Cause??? Are we EVER going to get any closer????

I find it more than somewhat discouraging that we, as a forum are not striving collectively to come closer to understanding what is causing this in all of us.
I continue to work with Dr Moschini here in Massa, Italy, who begs me to be patient, but promises that the treatment I am undergoing - a combination of homeopathic remedies to address the underlying viruses (heliobacter pylori, Epstein Barr, citomeglovirus) and advanced stem cell therapy which he is obtaining through the German company Wala. I cannot report results yet, however I continue to be grateful and amazed that in the face of all odds (commerical!) this man continues, off the radar to genuinely try to cure people of this nightmare. He is also using a 'Mora' device as a diagnostic tool, about which I have written about previously.
I have been working with him since July, and I'm not 'there' yet, and maybe I never will be, and too cautious for now to attempt to proclaim cure/improvement. I will not hold back when that day comes.
If we can't focus on the causes of this, we will remain at the mercy of the ablationists and vitamin sellers....something has to work, right? In what combination? Why for me and not for you?
Where are we heading? And why is this forum no longer trying to move in the direction of understanding this illness, instead of band-aid 'solutions'.

Francesca,

Let us know when you have real evidence it works? .. we are all ears .. but one or two or even just a handful of anecdotal reports isn't likely to cut it. There would have to be some real solid extended evidence, not only in number of afibbers at various stages of the condition that experience either a complete long term 'cure' (much less likely) or even extended significant success, but short of a 'cure', by dramatically lessening breakthroughs and total AFIB burden over long periods of time.

Any consistent and repeatable benefits confirmed by clear and reliable data, beyond what is already acheivable that many have found works for a sustained period with our nutritional protocols, would be most welcome. However, its going to take some solid evidence to convince most of us who have looked under nearly every nook and cranny for just such a metabolic solution for decades. Good luck with your search!

Cheers!
Shannon

In recent years there has been a lot of research etiology of lone atrial fibrillation. However, the more we learn, the more we understand that underlying causes of AF are highly complex and heterogeneous. There have been several genetic mutations identified with early onset AF. For example, researchers have identified several mutations in acetylcholine-sensitive potassium channels in atrial myocites that are believed to be responsible for causes atrial electrical instability, resulting in creation of areas of functional re-entry that result in atrial fibrillation. Other genetic mutations result in excessive inflammatory response, which results in fibrosis, atrial enlargement and creates favorable substrate for AF. Furthermore, there have been several studies which indicate that myocarditis, caused by viral or bacterial infection, can be very arrhythmogenic, as it effects both the anatomic and autonomic substrates. Auto-immune reactions are also believe to play a role in a subset of patients with AF. Another area of research indicates that the age-related decline in autonomic nervous system leads to hyperactivity of cardiac intrinsic autonomic nervous system. In lay terms, if the signals from the brain to the heart become too 'weak', then the cardiac autonomic control centers (the ganglionated plexi) become hyperactive. This autonomic hyperactivity results in ectopic bursts from pulmonary veins (triggering atrial ectopic beats and atrial tachycardia) and results in creation of areas of heterogeneous conduction ('fibrillar myocardium') that maintains atrial fibrillation. Therefore, some researchers hypothesize that decline in extrinsic signalling from the vagosympathetic trunk leads to hyperactivity of the intrinsic cardiac autonomic system that results in PV ectopy and creation of areas of functional re-entry that initiate and maintain AF. The resulting atrial fibrillation leads to further anatomic and autonomic remodeling (AF begets AF), as the autonomic dysfunction triggered paroxysmal AF progresses into more anatomically based persistent AF.

In conclusion, we can say that AF is a condition which has complex, poorly understood and highly heterogeneous causes. It likely has a strong genetic component, especially for people with early onset lone AF. Cardiac inflammation, ion-channel mutations and autonomic dysfunction are probably the primary underlying causes in majority of people with lone AF. As the disease progresses, anatomic substrate (atrial fibrosis) becomes more important in maintenance of AF.

You ask a very good question:
"And why is this forum no longer trying to move in the direction of understanding this illness, instead of band-aid 'solutions?"

My answer to you is how do you expect people on this forum to try to understand this illness, if best electrophysiologists on this planet are still far from having a complete understanding of it? What tools do we have that can unable us to understand AF? We all have this condition, however the underlying causes of our AFs can be completely different. As Hans Larsen said we are all experiments of one. How can we even begin to move towards understanding this disease?

It seems that many people on this forum are under an impression that electrolyte and amino-acid deficiencies are the primary causes behind lone AF. I do not agree with this hypothesis. While magnesium and potassium deficiencies are common in North American population, effecting close to 50% of the population by some estimates, they can not explain why only 0.1% under the age of 55 have AF. Even if that 0.1% are highly deficient in electrolytes, what about the other 49.9% of people with deficiencies that do not have AF? While it is probably true that electrolyte deficiencies can contribute to AF in people with genetic predisposition to this disease, I do not believe that they are a primary underlying cause in majority of AFibbers. I believe that Mg and K supplements help some due to their anti-arrhythmic effects, not only because we replenishing our depleted intracellular supplies. Various supplementation routines might slow down the progression of the disease, but I believe it is highly unreasonable to expect a cure from such a regiment. Nobody knows what caused your AFib in particular and more importantly we do not have any reliable means to answer that question. One thing we should not do is to look for a common denominator that caused our AF, as this denominator might not exist.



Edited 1 time(s). Last edit at 11/03/2012 10:25PM by Namor.

Francesca,

I agree with your first and last sentence, and think that their ARE things an actual paroxysmal AF sufferer CAN do, particularly in terms of "on the spot", "hour to hour" experimentation which labs cannot do or are not doing. See my suggestion in the current thread: "Cardymeter Session in Conference Room", for people to monitor their saliva Calcium with a meter, just like the Potassium meter which has proven very useful.

"...even just a handful of anecdotal reports isn't likely to cut it...."

Shannon. i have a question for you. Is 50 people still a handful? That is how many people were listed in conf. rm. session 61, where people who had controlled or eliminated their afib episodes by means other than surgery or heart drugs were listed. At that time there were about that many more still further back in the archives, but Hans asked me to stop there because we were running out of room. My understanding of computers is faulty so i cannot explain how the internet can run out of room, but Hans is still with us so he can explain that if you are curious about that detail.

Shannon. if 50 is still a handful, please tell me what number would no longer qualify to be called a handful, and i think that number of List members can be pulled from the archives either from before the date of the oldest ones in session 61 or from the people Listed more recently, since session 61 ended. We would have to get another volunteer to do the actual extracting from the archives, because i am growing progressively more decrepit as time goes on and especially with the new forum format, i am finding it much more difficult to use the archives. I am just guessing here, but i think 200 might be an approximate number.

Shannon or Researcher or anybody who can respond to this, can a report made here as the
Listmembers have done ever be called anything but an anecdote? This word bothers me. It seems to me to have connotations of "story" rather than of a factual report, which is what i take these posts from correspondents here to be.

PeggyM

Namur

Thank you for your very useful and interesting post. Seems to me that looking for a single cause for lone AF is like looking for a single cause for stomach pain - it can be many things, singly or in combination. Supplementation is worth trying, and if it works for you that's great, but for many (most?) people it doesn't. Your point about 0.1% of people under 55 having LAF when close to 50% of them are deficient in electrolytes is particularly telling.

Ablation may not be a cure in the sense that it removes the root cause but it is the best 'fix' that we have at the moment. If I had gangrene in my foot I would have to accept that amputation was the best available treatment and would save my life even though it was not a cure.

Gill

PeggyM,
Anecdotal generally means reporting in an unscientific fashion, which is how personal accounts are usually presented. The word does not mean that such accounts are not valuable, it simply means they are not done in the form of a study (or other format) with scientific controls.
Tom

Hi Namor,

In your reply you said

" the age-related decline in autonomic nervous system leads to hyperactivity of cardiac intrinsic autonomic nervous system. In lay terms, if the signals from the brain to the heart become too 'weak', then the cardiac autonomic control centers (the ganglionated plexi) become hyperactive"

I ask from all, how can we improve these weak signals?
Is there a supplement we can take, is there a food that would help?

Colin

PS. Just found this

digestion is controlled by the autonomic nervous system. When the ANS malfunctions, the "victim" commonly develops gastrointestinal problems.

Every Afibber I know has a digestion problem.



Edited 3 time(s). Last edit at 11/04/2012 06:57PM by colindo.

I discovered this site eight years ago and must say it has provided me with a wealth of information as well as hope. If you go and talk to your cardiologist, do you leave there feeling optimistic about your afib issues? More than likely you leave with a prescription in your pocket for yet another toxic drug. Countless afibbers have been helped by suggestions on this forum. We all know that supplementing, diet change, avoiding triggers etc. can make a huge difference. I would never say that this forum is not moving in the right direction. Unfortunately, right now the closest thing to a cure is ablation. I guess we can call everything else we try a band - aid solution because afib is not an easy fix. Afib has such varying degrees of symptoms and severity, and what works for one person may not work for others.

I think the future for afib treatment is very exciting and promising. There will never be a wonder drug that cures afib, but the continuing advancement with ablation procedures offers real hope. In the mean time, I want to thank and encourage the people on this board who spend so much time and effort into offering the rest of us these so called band - aid solutions.

Cheers to everyone,
Lou

The only hope we have to get closer to a "cure" right now is the work of Dr Narayan with FIRM ablations who actually targets the 2 or 3 rotors that sustain afib.
Everything else has just been a ban-aid till now with some people actually "cured" with current ablation strategy. A Mt Sinai EP and the top Cleveland Clinic EP's also echo the same thing anybody that tells you right now with current ablations we have a cure is full of it.



Edited 1 time(s). Last edit at 11/04/2012 07:00PM by McHale.

Colindo:

I have had episodes of AF, starting in 1996, I have never had digestion problems and still don't. I get AF episodes maybe once every 3 months or so, I do take magnesium which I believes has helped me the most even though I am still on the low end in my labs.

Liz

McHale,

FIRM may well be a great break-through, but we have absolutely no data to support the assumption that it will be a long-term "cure".

Hans

Excellent overview of what we know to date Namur,

Which as you imply only underlines how complex and challenging it would be to drill down to one core 'cause' if there even is just one. The genetic predisposition no doubt is a strong driver for many of us, but to what degree and how that manifests in each of us that may have such unhandy genes, depends on a myriad of variables itself as you also discuss.

And PeggyM, I get the impression from your posts above that you somehow take it from what I have written that I am actually down on nutritional attempts to deal with this?? If that is your impression, then you must have missed or only skimmed over too quickly the vast majority of my postings on afibbers.com over the years!

I was speaking SPECIFICALLY about the European doctor in question that Francesca mentioned seeing who is trying, laudably enough I am sure, for a combined Homeopathic/stem cell treatment AFIB 'cure'. I'm all for such experiments and my main caution was solely to suggest he will need more than a handful of personal reports and ones that demostrate long-term success that his method is bringing before we can get too excited about it being anything close to a real cure.Also we would want to have some evidence that it is better than what many here have already found some modest relief in some cases, to excellent relief imn other cases through the Strategy and other modalities.

Thus, it really seems you must have truly misread my post entirely. As far 'cures' go, that word implies a real long term fix which eliminates AFIB such that even if we stopped the protocol that apparently was the agent of the 'cure', there would still be no more likelihood of us having any more episodes of AFIB than there was in our youth when we could never have even dreamed of such a condition, and regardless of what we ate or what supplements we took. That to me is a real cure.

But I'm 100% in favor of anything with a valid and repeatable efficiacy for the majority of the people who suffer with AFIB.
Shannon

Namor (which is Roman in reverse) writes:

"In conclusion, we can say that AF is a condition which has complex, poorly understood and highly heterogeneous causes. It likely has a strong genetic component, especially for people with early onset lone AF. Cardiac inflammation, ion-channel mutations and autonomic dysfunction are probably the primary underlying causes in majority of people with lone AF. As the disease progresses, anatomic substrate (atrial fibrosis) becomes more important in maintenance of AF. "

It's a very sobering and rational statement and is a great summary of where the medical community, and we as afibbers, stand in dealing with this disease. Wouldn't it be great if there was a pill or supplement to take that would knock this out and then you get your life back? Unless you are one of the genetically lucky few that is not how it works. Multiple CAs, or surgery, end up being the "cure" for many although perhaps "remission" would be a better term following a successful procedure.

Francesca's stem cell treatment is a fascinating new angle- please keep us informed on that.

EB

Regarding Namor's statistic that only 0.1% of people under the age of 55 have AFib, I'd like to know exactly what he means by that? Does this statistic apply to people ages 0 to 54, or to ages 50-54? Do people ages 50-54 have a rate of AFib a lot higher than 0.1%? I would just like to have this clarified. Because if the actual occurrence of AFib in people ages 50-54 is just 0.1%, then it is likely that nutritional approaches or lifestyle changes will be a waste of time, because there is probably a lot of people in that age group in the U.S. who have nutritional deficiencies due to the poor American diet, plus a much larger percentage than that participate in endurance sports.

I'd also like to mention a study I found when I went out looking for information on endurance exercise and AFib, where the members of an Olympic level cross-country ski team was checked in their 50's and 30% of them had lone AFib. That's a very large number (not like 3% or 1%). I wish I had the Internet link to that study to post here. Other studies I found had similar high percentages of endurance athletes getting AFib as they got into their 50's. My guess is that endurance exercise over the long term might cause autonomic dysfunction.

I need to answer these questions for myself, to determine whether it's worth my time and energy to pursue alternative remedies, or to just go ahead and get an ablation, and don't bother to change my diet or cut back on endurance exercise.

Dianne,

You may be interested in my report Endurance Exercise: Is it worth it? [afibbers.org]

Hans

Diane,

Be careful about that loose talk of not paying attention to diet; you might get accused of heresy on this website. ;-)

As I recall, you were taking flecainide, if it reduces your afib burden without negative side effects, that might be a long term solution for you. In some cases flecainide reduces exercise tolerance, although it didn't for me.

I am familar with the cross country skier study that you refer to (I couldn't locate it with a quick search) but there isn't any question about the link between long term aerobic exercise and afib.

Regarding detraining- I detained, although I am still doing what would qualify as aerobic training 20 min/day 4 days/week. The difference is that my pulse is in the 130s rather than the 160s during the training. On other websites I have read posts of individuals continuing to train while in afib; those guys are OCD maniacs IMO.

You will know when your afib burden gets to the point that it is time for the procedure, and one significant factor is when you are tired of having it hang over your head.

You sound like the sort of person who identifies closely with your training level- you should not have to abandon that due to afib. The trick is to find a balance between a fitness level that keeps you feeling good versus a fitness level that exacerbates your afib.

EB

Diane98683 Wrote:
-------------------------------------------------------
. My guess is that
> endurance exercise over the long term might cause
> autonomic dysfunction.
>
> I need to answer these questions for myself, to
> determine whether it's worth my time and energy to
> pursue alternative remedies, or to just go ahead
> and get an ablation, and don't bother to change my
> diet or cut back on endurance exercise.

Diane,
That's my guess too, as my afib began in my early 50's and is definitely tied to autonomic dysfunction. I too have been an endurance player. But...
as I have noticed even following my ablation of 20 days ago, diet is still key to keeping the heart stable. If I do not consume a lot of potassium-rich foods, I have many more PVC's, more heart pain, and a general instability that has twice led to post-ablation tachy. Will the ablation procedure eventually "cure" that need? - I doubt it.

For some of us, discovering and establishing a diet (with or without supplements) that mitigates afib (or heart instability in general) prior to an ablation may prove beneficial afterwards - it certainly seems to be a key element for stability during my ablation recovery period.

Tom

Tom, Dianne, et al,
"as I have noticed even following my ablation of 20 days ago, diet is still key to keeping the heart stable. If I do not consume a lot of potassium-rich foods, I have many more PVC's, more heart pain, and a general instability that has twice led to post-ablation tachy. Will the ablation procedure eventually "cure" that need? - I doubt it. "
And well you should doubt that. The body will not be cured of needing appropriate nutrition in order to operate, just as cars are not cured of needing gasoline in order to run. We need to eat food that contains the kind of fuel we operate on, like the car needs gasoline. Our fuel must contain the trace elements used by our bodies for normal operations, such as a normal heartbeat. Or else we must, as a stopgap, provide these necessary trace elements in capsule, pill, or powder form. Either way these items must be provided or abnormal operations will ensue.

PeggyM

Tom B,

You are spot on- but remember, you are only 20 days out. In 6 months, after you have healed, hopefully your successful ablation will result in your heart being less susceptable to triggers. That post-ablation "tachy" is probably flutter and it just takes time to resolve the inflammation (at least that is what my surgeon told me after my procedure).

EB

That's my thinking as well. Of course, it's best to follow a good diet, for other health reasons, but if you have a healthy heart, these triggers we talk about here won't cause AFib. Once our AFib is truely cured, none of these food triggers should cause it (except for maybe alcohol). If we have to keep watching for triggers post ablation, that means that the ablation hasn't really cured us.

There were several large epidemiological studies which evaluated the prevalence of AF in adult population. Prevalence increased from 0.1% among adults younger than 55 years (0-55 years) to 9.0% in persons aged 80 years (80 to infinity) or older. Early onset lone atrial fibrillation is a rare disease. If the primary causes of AF were nutritional deficiencies, there would be a lone-AF epidemic in third world countries. Such epidemic does not exist, rather AF is more common in developed nations were people have better nutrition. The association between AF, obesity and hypertension is stronger than the association between AF and electrolyte deficiencies.

It is very important to keep these basic facts in mind when analyzing the potential causes of atrial fibrillation. There are millions of people who do not consume enough Mg, K+, Taurine, etc on a daily basis and never develop AF. As a matter of fact the vast majority of people who have nutritional deficiencies do not develop AF. Even if most Afibers are Mg and K deficient, it does not mean that there AF was caused by these deficincies. I am not saying that keeping a proper electrolyte balance is not good for Afibers, as I think it is essential, however I do not think that electrolyte imbalance caused by poor nutrition is the root cause for majority of people with AF.

References:

Go AS, Hylek EM, Phillips KA, et al. Prevalence of Diagnosed Atrial Fibrillation in Adults: National Implications for Rhythm Management and Stroke Prevention: the AnTicoagulation and Risk Factors In Atrial Fibrillation (ATRIA) Study. JAMA. 2001;285(18):2370-2375. doi:10.1001/jama.285.18.2370.



Edited 1 time(s). Last edit at 11/05/2012 08:02PM by Namor.

Diane98683 Wrote:
-------------------------------------------------------
. Once our AFib
> is truely cured, none of these food triggers
> should cause it (except for maybe alcohol). If we
> have to keep watching for triggers post ablation,
> that means that the ablation hasn't really cured
> us.
As I understand it, PVI ablations are essentially a means to isolate irritable foci from conductive atrial pathways by destroying conductive tissue with heat. One has to assume that an ablation is not a cure as long as the process that created those irritable foci still exists. The ablation is a reprieve... a way to extend our lives. Irritable foci don't spring up overnight, they multiply as time goes on - If one indulges in foods and drink that have been triggers in the past, they may still be feeding the process that got them to the point of afib to begin with. How can any of us know what the pathways to afib for each of our unique physical makeups are? Irritable foci can appear in virtually all parts of the heart...so why rely only on an ablation that has isolated only those formed thus far?

Afib is but one element of heart instability, PVC's are a whole other animal, yet may be tied to afib in some situations. As Hans noted in an earlier post, potassium is often under-utilized in persons with PVC's - When my heart is unusually unstable, I can get multi-focal PVC's (I have an EKG machine) and not have problems with afib. Other times, PVC's indicate afib is likely lurking...the "ramp-up" to afib is complex to say the least and likely not the same for many of us.

A PVI ablation does not extend into the ventricles where PVC's occur, yet PVC's may indicate the entire heart's (all chambers) muscle function is impaired to some degree. After all, a PVC is another irritable focus firing due to some stimulant, lack of oxygen or nutrient. Just musing...at a primary level, diet can obviously affect atrial function. and though having nothing to do with previous discrete afib triggers, may affect the heart's ionic pathways during the post-ablation healing process in such a way that ablation success may be greatly affected. As noted by Fivebox, the blanking period is one of healing during inflammation, but can it also be a time when dietary balance can possibly deter incorrect pathways while enhancing the correct metabolic pathways, thus affecting long-term outcome? Hans has provided some studies regarding ablation success and the number and duration of afib incidents during the blanking period. Bottom line, the fewer and shorter the arrhythmias, the more likely the success...so if diet stabilizes the heart (as in my case so far) it may be an important element in achieving ablation long-term success. Many EP's prescribe both rhythm and rate control drugs during the blanking period which may improve final outcomes - so why not use diet (and or supplements) to do the same thing?

Shannon, i am oversensitive on this subject and have over-reacted to your post. Please allow me to apologise.

PeggyM

Namor,

Certainly there is a genetic component. Eight years ago, when I was working with my primary care physician to monitor and balance my electrolytes (he was following my direction for testing & etc), he commented, "I spend my day putting people into hypokalemia (with diuretics), why don't they all have afib. My response was genetics.

That being said, for many of us who are genetically prone to lone afib, electrolytes do make a big difference.

George

George N, I absolutely agree with you. There are many people who have severe hypokalemia and hypomagnesemia and never develop AF. However, if you are genetically predisposed to AF, or already have favorable autonomic and/or anatomic substrate, maintaining a proper electrolyte balance is essential. The point I am trying to make is that I do not believe that essential electrolyte and amino acid deficiencies are the root cause for development of AF and frequent ectopics in vast majority of cases. However, individuals with cardiac ANS dysfunction (cardiac dysautonomia) tend to be very sensitive to naturally occurring electrolyte fluctuations and minor deficiencies which commonly occur in the general population and do not cause any major rhythm abnormalities in the vast majority of people.



Edited 1 time(s). Last edit at 11/07/2012 12:11AM by Namor.

Diane98683 Wrote:
-------------------------------------------------------
> That's my thinking as well. Of course, it's best
> to follow a good diet, for other health reasons,
> but if you have a healthy heart, these triggers we
> talk about here won't cause AFib. Once our AFib
> is truely cured, none of these food triggers
> should cause it (except for maybe alcohol). If we
> have to keep watching for triggers post ablation,
> that means that the ablation hasn't really cured
> us.

Just curious, here, but why would alcohol be any different than any other trigger? Pre or Post Ablation. If what ever the trigger was Pre, and it no longer triggers AF, it's a success. If it still triggers AF, then it's not.

lisa
__________________________

So much of medicine is looking solely down the wrong end of the gun barrel, and that is really a pity for all of us---Shannon

Lisa - one of Shannon's posts offered this:

Shannon
Re: Alchohol in the blanking period
October 14, 2012 10:50PM IP/Host: ---.npg.sta.suddenlink.net

Dr. Natale warns strongly about drinking ANY alcohol after an ablation. Especially in the blanking period and for up to a good year or more at least until you know for sure you are stable and out the woods. In reality, any afibber that has required ablation should just swear off for good if they are smart about it at all.

A glass of wine on a special event might be okay after some time. But anyone drinking at all in those first 3 to 6 months and really first year after an extensive ablation are truly playing russian roulette with their ablation.

Dr.Natale told me in August after my LAA isolation ablation when we were discussing post-ablation triggers that about the onlky one he is really strong everyone avoiding is Alcohol.

Having seen first hand the effects of more ablation outcomes that he has performed than any other person on earth, I'd think he is a man worth listening too on the subject!

If you need to get loose and relaxed learn some breathing exercises/ some meditation or take a few Theanine or a small dose of Xanax or Ativan if need be for the time being.. just stay away from wine, beer and especially hard liquor. Some people seemingly get away with it ... for a while .. but it usually will catch up to most people who ignore this common-sense advice.

Shannon
[www.afibbers.org]

>
> Just curious, here, but why would alcohol be any
> different than any other trigger? Pre or Post
> Ablation. If what ever the trigger was Pre, and
> it no longer triggers AF, it's a success. If it
> still triggers AF, then it's not.

I don't think your definition of ablation success is in line with most medical observers.

I'll repeat what I've said before; an ablation simply isolates or destroys the foci that initiate afib, it does not prevent afib's recurrence if other foci become irritable later (burn breakthroughs aside). The ablation process isolates very few of the total number of foci cells that exist in the heart - any of which can cause atrial or ventricular arrhythmias. The average afib-free term following a successful ablation is something like 5-6 years. I suspect very much that the same set of circumstances that brought about the first afib presentation are likely diligently continuing to work to bring about yet another. If those circumstances include alchohol or any other trigger...or diet...or stress....or over-exertion..or high BP, etc...it seems the smart thing to do would be to mitigate what you CAN control so as to extend the ablation reprieve as long as possible. Why needlessly introduce stimulants or other detrimental factors to those still-healthy foci so that they may also begin to fail under such circumstances?

No ablation cures the process that led to afib in the first place.

Tom

Tom:

The only way to know would be to survey those who had an ablation and it appears to be successful--divide them into two groups, survey those that eat, drink whatever they want and the other group that watch what they eat, take supplements etc., what is the long term success rate of both groups. We are only assuming because we believe that taking supplements, eating correctly is the right course to prevent any occurances of AF, perhaps it is but is it?

Liz

No one has answered my question. Why is alcohol a different kind of trigger? Lots of opinions, no reasons. My question wasn't about introducing prior triggers during the blanking period.

lisa
__________________________

So much of medicine is looking solely down the wrong end of the gun barrel, and that is really a pity for all of us---Shannon

"Lots of opinions, no reasons."

Opinions are all we have to offer, Lisa. Informed opinions, to be sure, but opinions none the less. My own opinion about alcohol as a trigger is that it is not different from other triggers .Alcohol does not seem to act as a trigger for me personally, but it sure does for a lot of other afibbers.

I think the reason that afibbers can be so different from one another is that afib is not a disease entity in itself, but is a symptom which can be caused by many different disease processes and sub optimal nutrition states, most of which are even now poorly understood if understood at all. Also several of these poorly understood processes and conditions can interact together in the same poor suffering afibber. Personally i do not think we will ever isolate one thing as a cause for all afib, because there is not one cause, but many. That is, of course, another opinion.

People here have often succeeded in getting control of their own afib situations, but not everybody has found success by using these same methods. We cannot tell why so far, but doubtless as time goes on we will find out more about it.

PeggyM

Lisa - fundamentally, alcohol acts as a diuretic and flushes out essential heart electrolytes, especially magnesium.
Additionally, in some individuals, there is a quasi- or pseudo-reaction to alcohol acting like a sugar and producing hypoglycemic symptoms... and the rush of adrenaline that accompanies hypoglycemia. This could be exacerbated by consuming alcohol on an empty stomach with the previous meal many hours prior.

As we know, for some, alcohol isn't a trigger... but as long as EPs such as Dr. Natale note that it is a persistent source of trouble, it makes sense that there is some depletion or interference mechanism from alcohol’s effects on rhythmicity and on conductivity in the heart

I recall the magnesium researchers, the Alturas, (B.M. and B.T) had published reports..at least one... about alcohol's effect on magnesium depletion and the consequences for the heart and brain. If you are motivated, you may find it in Paul Mason's Magnesium Water website or by Googling Altura, magnesium and alcohol. [www.mgwater.com]

Jackie

Lisa,

Alcohol affects the autonomic nervous system and is associated with an increased vagal response. So it may be particularly detrimental for vagal afibbers [www.ncbi.nlm.nih.gov]. LAFS III found that alcohol was a trigger for 33% of vagal afibbers and 19% of adrenergic afibbers.

The extent to which you need to avoid pre-ablation triggers after an ablation depends on whether the procedure was a success or not. If it was, only 5% definitely had to avoid previous triggers while 16% were uncertain whether they had to as per the 2008 ablation/maze survey [afibbers.org]. Trigger avoidance during the blanking period is however, a very good idea.

Hans