Hi!

Hi All!
I'm new to the forum. My journey started five years ago with first, an episode of SVT with ectopics and a year or two later, a two and a half hour episode of a-fib. After a couple more years I started having nightly sinus tachycardia/atrial tachycardia episodes (about 3 am), which eventually were more a-fib. They usually go away when I get up.
This past week I had an EP study. I was hoping for some type of re-entrant tachycardia that degraded to a-fib so it would be 100% curable, but it was just a-fib, so more complex to fix. I was told I went into it easily and I had to be shocked three separate times. My doctor didn't do an ablation. I was bummed! They put me on Flecainide and I don't like it at all. I woke up last night short of breath and a regular heart rate of 120 bpm.
I'm appreciative of the support this site offers.

Hi, so what did you mean by you had to be shocked 3 times? And why didn't your doctor do an ablation? I hope you get some more clarity on that. Do you take magnesium? Cindy

Sounds like the Dr. intentionally put her into AFIB, as part of the EP Study, thus the need the Shock the Heart back into NSR after completing the Study.

I had side effects that subsided after the first week from Flecainide. It made me irritable and aggressive at times. What dosage are you on? Maybe you need to start at a lower dose?

Welcome Libby,

I'm glad your doc did not do an AFIB ablation right away so early in the process of your discovery you had an atrial arrhythmia. At least this way, giving you the chance then to learn more about the whole process and perhaps make a better choice for who to handle this very highly skilled-dependent procedure in which one's total future history experience with AFIB is so often mediated and influenced so directly and significantly based on that one most important choice you make in this whole game! ... And that is ... who you chose to handle and guide the catheters inside your heart for those critical few hours.

This is NOT a procedure you want relagated to a local hospital cardio or EP as a rule of thumb. Occasionally you might land a good ablationist, but its very much a crap shoot going about it that way.

SVT (supra-ventricular tachycardia) ... especially the type that degrades into AFIB ... very much predisposes the person to develop ongoing full blown AFIB long term, until and unless it is dealt with effectively via re-establishment of durable NSR ... by what ever means or combination of means that goal is brought about.

The same is largely true with CTI-Flutter (Cavo-Tricuspid Isthmus Flutter), otherwise known as 'common' or 'typical' Right Atrial Flutter. This CTI-Flutter is a frequently detected high speed RA tachy-arrhythmia that generally evolves directly over time into AFIB itself, and mostly via genetic influence. In fact, CTI Flutter is really an early manifestation of AFIB .. more like a precursor to AFIB.

Also, those who develop SVT that degrades into AFIB, as well as those with CTI Flutter, both groups of patients thus almost invariably go on to full-blown AFIB as well. In fact, Atrial Flutter is already a manifestation of AFIB in essence.

Leading many front line EP ablation experts to suggest to their patients who first come to them with either this kind of SVT that degrades into AFIB, or CTI-Flutter, that they should consider undergoing not only the rather straight-forward CTI Flutter or SVT ablation in the RA, but add in a full PVI as well as a kind of prophylactic to possibly prevent the evolution of these early stage 'canary in the coal mine' arrhythmias from morphing into full-on AFIB as well, as it almost inevitably will.
Hopefully, thereby, killing two birds with one stone.

While having a stand-alone SVT or CTI-Flutter ablation first, which are both only in the right atria alone, and present very well-defined anatomical-only lesion sets, is certainly an okay step to take. Especially, if the person suffers from frequent bouts of high speed tachy-arrhythmia by either of these names. Nevertheless, it still behooves one to discuss these options with a highly experienced ablation EP to more methodically plan out your best course of action, including discussing when might be the best time to include any left atrial work to possibly stave off AFIB altogether.

Best wishes Libby,
Shannon



Edited 3 time(s). Last edit at 09/04/2017 12:47PM by Shannon.

During the EP study they were trying to see what rhythms I'd go into. A-fib happened 3 times and they shocked me to get me out of it.

Thanks! I'm on 100 mg twice a day. My rhythm seems better this week. I've felt more short of breath going up stairs lately and have some visual stuff at times. Not sure how to describe. A little blurriness at times or sometimes it's like I see peripheral movement when I move. It might have to do with the lighting. I don't notice it all the time.

Thank you Shannon. Lots of good information! It feels so complex. Do you think in the general EP study the doc would weed out if the a-fib is from the right or left side? I read his note. I don't think he went into the left side. There were two catheters in the right and one in the coronary sinus.
I do agree about timing and having the right doc. I did research on docs, but I'm feeling unsure now. Does anyone have any recommendations for the Minneapolis area? I work in the medical field and had a patient that had an ablation for a-fib using cryoablation instead of heat. He said the doctor said he had better luck with this. Does anyone here have an opinion?
Thanks so much for your help everyone!

Quote
libby
Thank you Shannon. Lots of good information! It feels so complex. Do you think in the general EP study the doc would weed out if the a-fib is from the right or left side? I read his note. I don't think he went into the left side. There were two catheters in the right and one in the coronary sinus.

He didn't go to the left side. You would have seen mention of a septal puncture if he had.

Quote

I do agree about timing and having the right doc. I did research on docs, but I'm feeling unsure now. Does anyone have any recommendations for the Minneapolis area? I work in the medical field and had a patient that had an ablation for a-fib using cryoablation instead of heat. He said the doctor said he had better luck with this. Does anyone here have an opinion?

Sure, I've got lots of opinions. :-) My first opinion would be that if you're going to pursue the ablation route that you need to find the absolute best ablationist you can. If it means travel, so be it. It's easily worth a thousand bucks of travel costs one time to avoid years of failure and $10s of thousands in added medical expenses. (I've had more than a couple of ablations, so this is a long, bitter lesson I know all too well.)

Cryo vs RF is another really good question. I'm not well versed in cryo but I know it can be effective in the right hands with the right patient. The biggest problem with cryo might be the small number of EPs performing cryos. There's only so much experience out there as compared to RF.



Edited 1 time(s). Last edit at 08/31/2017 01:15AM by Carey.

I'm so sorry you've had some hard learning. It's traumatic. Thank you for sharing your expertise!
I'd be ok to travel somewhere. What kind of questions would you ask when researching doctors? I tried to ask about how many a-fib ablations were done per year and success rates, but the lady on the phone scoffed at me saying how important and well thought of the particular doc was. She basically said she didn't know, but that can't be. Someone keeps track of that. He did have all the right credentialing stuff, which doesn't necessarily mean he's good, just that he jumped through the right hoops. I also looked at reviews online.

Quote
libby
I'd be ok to travel somewhere. What kind of questions would you ask when researching doctors? I tried to ask about how many a-fib ablations were done per year and success rates, but the lady on the phone scoffed at me saying how important and well thought of the particular doc was. She basically said she didn't know, but that can't be.

That kind of response would get him stricken off my list right away. It's a perfectly valid question and they should be able to provide an answer.

My favorite resource for finding out how many procedures an EP has done is Medicare data. Find the EP you're interested in and then scroll down and look for entries for "Destruction of tissue of right or left upper heart chamber via catheter for treatment of abnormal heart rhythm". Those are the actual ablations they've performed. It's important to look for that entry because many EPs do a lot of procedures other than afib ablations (pacemaker insertions and replacements, for example).

Only 2012 through 2014 data is currently available, but that should be good enough to give you a pretty good idea how experienced someone is. For example, if you look up Andrea Natale, you'll find that he did 196 ablations in 2014.

Thank you!!

I've been reading online, trying to understand a root cause for lone a-fib. I see suggestions of it being a mitochondrial disorder, B1 deficiency, hyperhomocysteinemia or specific forms of B6 deficiency (whatever that means). That lead me to the mitochondrial diet, methylation defects, lifestyle (sleep, stress, inflammation...)....
Some people seem to say they are living without meds and in normal rhythm after addressing the above. Does anyone have experience with this?
What is the success rate of a-fib ablation in good hands? Any stories out there of successful procedures?

Libby - There is an archived section titled Conference Room Sessions and one is titled, The List, which is a collection of success stories of afibbers who managed to control their arrhythmia by various methods that did not involved ablation.
It's dated, so we don't know how long their successes lasted, but it does give readers an idea of the variety of contributing factors that can cause arrhythmia and also various things that can help reduce them ... even if just temporary.[www.afibbers.org]

Finding the root cause of Afib has been one of my goals, too. There is a study that indicates a gene flaw that prevents proper absorption and therefore, limited utilization of magnesium which definitely is one of the critical electrolytes involved with maintaining normal sinus rhythm (NSR). And we now know that we can often influence whether or not the gene defect is able to 'express' or not, thanks to the field of Epigenetics, so it makes sense to consider that some of us may have success with overcoming the genetics factor. Here's a search result with some of these discussions.
[www.afibbers.org]

Cardiac Fibrosis or Remodeling also contributes to arrhythmia. Here's a CR session on that topic [www.afibbers.org]

Keep in mind, the links I've provided are just for background and were collected some years back.

The current forum has many posts by GeorgeN who has managed his arrhythmia by special eating plans and is definitely worth calling up by using the Advanced Search method at this link [www.afibbers.org]

As for ablation success, definitely, it depends on the knowledge, skill and experience of the EP. I've had three ablations by Dr. Natale for which I am most grateful. The first was in 2003 which lasted for 11 years. Then I developed a-flutter and had the second ablation in 2014 followed by a touch up in 2015.

Hope this helps as a start to your research.

Best to you,
Jackie

Jackie,
Thank you so, so much!!
One more question. I know my chamber sizes are normal. I think that means there's no remodeling? I'm guessing that fibrosis is not seen? Is that correct?
I so appreciate the information you've provided!
Wishing you the best,
Libby

The big question is whether "lone" afib is really lone afib. In other words, are those of us diagnosed as lone affibers really free of structural heart disease or is afib itself a type of structural heart disease? The thinking is leaning in that direction these days, with the term atrial myopathy being used. Personally, I think almost without doubt this will be found to be the case in the end. I think afib is primarily a genetic disease, enhanced or inhibited by lifestyle, and it has a pathological cellular basis. The cure will be via gene therapy, but unfortunately only the youngest ones here will benefit from it.

Your normal atria size is good prognostic indicator. The degree to which you might have fibrotic changes is unknown unless someone does a delayed enhancement MRI. Anyway, things like atrial size and fibrosis are signs of the disease, not causes. It's good if they're absent just because it improves outlook, but otherwise they're just kind of "nice to know" things.

As for ablations, figure 60-70% success with paroxsymal afib by the average EP. If you stop and think about it, those are pretty poor numbers. A 40% chance of failure? Really? That's not good. With ablations, my advice is to head to the most experienced ablationist you can find regardless of distance. Experience means everything with these procedures. In other words, don't do what I did (just completed ablation #6, my first with Natale, who I should have had do #1, in which case I wouldn't be on #6).

Carey - Cardiac Fibrosis can interfere with the electrical pathway conductivity mechanisms and definitely does cause arrhythmia.

Refer to CR Session 24 Cardiac Fibrotic Remodeling – The Role of Fibrosis in LAF which quotes David VanWagoner, PhD, Lerner Research Institute of the Cleveland Clinic Foundation. Excerpts taken from his papers and presentations.

Jackie

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Jackie
Carey - Cardiac Fibrosis can interfere with the electrical pathway conductivity mechanisms and definitely does cause arrhythmia.

I understand that, but what causes the fibrosis? That's the point. Fibrosis is a result of disease, not disease in and of itself.

I had Disseminated Histoplasmosis in my 20's (I'm 59 now). I had bigeminy at times then. I've heard it can involve conduction. I'm not sure if that could have contributed. But, my Dad has a-fib and so does one of his brothers.
Dr Natale sounds awesome! Is it hard to get into him?
I guess I'll dink around with the meds and lifestyle changes a little longer. What's the best timing for ablation? Before chambers stretch out and while it's still intermittent.

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libby
I had Disseminated Histoplasmosis in my 20's (I'm 59 now). I had bigeminy at times then. I've heard it can involve conduction. I'm not sure if that could have contributed. But, my Dad has a-fib and so does one of his brothers.
Dr Natale sounds awesome! Is it hard to get into him?
I guess I'll dink around with the meds and lifestyle changes a little longer. What's the best timing for ablation? Before chambers stretch out and while it's still intermittent.

You should expect it to take several months to get in to see Natale. I made first contact last April and ended up with a late August appointment, so if you call tomorrow you're probably looking at a January/February appointment.

When it comes to ablations, the sooner the better is the rule. There is nothing to be gained by delay, and there are things to be lost. Delay means more time in afib, which means more potential for remodeling, atrial enlargement, and all the other negatives that go with afib. After dealing with this beast for 15 years and six ablations, I cannot recommend strongly enough that you pick up the phone tomorrow morning and make it so.

Carey You said: I understand that, but what causes the fibrosis?

The cause of fibrosis - from William Wong’s report, "Fibrosis… The enemy of life"… lack of fibrinolytic enzymes. While he does not focus on fibrosis in the heart, the association is obvious. He says that around age 27 we start producing less of these important, protective enzymes.

In CR 24, the various speculations for what promotes formation of fibrosis is outlined.

William Rowe MD – reports on endurance runner Sy Mah and the unremitting stress from extreme exercise observation (see below) and also David Van Wagoner’s 2013 paper [www.ncbi.nlm.nih.gov] mentions fibrosis 26 times.

Fundamentally, it would be logical to say it’s a collective of ROS (oxidative stress) from free radical damage as occurs in heavy, prolonged exercise.. which allows the oxidative stress damage to occur and the fibrosis is a response of that…. and in the presence of magnesium deficiency. Plus, managing the effects of ROS by optimizing both the fibrinolytic enzymes and abundant anti-oxidants.

[www.totalityofbeing.com]

[www.femsinspace.com]

Dr. Rowe published in LANCET that extraordinary unremitting endurance exercise can injure a perfectly normal heart


Mayo Clinic [www.ncbi.nlm.nih.gov]
Abstract
A routine of regular exercise is highly effective for prevention and treatment of many common chronic diseases and improves cardiovascular (CV) health and longevity. However, long-term excessive endurance exercise may induce pathologic structural remodeling of the heart and large arteries. Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias. Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening. However, this concept is still hypothetical and there is some inconsistency in the reported findings. Furthermore, lifelong vigorous exercisers generally have low mortality rates and excellent functional capacity. Notwithstanding, the hypothesis that long-term excessive endurance exercise may induce adverse CV remodeling warrants further investigation to identify at-risk individuals and formulate physical fitness regimens for conferring optimal CV health and longevity.

Dr. Rowe on Mah’s heart autopsy… mentions fibrosis.
[clinmedjournals.org]

Jackie

Thanks Carey!
Thanks all! Great website with great information!

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Jackie
Dr. Rowe published in LANCET that extraordinary unremitting endurance exercise can injure a perfectly normal heart

Okay, sure, maybe we understand a little bit about what causes fibrosis in a small percentage of afib patients. But the majority who are not endurance athletes remain unexplained, and they're the much more interesting question, especially the ones who lack all the usual risk factors like obesity, diabetes, CAD, HF, smoking, etc. What's to explain their fibrosis and afib? You're not going to find the answer in existing research because the folks doing the research don't know yet. They just know they suspect an atrial myopathy that has not yet been identified.

Personally, I think the answer is genetics. After all, most endurance athletes don't get afib, and most obese people with diabetes who smoke don't either. No explanation that points to any of those things can be a complete answer. I also think the ultimate cure for afib will be gene therapy. Unfortunately, I also think only the very youngest here will live long enough to see that come to fruition in the form of effective treatments.

Carey:

I have been saying that for years, I too believe that our genes are mainly to blame for our AF., my mother had AF. I know many people that are overweight, smoke, bad diets they don't take Mag. or Potassium, yet they do not have AF.

Liz

As we have noted in past explorations of fibrosis and its undeniably close relationship/association with many forms or stages of AFIB, most respected AFIB researchers are careful not to list Fibrosis as a 'primal 'cause' of AFIB. Nevertheless, in the same breath they will underscore the observation that fibrotic changes to the atrial substrate is often a very strong contributor to the milieu of interconnected ... and so far not completely understood ... combined factors that help sustain AFIB and often contribute to its progression.

The degree of fibrotic changes manifest in any given Afibber is also strongly mediated by genetics, with some folks showing very little to no fibrotic changes in the atria even a decade or more of active AFIB, while a majority of Afibbers will show a notable progression in fibrotic substrate changes to the atria more or less in sync with the progression of their condition toward greater persistence. But the fact that even some LSPAF patients reveal little to no fibrotic changes throws a significant monkey-wrench into the theory that fibrosis is THE core primal cause of AFIB and that thus reducing fibrosis will result consistently in a corresponding reduction in AFIB burden.

Carey, your question above on whether the term 'Lone AFIB' is even applicable any longer in a time now with greater detection and understanding of more subtle forms of vascular and structural CVD issues that only in recent years were even detectable, is well taken.

In issue 139 of The AFIB Report, I led off with a summary of a cogent editorial about this same topic that our readers can find here by this title .... Lone AFIB: Is There a Rationale (Still)? that I think many of you will find interesting.

After writing this summary in issue 139 of the newsletter, I removed the word 'Lone' ( as in 'Lone AFIB') from the original title of our website to reflect the all-inclusive nature of AFIB that we address on this website and forum and always truly have.

Also, the issue of Fibrosis and its significant role in the progression of AFIB in the vast majority of cases I discussed on page 5 of: Issue 140 of The AFIB Report .

The following is the excerpt from page 5 of issue 140 regarding Fibrosis and its very strong association with progression of AFIB, especially in persistent and LSPAF evolution of the condition, but which falls significantly short of a true 'core causal' relationship to AFIB genesis across the board.

Fibrosis

Without question, the development of cardiac fibrosis has a strong association with AFIB and its
progression. Such increases in fibrotic changes are often a reflection of structural remodeling which
tends to expand the greater one’s cumulative AFIB burden.

However, the idea that fibrosis is ‘the’ core cause of AFIB doesn’t hold much water now with increased
understanding of the disease process. The degree of fibrosis is strongly mediated by genetic
predisposition, and not solely by length of time with the disease or overall AFIB burden.

Some long standing persistent AFIB patients who lack the genetic tendency to for laying down fibrotic
scarring, may have very little fibrotic burden even after many years of AFIB. While even short timer’s in
the first year or two of paroxysmal AFIB episodes can demonstrate substantial fibrosis. These are
exceptions, not the rule, to be sure, yet indicate a heterogeneous association of fibrosis with AFIB.
Renowned AFIB researcher Dr. Jose (Pepe) Jalife of University of Michigan, and pioneer of the ‘rotors
as drivers of AFIB’ theory, asked the question: ‘Is fibrosis the cause or consequence of AFIB?”

To study this question, and to investigate a potential upstream therapy to prevent fibrosis, the
aldosterone antagonist drug Eplerenone was compared to a Galectin-(GAL-3) inhibitor. GAL-3 is a
protein that regulates inflammation, immunity and cancer as well as fibrosis. Serum levels of GAL-3
increase in persistent AFIB, but interestingly inflammation markers do not rise with increases in GAL-3.
Administering a GAL-3 inhibitor reduces rotor frequency seen during AFIB mapping.

Keep in mind that sustained AF tends to increase atrial dilatation, collagen formation and increases fibrosis as a result.
The theory then, was that since the adrenal mineralocorticoid hormone, Aldosterone, in excess levels
promotes a fibrotic substrate, then perhaps blocking Aldosterone would mitigate AFIB cellular
hypertrophy and dilatation, and also should reduce serum evidence of fibrosis and P3NP. Indeed,
Eplerenone did show reduction in fibrosis on direct tissue examination.

However, there was zero change in AFIB dominant frequency (DF) with Eplerenone! Only the Galectin 3
inhibitor prevented sustained AFIB, not Eplerenone, though both drugs reduced cardiac fibrosis! This is
a key finding. It underscores the reality that though fibrosis is an important factor in AFIB, in many cases
its only a consequence and not a cause of AFIB triggering or maintenance.

Hence, the story isn't quite so simple as the 'fibrosis causes AFIB' ideas would have us believe, and underscores as another classic example of the old adage that in scientific research it is always incumbent upon the investigators not to get too far out in front with causation theories, when the real connection may be limited to even a powerful 'association' as opposed to a core causal relationship.

Now this fact does not mean that some afibbers might not still benefit from a reduction in fibrosis, if and by whatever means, a durable reduction in structural atrial fibrosis might be achieved ... such as via restoration of NSR from an expert ablation process resulting in a reduction in fibrotic structural changes to some degree after many years of dealing with progression of the beast!

But it does highlight the potential pitfalls of making sweeping assumptions of 'cause and effect' without a clear unequivocal causal relationship being demonstrated.

And as Jackie noted above, when dealing with various supplements that the majority of us anecdotally report some degree of benefit from using, it does not mean every one will benefit, nor that the effect is predictable for all users. Again, we are all an experiment of one, especially with biochemical responses to various supplements, diets and drugs.

Shannon



Edited 3 time(s). Last edit at 09/06/2017 02:32PM by Shannon.

Yes Carey - I agree. You asked what caused fibrosis and I attempted to respond to that in that it could be the natural lack of enzymes quoting Dr. Wong and also the ROS factor in some. Shannon has extended the overview much more thoroughly. When I first was researching fibrosis, the observations were that not everyone would form fibrosis, but when you had the tendency, it was apparently quite easily to build and not just in the heart tissue.

As for genetics, again, I agree... and I also think that Epigenetic methodology can help; we just haven't quite arrived at that place yet (for AF) and it may not happen for some time. But there was a post from several years ago and last year Travis brought up the topic at this link: [www.afibbers.org]. and in I had posted about this study indicating the hypo-magnesemia gene mutation made sense in the case of afibbers. Could obviously be one of many not yet discovered.

In another previous post (following) that I couldn't locate in the archives, these observations were listed:

For readers who have emailed me about this recent Genetic Expression and Methylation post asking for more reading references, here are links to Erling’s previous contributions on Methylation and my earlier Genetics and AF post in 2012 followed by reference list of books written by highly-credentialed and respected professionals who discuss the importance of and effects on DNA by methylation and Epigenetics which point the way to controlling our destiny.

Moreover this topic is something that (unless we are consulting with those who practice functional medicine), we are unlikely to know about tests to assess our methylation status since they are not typically considered standard or routine. I’ve mentioned previously that many labs are currently are offering Metabolic Profile type testing assessments that zero-in on how we metabolize the food we consume and show imbalances that exist. These are especially useful in for those with arrhythmias. Most importantly, if AF tends to run in one’s family, all the more reason to learn what needs to be enhanced or toned down.

Healthy is wealthy!
Jackie

Resources:
Search Messages: 'Introduction to 'epigenetics' and 'methylation' - All Forums, All Dates, Exact Phrase - 16 results:
[www.afibbers.net]
1,match_type=PHRASE,match_dates=0,match_forum=ALL,match_threads=0

Introduction to 'epigenetics' and 'methylation' Sept. 18, 2010
[www.afibbers.net]

Genetics and AF ( May 20, 2012)
[www.afibbers.net]

Epigenetics

Biology of Belief – Bruce H. Lipton, PhD

Genie in Your Genes, Dawson Church, PhD

Genetic Nutritioneering
Jeffrey S. Bland, PhD, FACN, CNS

Transcend – 9 Steps to Living Well Forever
Ray Kurzweil, PhD and Terry Grossman, MD

In the last post link dated 2012, I’ve brought it forward and highlighted the comments by Drs Gordon and Bland for emphasis… but be sure to get into the other referenced links as well. It’s time well spent.

Jackie
Genetics and AF
May 20, 2012
We often see posts indicating that afibbers are told the cause of their afib is genetic.

As stated in a Dec. ‘11 post, the missing portion of that statement is: “While some individuals may have a genetic or familial tendency toward developing atrial fibrillation, the world now knows that by understanding Epigenetics, we are no longer held hostage to a genetic link since we are able to control or influence genetic expression. Expression is the operative word. A flaw may be the inability of that body to perform a specific metabolic function … such as absorb and metabolize magnesium efficiently or methylate properly which sets the stage for afib. These flaws are modifiable once recognized. Influencing factors include lifestyle, diet and environment.

Through nutritional and other interventions, we have have strong influence over the Expression The concept isn’t new but is a major breakthrough from conventional thinking that “our genes are our destiny.” Success stories abound. Crusading actively to enlighten patients and doctors is Garry Gordon, MD, who is living proof that one can over-ride gene flaws. No longer are we victims of our genetics, thanks to Epigenetics.

In a book written specifically for non-scientists to understand the principles of our ability to modify inherited traits, biochemist and leader in the field of functional medicine, Jeffrey S. Bland, PhD wrote Genetic Nutritioneering back in 1999. He explains how food and nutrients improve gene expression and how we can reprogram our genes…just as Garry Gordon demonstrates his own personal success story.

Correcting gene flaws isn’t just a concept for afib….there are many familial tendencies that can be reversed or prevented from occurring in the first place. The most important thought for everyone is when “genetics as a cause” is mentioned, is to start thinking, "what can I learn about reversing the tendency for that gene flaw expression?" We don’t have to throw up our hands and give in to “the sentence” of just living with it. We can actively participate to reverse or alter the course ahead.

As exemplified by the many success stories in CR 61 where afibbers have successfully reversed their AF trend, we are living proof that diligence and attentiveness can pay big dividends.

Hold in your mind the following comments on Epigenetics by Dr. Gordon. This is specific to cancer, but emphasizes the concept of Epigenetics.

Jackie


Dear Readers:
Please read this carefully; Epigenetics is understandable. Those who advise patients with BRCA 1 or 2 issues are one day going to wake up and realize that removing breasts and ovaries because of BRCA test results is not state of the art medicine, it is medieval medicine.

The role of Epigenetics in health and disease is becoming ever clearer, and I firmly believe this field of study will eventually supplant the current medical paradigm. The conventional belief has been that genes controlled their own expression and were therefore the direct cause of certain diseases. This laid the groundwork for the idea that your genes predetermined your health.

But genes are in fact NOT self-regulating. Having "bad genes," does not at all mean you're doomed to suffer some inevitable fate like cancer!

Genes are merely blueprints, and these blueprints are activated and controlled by something else entirely, namely their environment. This environmental information, which includes diet, toxic exposures, as well as thoughts and emotions, and more, can create more than 30,000 different variations from each blueprint, allowing for an astounding amount of leeway in modifying the expression or "read-out" of each gene. As a result of these findings, we're now finally seeing science alter its course to investigate the power of optimal nutrition to improve health and prevent chronic disease from occurring in the first place

I hope all of you become more interested in OPTIMIZING ENVIRONMENT. For example, since that means diet and exercise, learn about my M.I.C.E. (magnetically induced cellular Exercise) concept that lowers cancer risk through autophagy.

Also the 72 gene panel I am doing on my patients in Australia with a company called SMART DNA finds the genes that nutrition can optimize to really offer advanced dietary supplement assistance to anyone looking for optimizing their environment so that the genes for their parents are not expressed in their bodies.

The information in this link will make you understand why Kobayashi’s program eliminated clinical (we all have subclinical all the time) cancer for 10 years for nearly 10,000 patients no matter what the family history was or the gene tests showed.

Sincerely,
Dr. Garry F. Gordon, MD, DO, MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Gene Expression and Epigenetics have been discussed frequently in other posts with mention observations by Bruce Lipton, PhD (Biology of Belief) and Dawson Church, PhD (Genie in Your Genes), two important books of many reading resources.

Jeffrey S. Bland, PhD, FACN, CNS
Genetic Nutritioneering
© 1999

Video clip on Epigenomics….A Tale of Two Mice
[www.pbs.org]

"As exemplified by the many success stories in CR 61"
What's CR 61?

Libby - Sorry... CR is Conference Room 61... at the top of this page there is a yellow box that says.... Afibbers.org.

Click there and it opens up a menu of various links to research reports and more about Afib. One segment was titled Conference Room Proceedings or Sessions... where a topic would be presented... such as CR 61 was "The List" of afibbers who had managed to reverse their afib by various methods...that didn't involve ablations. Peggy M. at the time was collecting the testimonies and Hans used several in his book as examples. We always meant to do an update as many more had also reported successes but we just never did, unfortunately.

So.. click there and then scroll down through the CR topics to #61 or
SESSION 61: Protocols for reducing/eliminating afib (November 5 -December 15, 2007)
which is here: [www.afibbers.org]

Another helpful yellow block, Libby, is the one right below Afibbers.org
which is Afib Resources... there are many reports there that have useful information for new readers.
[www.afibbers.org]

Jackie

Thanks so much, Jackie!