Toni's survey

Toni.

I've pondered on this for a while -

like most other folks I've had my share of 'usual' stressors, eaten things I shouldn't have, esp sugary things in the past, had/have a lot of exercise and have done heavy work [farming] had an over active thyroid 30 years ago, had 3 children, 2 hip resurfs and now have medication to lower eye pressure.

However I truly believe that genetics has to play a HUGE part in afib [and most other afflictions!]

Both my parents were physically active [farming] both had both hip joints replaced in their early 60's, both developed a-fib. Father died of a massive coronary heart attack at 71. Mother is very incapacitated with temporal arteritis at 88, though she was in very good health till she was 80 [no meds or supplements].
Mother always cooked home grown food as have I most of my life [couple of years eating not so well when I worked full time]

On the other hand my husband, whose parents were both in good health til their 80's can eat what he likes, dislikes veggies, fruit and exercise, has 2 tsp sugar in every cup of tea or coffee, and as far as anyone can tell is in pretty good health!

Jealous? You bet!!

Joyce

Joyce: The words jealousy, envy, and admiration have become misused during the last few decades.

Jealousy is a word used to describe the emotion one feels when another person is attempting to take away something one owns.

Envy is a word used to describe the emotion one feels when one is impotent in the face of evidence that one is less in some way.

Admiration is a word used to describe the emotion one feels when one is grateful that another person is better in some way.

Must disagree - everyone has always had genetics, but afib is a modern disease, so it must be some change in our environment that happened within the last 60 years or so.

Hip replacement was common for my farming aunts and uncles, but never happened to my parents or their friends, city folks all.

For example here is one way the environment has been changed for many people:
[www.relfe.com]

William

William

>>afib is a modern disease<<

A lot of the people alive now would, in the past, have been killed off by other diseases so would not have lived long enough to develop afib.

The work on the human genome is finding more and more illnesses with a genetic base. I'm with Joyce on this one.

Gill

Joyce - I don't mean to hijack your post but since you bring up the genetic link, this is a perfect opportunity to share some publications on sources of afib incluging the genetic factor.

I think in the future, if genetic research ever seriously targets afib, we'll see that there is some form of damage to DNA that creates a gene expression as a result of some environmental influence that either influences or creates some form of deterioration that enables AF.

I agree with William that years back, people didn't have this epidemic of afib. Something is bringing on the variation in the genetic expression and it could be the toxic food additives, preservatives, chemicals... or something in the air or water that is more prevalent and toxic than it was in the earlier populations.

Then there could be a related issue once again, etiology unknown, as discussed in the current Conference Room "dysautonomia" ....but it still doesn't address the origin or cause.

Note some of these publications regarding thoughts on causal influences for afib.... Plenty to ponder.

Jackie

"Gene variants with possible links to atrial fibrillation identified"

May 22, 2007 Steve Stiles

Denver, CO - In another example of what the Human Genome Project hath wrought, researchers have preliminarily identified 35 gene variants that have a significant association with atrial fibrillation, apparently either promoting the arrhythmia or protecting against it [1].

The gene variants in what appears to be the first whole-genome association (WGA) study to focus on AF, according to coauthor Dr Mina K Chung (Cleveland Clinic, OH), are tied to a variety of physiologic functions. Whereas individual candidate genes previously linked to some rare forms of familial AF are related to potassium- and sodium-channel function, "if you look at common AF, it's a more complex phenotype and more likely to be polygenic," she said.
Continue here: - [www.theheart.org]

=====

"Some lone atrial fibrillation attributed to gene mutations found only in atrial tissue"

June 21, 2006 Steve Stiles

Boston, MA - Their lone atrial fibrillation (AF) seemed idiopathic no more—mutations in a specific gene encoding for a protein needed for myocardial electrical conduction were found in cells scattered throughout the atrial tissue of three patients, according to a new report [1]. The mutations could be detected in atrial myocardium but not in peripheral lymphocytes, suggesting they were somatic—that is, they weren't inherited but developed after conception in some young cells destined to become atrial myocytes.

A mutation stemming from germ cells and related to the same protein was identified in atrial tissue from a fourth patient with idiopathic AF, whose two sons also carried the variant gene and were free of AF but found to have P-wave prolongation.

The four patients each showed atrial cells with distinct nucleotide substitutions in the gene GJA5, which encodes for connexin 40, a protein that forms the gap junctions between myocytes that allow transmission of electrical and chemical signals. Dr Michael H Gollob (University of Ottawa Heart Institute, ON) and colleagues conducted the laboratory work that defined the novel mutations and outlined their proposed effect on myocyte electrical coupling. Their report appears in the June 22, 2006 issue of the New England Journal of Medicine.

Continue: [www.theheart.org]

==============

Curr Opin Cardiol. 2006 May;21(3):155-8.

"Cardiac connexins as candidate genes for idiopathic atrial fibrillation"

•Gollob MH. University of Ottawa Heart Institute, Ottawa, Ontario, Canada. MGollob@ottawaheart.ca

PURPOSE OF REVIEW: Atrial fibrillation is the most common sustained cardiac arrhythmia and may cause significant morbidity. Current management strategies offer only modest success and may be associated with intolerable drug side effects or risk of procedural complications. As with other cardiac arrhythmias, the identification of genetic determinants predisposing to atrial fibrillation may provide novel molecular targets for drug development. This review discusses the role of cardiac connexins in the heart and suggests that genetic defects in cardiac connexins may predispose to arrhythmia vulnerability.

RECENT FINDINGS: Animal models deficient in cardiac connexins demonstrate abnormalities in myocardial tissue conduction and vulnerability to re-entrant arrhythmias, including ventricular tachycardia and atrial fibrillation. Atrial tissue analyses from human patients with atrial fibrillation consistently demonstrate alterations in connexin distribution and protein levels, suggesting a role of connexins in the perpetuation of the arrhythmia. Most recently, genetic studies of Cx43 and Cx40 indicate that genetic variations in these genes may predispose to arrhythmia vulnerability in humans.

SUMMARY: Current data support the critical role of cardiac connexins in mediating coordinated electrical activation and conduction through myocardial tissue. Alterations in the tissue distribution or function of cardiac connexins may predispose to cardiac arrhythmias, supporting a previously proposed hypothesis that cardiac connexins should be considered a major therapeutic target in the management of atrial fibrillation.

===

"Na-channel gene mutations tied to both atrial fib and dilated cardiomyopathy"

Jan 25, 2005 Steve Stiles

Rochester, MN - Mutations in a gene associated with the cardiac sodium channel seem to predispose affected individuals to dilated cardiomyopathy (DCM), atrial fibrillation, or both, according to a study reported in the January 26, 2005 issue of the Journal of the American Medical Association.[1] The novel finding—mutations that produce cardiomyopathies typically affect myofibrillary proteins—supports a pathophysiologic role for cardiac ion-channel dysfunction in some cases of heart failure, report Dr Timothy M Olson (Mayo Clinic, Rochester, MN) and colleagues.
Adding to the discovery's intrigue, the implicated mutations were in a gene that has previously been associated with a spectrum of rhythm disturbances, some potentially life-threatening.

We were surprised to find that a gene that is very strongly linked to a predisposition to arrhythmia could also be associated with heart-muscle disease.

"Mutations in the sodium channel have been identified in a broad spectrum of heritable arrhythmia syndromes, so we were surprised to find that a gene that is very strongly linked to a predisposition to arrhythmia could also be associated with heart-muscle disease," Olson told heartwire. His team found mutations in SCN5A, a gene previously linked to long-QT syndrome, Brugada syndrome, idiopathic VF, heart block, and bradycardia.
The finding, Olson said, "further emphasizes the heritable nature of many cardiac diseases and the importance of family history as well as, for patients without traditional risk factors, the need for clinical screening of first-degree relatives." Such screening should include both echocardiography and electrocardiography, he said.

Continue:[www.theheart.org]

=================

Clin Pharmacol Ther. 2007 Jan;81(1):35-41. Comment in:
Clin Pharmacol Ther. 2007 Jan;81(1):26-8.

"A common polymorphism in SCN5A is associated with lone atrial fibrillation"

• Chen LY, Ballew JD, Herron KJ, Rodeheffer RJ, Olson TM.

Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.

The cardiac sodium channel (SCN5A) is a target for the treatment of arrhythmias. We hypothesized that vulnerability to atrial fibrillation (AF) could be caused by genetic variation in SCN5A. We recruited 157 patients with early-onset AF who lacked traditional risk factors, and 314 matched controls. SCN5A was subject to targeted genotyping of a common loss-of-function H558R polymorphism and comprehensive mutation scanning.

Genotype frequencies in the AF cohort vs controls were as follows: HH, 50 vs 63%; HR, 40 vs 33%; and RR, 10 vs 4% (P=0.008). Additional coding sequence mutations were ruled out. The R558 allele was more common in patients than in controls (30 vs 21%, P=0.002), conferring an odds ratios for AF of 1.6 (95% confidence interval 1.2-2.2). The SCN5A R558 allele, present in one-third of the population, thus constitutes a risk factor for lone AF and may increase susceptibility to sodium channel blocker-induced proarrhythmia.

===

J Cardiovasc Electrophysiol. 2006 May;17(5):480-5.

"SCN5A mutation associated with cardiac conduction defect and atrial arrhythmias"

Laitinen-Forsblom PJ, Makynen P, Makynen H, Yli-Mayry S, Virtanen V, Kontula K, Aalto-Setala K.

Department of Medicine, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.

INTRODUCTION: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias.

METHODS AND RESULTS: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms.

CONCLUSIONS: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger.

==========
"Familial risk for atrial fib seen in Framingham offspring"

Tue, 15 Jun 2004 Steve Stiles

Framingham, MA -Atrial fibrillation (AF) might belong on the list of heart disorders for which a predisposition can be inherited, according to a prospective study of offspring from the original Framingham Heart Study participants.1

"Parental AF increases the risk of future offspring AF events, consistent with a genetic contribution to the etiology of AF," write Dr Caroline S Fox (Brigham and Women's Hospital, Boston, MA) and associates in the June 16, 2004 issue of Journal of the American Medical Association. Among Framingham offspring, having at least one parent with AF was associated with a significant 85% relative increase in the development of one or more AF episodes over four years. The relative risk was much higher when both parent and offspring developed AF at younger than 75 years.

"To our knowledge, our study is the first to demonstrate that a familial component exists for AF among unselected community-based individuals," the group writes, which suggests there are "potentially unaccounted-for genetic mechanisms" that promote AF.
The Framingham scientists followed 1078 sons and 1165 daughters of the original Framingham cohort who were at least 30 years old and initially free of AF. Of these, 30% had at least one parent with documented AF, the group reported.

Continue: [www.theheart.org]

===========

"Genetic mutation found for one heritable form of atrial fibrillation"

Thu, 09 Jan 2003 Shelley Wood

Shanghai, China - Chinese researchers have pinpointed a genetic mutation they believe is responsible for initiating and maintaining atrial fibrillation (AF) in 4 generations of the same family in Shandong Province, China.
Writing in the January 10, 2003 issue of Science, Drs Yi-Han Chen, Shi-Jie Xu, and colleagues observed that a missense mutation in the KCNQ1 gene on chromosome 11 was present in 17 family members, all of whom also had AF.1 In family members with no AF, the mutation in KCNQ1 was not found, with the exception of 1 member in whom the authors speculate manifestation of AF may have been delayed or there may have been incomplete phenotype penetrance. The mutation was also absent in 188 healthy controls.

Potassium channel function enhanced
Of note, Chen et al write, KCNQ1 is already known to arrhythmia researchers, who have shown KCNQ1 mutations to be associated with long QT syndrome. In the current study, 9 of 16 affected subjects also had prolonged QTc. "It is not clear whether part of the prolonged QT interval is attributable to secondary effects of AF (eg, heart muscle disease)," they write. "The value of the QT interval does not appear to correlated with AF persistent time."

Additional experiments by Chen and colleagues showed that KCNQ1 can form potassium channels, and that, in combination with other genes, the mutated KCNQ1 gene appeared to enhance potassium channel function and increase electrical activity in the heart. "The mutation in KCNQ1 causes a marked enhancement of its function, tips the normal balance of the process, and renders the cardiac myocytes more susceptible to atrial fibrillation," Chen and Xu stated in a press release. T

They postulate that the mutation in KCNQ1 that leads to AF keeps the potassium channel open, while a KCNQ1 mutation for long QT syndrome does the reverse. The new findings may mean that agents that block the potassium channel affected by KCNQ1 "may offer therapeutic benefit for a subset of patients with AF," the authors conclude.
Source KCNQ1 gain-of-function mutation in familial atrial fibrillation.2003 Jan 10; 299(5604):251-4
=====

"Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring"

Fox CS, Parise H, D'Agostino RB, Lloyd-Jones DM, Vasan RS, Wang TJ, Levy D, Wolf PA, Benjamin EJ.

National Heart, Lung, and Blood Institute Framingham Heart Study, Framingham, Mass 01702-5827, USA. foxca@nhlbi.nih.gov

CONTEXT: Atrial fibrillation (AF) is the most common cardiac dysrhythmia in the United States. Whereas rare cases of familial AF have been reported, it is unknown if AF among unselected individuals is a heritable condition.

OBJECTIVE: To determine whether parental AF increases the risk for the development of offspring AF.

DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study (1983-2002) within the Framingham Heart Study, a population-based epidemiologic study. Participants were 2243 offspring (1165 women, 1078 men) at least 30 years of age and free of AF whose parents had both been evaluated in the original cohort.

MAIN OUTCOME MEASURES: Development of new-onset AF in the offspring was prospectively examined in association with previously documented parental AF. RESULTS: Among 2243 offspring participants, 681 (30%) had at least 1 parent with documented AF; 70 offspring participants (23 women; mean age, 62 [range, 40-81] years) developed AF in follow-up. Compared with no parental AF, AF in at least 1 parent increased the risk of offspring AF (multivariable-adjusted odds ratio [OR], 1.85; 95% confidence interval [CI], 1.12-3.06; P =.02). These results were stronger when age was limited to younger than 75 years in both parents and offspring (multivariable-adjusted OR, 3.23; 95% CI, 1.87-5.58; P<.001) and when the sample was further limited to those without antecedent myocardial infarction, heart failure, or valve disease (multivariable-adjusted OR, 3.17; 95% CI, 1.71-5.86; P<.001).

CONCLUSIONS: Parental AF increases the future risk for offspring AF, an observation supporting a genetic susceptibility to developing this dysrhythmia. Further research into the genetic factors predisposing to AF is warranted.


JAMA. 2004 Jun 16;291(23):2851-5.
Comment in:
JAMA. 2004 Sep 8;292(10):1174-5.
===================

"Blacks 50% less likely to have atrial fibrillation in heart failure"

Tue, 03 Feb 2004 Allison Gandey

Oakland, CA - A new study has found that atrial fibrillation in heart failure was significantly less common among blacks than whites.1

In the February 4, 2004 issue of the Journal of the American College of Cardiology, the researchers write that this variation could not be explained by differences in traditional risk factors for atrial fibrillation, the etiology and severity of heart failure, or treatment.

In an interview with heartwire, senior author Dr Alan Go (Kaiser Permanente of Northern California, Oakland) added that the variation between races couldn't be explained by socioeconomic variables, either. "All of these patients were insured and hospitalized. They had the same duration of membership in their insurance plans and similar outpatient-utilization rates."
Continue: [www.theheart.org]

==============================

Curr Opin Cardiol. 2004 Jan;19(1):2-11.

"Autonomic aspects of arrhythmogenesis: the enduring and the new"

Verrier RL, Antzelevitch C.

Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

PURPOSE OF REVIEW: Recent progress in understanding the role of the autonomic nervous system in the development of cardiac arrhythmias is reviewed. The focus is on the translation of basic principles of neural control of heart rhythm that have emerged from experimental studies to clinical applications.

RECENT FINDINGS: Recent studies have made significant strides in defining the function of intrinsic cardiac innervation and the importance of nerve sprouting in electrical remodeling. A recurring theme is that heterogeneity of sympathetic innervation in response to injury is highly arrhythmogenic. In addition, both sympathetic and parasympathetic influences on ion channel activity have been found to accentuate electrical heterogeneities and thus to contribute to arrhythmogenesis in the long QT and Brugada syndromes. In the clinic, heart rate variability continues to be a useful tool in delineating pathophysiologic changes that result from the progression of heart disease and the impact of diabetic neuropathy.

Heart rate turbulence, a noninvasive indicator of baroreceptor sensitivity, has emerged as a simple, practical tool to assess risk for cardiovascular mortality in patients with ischemic heart disease and heart failure. Evidence of the proarrhythmic influence of behavioral stress has been further bolstered by defibrillator discharge studies and ambulatory ECG-based T-wave alternans measurement.

SUMMARY: The results of recent investigations underscore the importance of the autonomic influences as triggers of arrhythmia and provide important mechanistic insights into the ionic and cellular mechanisms involved.

=============

"Stress, depression and cardiac arrhythmias"

Brunckhorst CB, Holzmeister J, Scharf C, Binggeli C, Duru F.

Kardiologische Abteilung, Universitats-Spital Zurich. corinna.brunckhorst@usz.ch

A relationship between behavioural factors and cardiac arrhythmogenesis in humans has been described.

Three sets of conditions contribute to the occurrence of arrhythmias: myocardial electrical instability, most often due to coronary artery disease; an acute triggering event, frequently related to mental stress; and a chronic, pervasive, and intense psychological state, often including depression and hopelessness.

The autonomic nervous system plays an important role in the occurrence of cardiac arrhythmias and it is well documented that mood alterations as mental stress and depression influence cardiac autonomic balance.

There is an increasing body of evidence that patients with the greatest changes in cardiac neural regulation with decreased parasympathetic tone coupled with increased sympathetic activity are at the greatest risk for developing fatal ventricular arrhythmias. These patients have a reduced heart rate variability, increased QT-dispersion and a decreased baroreceptor sensitivity.

====================

"The influence of stress and depression on the autonomic nervous system and the impact on the occurrence of both atrial and ventricular arrhythmias is being discussed"

Shimazu T, Tamura N, Shimazu K.
Department of Neurology, Saitama Medical School.

Aging is associated with structural and functional changes in the autonomic nervous system (ANS), which innervates the whole body, and its altered function may influence almost all body systems.

Changes related to aging are found in autonomic nerves and ganglia, and ANS controlled functions including cardiovascular functions. Much of the current knowledge about age-related changes in sympathetic nervous function is derived from studies of circulating catecholamine levels, norepinephrine kinetics and microneurographic recordings from sympathetic nerves of skeletal muscle. Significant evidence suggests that basal plasma noradrenaline levels increase with age.

These data indicates that healthy aging is associated with elevated basal sympathetic nervous activity. In contrast, the reactivity of the sympathetic and the parasympathetic nervous activity are reduced with aging.

===========================

Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6818-23. Epub 2007 Apr 9. Links

"A cortical potential reflecting cardiac function"

Functional Imaging Laboratory, Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, 12 Queen Square, London WC1N 3BG, United Kingdom. M.A.Gray@bsms.ac.uk

Emotional trauma and psychological stress can precipitate cardiac arrhythmia and sudden death through arrhythmogenic effects of efferent sympathetic drive.

Patients with preexisting heart disease are particularly at risk. Moreover, generation of proarrhythmic activity patterns within cerebral autonomic centers may be amplified by afferent feedback from a dysfunctional myocardium. An electrocortical potential reflecting afferent cardiac information has been described, reflecting individual differences in interoceptive sensitivity (awareness of one's own heartbeats).

To inform our understanding of mechanisms underlying arrhythmogenesis, we extended this approach, identifying electrocortical potentials corresponding to the cortical expression of afferent information about the integrity of myocardial function during stress. We measured changes in cardiac response simultaneously with electroencephalography in patients with established ventricular dysfunction. Experimentally induced mental stress enhanced cardiovascular indices of sympathetic activity (systolic blood pressure, heart rate, ventricular ejection fraction, and skin conductance) across all patients.

However, the functional response of the myocardium varied; some patients increased, whereas others decreased, cardiac output during stress. Across patients, heartbeat-evoked potential amplitude at left temporal and lateral frontal electrode locations correlated with stress-induced changes in cardiac output, consistent with an afferent cortical representation of myocardial function during stress.

Moreover, the amplitude of the heartbeat-evoked potential in the left temporal region reflected the proarrhythmic status of the heart (inhomogeneity of left ventricular repolarization). These observations delineate a cortical representation of cardiac function predictive of proarrhythmic abnormalities in cardiac repolarization. Our findings highlight the dynamic interaction of heart and brain in stress-induced cardiovascular morbidity.

=====

Folks may also find this interesting...


The changing epidemiology of non-valvular atrial fibrillation: the role of novel risk factors

Age plays and enormous part in AF, 10% of people over 80 have it (and account for a third of the AF population)

Since octogenarians are the fastest growing part of society this must surely play a large part in the 'rising epidemic'.

I've no doubt that genetics plays it's part but so does an ageing heart.
If there is an environmental component it looks like it may be taking many years of exposure before AF appears. AF is a symptom of so many other problems that it's hard see which side of the coin a particular individual's problems comes from.

I say all this having got AF at 28(!) I've yet to spot any large study that is even prepared to give my age range a bar on the their age analysis of AF. I believe many posters here are the statistical anomalies rather than the norm.

--
James D

If you exclude the horrendous childhood death rate, the average age at death has been constant about 70 years. They had plenty of time to develope afib.

Genes can be turned on or off by food, and I'd guess by other modern environmental factors, so in that sense one might call afib genetic, except that there is too much evidence that the reaction is similar to poisoning - note that heart rhythm disturbances are quoted as one effect of some kinds of electromagnetic radiation.

Calling diseases "genetic" is convenient for innocent modern medical researchers who are too frightened to look at the true sources of modern diseases.

Noting the success of some who supplement with taurine, if I'm right that taurine is an amino acid or something normally present in raw meat and less or none in cooked meat, it confirms the idea that the neolithic habit of eating cooked meat is a bad one.
This is not genetic; I think it's political.

So James...then, the question becomes, at the tender age of 28, did something in your DNA change to the point where it became 'aged' and allowed afib to happen in a young person, just as it would in the elderly.

I totally agree that age is an influence, but what we don't know is what influences those telemeres unravel - earlier in some than others - and still others not at all.

If aging were the culprit 100%, then I think we'd see a much higher percentage of the elderly population suffering from AF.

William -I agree that genetics could be just a convenient explanation and perhaps not enough research is being done with the focus on nutritional deficiencies that allow afib to become pathology; although there are some studies on nutritional influences, we've not uncovered many offering conclusive evidence.

And I also agree that the enzymes and nutrients in the raw Paleo have far more merit than is typically recognized by mainstream medicine. I believe I remember, though, that it is present in either cooked or raw meat - probably more abundant in raw but in some meat nevertheless. The supplement form probably allows us to 'mainstream' it more efficiently.

Fascinating topic. Thanks for the stimulating input.

Jackie

Stress of modern living...?

Carol

Something in our water...?

Like the chemicals used to 'purify' it or the residues that are not able to be removed from public water. That's a topic for another discussion. And I already have some of a post prepared on just one segment of a toxin in water that isn't well known.

Jackie, you are always working on something interesting! I was actually wondering if maybe someone had gotten to our water supplies as a way of making a lot of people sick. Sort of like "water terrorist" In this day and time might not be too far fetched, except that if that happened it would probably affect everyone and not just a few million...so much for my wild water theory, I withdraw it. Yours is probably more logical Jackie, so I will wait to see it. Sharon

This is a very interesting thread of different yet also similar views!

Jackie, I'll have to have a thorough read of your long post, not in haste as it'll definitely cause indigestion!!! and that is a definite trigger for me - lol!

Although I'm so very sure of the genetic link to what used to be called a 'good constitution' I don't doubt that nutrition and environment play a major part in genetic expression.

What I think I started out with ..... is that despite years of apparent abuse some folks seem to get away with good health and others don't - but then I suppose that is 'individuality'!

Joyce

PS. Wil - my grasp of the English language often leaves much to be desired!

"So James...then, the question becomes, at the tender age of 28, did something in your DNA change to the point where it became 'aged' and allowed afib to happen in a young person, just as it would in the elderly."

Hi Jackie and all,
I think one of the frustrating parts of AF is that we want to point at a single thing that breaks in order that we can go fix it. For many I suspect it's the cumulation of several factors that results in AF and we may have to remove more than one to get bellow the AF threshold.

Jackie, I know you have unusual anatomy of the PVs and that mine are particularly large. I'm certain that this plays an large part in our AF but I'm also sure there a folks out there with similar anatomy that don't have AF. Did your thyroid problems contribute to AF? Does the fact I'm male contribute to my AF? Is it our unusual anatomy combined with slow resting heart rate? Do young AFers need unusual anatomy, unusual heart rates and unusual genes and the elderly just need unusual genes and an 'elderly' problem (fibrosis/CHF/MI...)?

I'm not necessarily saying that something in young AFers has been prematurely aged (though I'm not ruling it out either I'm saying that perhaps a number of things have to be wrong and it's just this combination that makes it rare in the young (and there are more common problems in the elderly that bring the AF threshold into view). My genes may have being expressing themselves this way all my life and just waiting for my heart to get large enough or some fibrosis line to appear in the ideal spot....

Does anyone know of any research that suggests AF is on the increase in the under 30s? (even that is a complicated question given how many AFers go undiagnosed until being hooked up to an ECG for something else!). The rising epidemic of obesity in the young might well be throwing up AF secondary to other heart conditions but what about this odd ball group of 'unkown cause' we find ourselves in? Is LAF in the young on the rise?


Does anyone else wish this was much simpler
Is there a prize for a poster who asks the most questions that nobody has the answer to ? ;-)

--
James D
(interesting thread)

And I can add an interesting piece of information to this topic: I have two first cousins who have A-Fib in the family.....maybe more....we're just finding some of this out! One is in her 80's and has had it for many years; and recently I became aware of another cousin - if he is LAF, I am not sure, but has had it for many year also.

Now here's the kicker: While gathering information to do a family story for my Dad's side of the family, an uncle spoke of his mother (my grandmother) and said that from time to time she would take a respite and go and live with one of her children for a short time......all he could remember was "she seemed to have palpitations or something..."

I found this interesting and expect our family situation is not only environmental triggers, but an inherited tendency in some of us!

Lois
Kalamazoo, Michigan

James, you said, "I think one of the frustrating parts of AF is that we want to point at a single thing that breaks in order that we can go fix it. For many I suspect it's the cumulation of several factors that results in AF and we may have to remove more than one to get bellow the AF threshold."

James, I think you are so right. We all might be guilty of looking for a single thing that causes our afib. But, that'shuman nature to not only look but hope we can find the "single thing." Maybe we need to take a look at our lives and families as Lois did, we may find some interesting connections. The only problem I have is that I have done a lot of research and have not been able to find a lot of health history. I don't remember my mother or father having anything like this and none of my siblings have afib, only me.

However, my youngest son had an episode a year or so ago that sounded just like afib. I can't seem to get him to ask for the exact diagnosis so I can see if it was afib. He is kind of protective of his health information because of his job. From what he was saying about how he felt, it sounds like afib. He is 43 and very healthy otherwise. He does work around high power lines and I often wonder about that also.

Anyway, we keep looking for answers for the young and the not so young. Sharon

I have shared our family history in past posts about how I think afib runs in our family.

My dad had it but still reached the age of 83. He told me he first started experiencing it in his 40's. My uncle my dad's brother has it and I also believe he got it in his 40's. My sister has had episodes and it is now controlled by medication. One of my uncle's daughters has it and I started having problems with afib in my 40's.

In addition to what I have just shared the men on my dad's side of the family died of either heart attacks or strokes in their 40's and 50's. My grandfather, my dad's father was the first to survive past his 60's and he died of an heart attack right after his 72th birthday. I don't however know if he had afib problems and my dad when I asked him said he didn't know either.

All of my doctors after researching our family medical history also believe the way that I do that afib is in our genes.

Chuck