What if it's something else that causes AF?

Here I am taking cranberry, ginger, magnesium, potassium, avoiding D, dairy and too little or too much O3 pufa, (plus several other things) and taking MulTaq again and getting ready for ECV # 2 but still in persistent AF.

But I keep thinking what if it's something else, like (and just throwing this out because we know it's out there) but from glycophosphate in our food and water?

[blog.daveasprey.com]

I did a little researching and tried to find out if AF was a thing 200 years ago but it seems there really isn't documentation on AF [www.ncbi.nlm.nih.gov]

Like there is on diabetes and sweet urine going back 3500 years ago.

[www.everydayhealth.com]

In general the more I read about other's AF here and elsewhere is the causes (or suspected causes) are as varied as we are as individuals.

If that's the case, then I start to wonder if these are really the causes or just, as in the case of atherosclerotic plaque, something like cholesterol that's always at the scene but not responsible for plaque.

The old when you only have a hammer, everything looks like a nail.

Anyone else ever thought maybe it's the __________ causing my AF? Our AF?

Or is just as simple as increased rates of hypertension, higher BMIs and things that accompany those like higher visceral fat, fructose, glycation, OSA, etc.

[www.ncbi.nlm.nih.gov]

Jaws - going to need a bigger boat.

Afib - going to need a bigger forum.

According to the US population projections by the US Census Bureau, the number of persons with AF is projected to be 12.1 million by 2050, assuming no further increase in age-adjusted incidence of AF, but 15.9 million if the increase in incidence continues.

[www.ncbi.nlm.nih.gov]

AF was known to the ancient Chinese, Greeks and Egyptians (so were strokes). No, they didn't know what caused it, but they were aware of the symptoms and that it existed. So looking for modern lifestyle explanations is futile. The more likely explanation is hypertension causing atrial stretch, which leads to atrial fibrosis, which leads to AF. Endurance sports, weight lifting, sleep apnea, hyperthyroidism, trauma, heart surgery, and artificial valves are also known causes and/or contributors.

Ultimately, I'm confident that it will be found to have a genetic basis in the sense that you have to have the genetic disposition in the first place, and then all these other things can flip the switch on. That would explain why among people leading similar lives with similar medical histories some will get AF but most won't.

Except for endurance sports, could it be diet? if you look at the world map below it shows the prevalence of AFIB and you will notice that USA lead the world and the least number of afibbers live in Japan.
I should point out that the Japanese diet includes Natto which is very high in vitamin K2. Vitamin K2 dissolves calcium and directs it to your bones.
Could it be that calcium has built up in our arteries, even the tiny ones in our heart causing it to run less efficient.
I haven't fully thought this through but think calcium has something to do with it.

The below report is about Nattokinase which is a bi-product of Natto which has vitamin K2 removed.
[www.ncbi.nlm.nih.gov]




Map.
[www.ncbi.nlm.nih.gov]

I think it's important to differentiate between calcium in plaque (where K2 MK7 helps to shuttle calcium via fetuin a and matrix GLA protein out of the arteries and into bones, as opposed to calcium channels in the heart. I have yet to see any research or inference that menaquinone affects heart rhythms.

Things like Tums and all of the -zol drugs aren't good for the arteries (read Malcolm Kendrick) and there seems to be some reason to believe that excess dietary calcium may not be good for the heart's electrical signalling.

I think Carey is correct. Considering all of the things I've done wrong in my life, it's a wonder I didn't have AF earlier.

High level cycling, excess carbohydrates (insulin and glucose spikes - glycation/neuropathy), eventually leading to higher BMI, T2, OSA and hsCRP, etc.

Quote
Carey
Ultimately, I'm confident that it will be found to have a genetic basis in the sense that you have to have the genetic disposition in the first place, and then all these other things can flip the switch on. That would explain why among people leading similar lives with similar medical histories some will get AF but most won't.

I concur. Very roughly, maybe 6% of those who chronically do endurance sports get afib. It is by no means a majority, but a large enough minority to be noticable. The very first paper I looked at in this regard was this one on Finnish orienteers. "However, in men without known risk factors, lone atrial fibrillation had been diagnosed in 12 of 228 (5.3% (2.8% to 9.0%)) orienteers and in 2 of 212 (0.9% (0.1% to 3.4%)) controls (P=0.012, two tailed Fisher’s exact test), the relative risk being 5.5 (1.3 to 24.4) in orienteers. The two controls with lone atrial fibrillation also took vigorous exercise. "

"Vigorous long term exercise is associated with atrial fibrillation in healthy middle aged men despite protecting against coronary heart disease and premature death. In population studies the average prevalence of atrial fibrillation, persistent or paroxysmal, is 0.5% in subjects aged 45-54 years, about 1% at 55-64 years, and 4% at 65-74 years. The prevalences of lone atrial fibrillation in our sportsmen were higher."

Most afibbers have comorbidities. The chronically fit generally don't fit this profile and represent a minor portion of the total afib population. In my experience here, it can be difficult for many of the chronically fit to change their exercise habits to be more optimal for their afib diagnosis.

George not only that, athletes often also have higher plaque burdens. When I was in training for the 1988 Olympics, I was often tested with lactic acid as high as 18 mmol. That is huge inflammation along with other molecules produced by doing training and racing at 189 BPM for about 52 minutes (40km time trial) and 4km pursuiting with heart rates of 194. Add in 10-12k of calories daily in carbs and that's just an insane amount of damage on a daily basis for 8 years + of competitive cycling.

Quote
Carey
Ultimately, I'm confident that it will be found to have a genetic basis in the sense that you have to have the genetic disposition in the first place, and then all these other things can flip the switch on. That would explain why among people leading similar lives with similar medical histories some will get AF but most won't.

Probably what happened to me. Genetics (both parents afibbers), endurance sport (cycling) and age (57 back then).
Afib came at rest likely because of my HR falling around 50BPM.

NotLying,

I did a bit of searching and found this,
[www.parathyroid.com]

Colindo Thank you so much - that is the likely smoking gun I've been looking for. Steve Carr also - thank you for opening up this idea.

I have to learn what Hyperparathyroidism is and if I have it.

What I know right now is T3 and T4 is fine, TSH has gone up and down at just right on the bubble 4.7 ish and Hasihimotos has been ruled out.

This is another good place to look. Thanks again. Great find !

Everything you wanted to know about hyperparathyroidism but were afraid to ask.

[www.niddk.nih.gov]

Colindo,

I've spent some time on this and it still looks like a good place to investigate further.

Multiple calcium readings over last 3 years of 9.7-10.0

No PTH labs - apparently not in the standard rotation.....

Will be looking into this.

Thanks

NLAMA

Steve Carr has a lot of stuff about Parathyroid: This is just a small sample


It could be as simple as the fact that VitD strongly suppresses parathyroid hormone secretion (and therefore PTH serum levels). Higher PTH also means more Ca absorption and less Ca secretion and other complex effects. And lower PTH means the opposite. But PTH also has a very pronounced natural diurnal range in the human body, with, very suspiciously from my point of view, its greatest variation in the morning hours -- around the sort of time when masses of vagal afibbers report their most frequent attacks! And, also very suspiciously, when I did not have my current lower Ca intake or as high serum VitD levels, my serum Ca levels (at the blood collection centre opening times when I gave the bloods, so 7am or 7.30am etc) used to be much more erratic -- still within the "normal" pathology lab "reference range", but often much further from the midpoint than they always are now.

So, as I say, these are my speculations (if they weren't speculations I'd be winning prizes), but I think that the natural, "solar-saturation" type VitD levels suppress the PT organ (suppress PTH levels) and thus stabilise it and the PTH levels in some way, resulting either not in excessive Ca absorption at certain times of the day which would otherwise occur, or enough Ca absorption at certain times of the day when it would otherwise not occur. Whatever the exact mechanism, my speculation (and small degree of evidence re my own bloods offered above) is that high-VitD/low-Ca-intake is much better for overall proper Ca metabolism than the reverse (low-VitD/high-Ca-intake, which is what most people in Western societies have), even tho on the face of it net Ca absorption seems like it might be similar; and the reason that it is better probably has to do with the high-VitD's suppressing and stabilising effect on the PT gland preventing large "excursions" of excessive Ca absorption or the opposite.

I have a PTH, Calcium and D lab scheduled tomorrow but losing a little hope because # 1 ECV labs mar 25th showed 8.7 calcium so it may not be this

High normal calcium maybe enough to effect afib. It would be interesting to know what afibbers levels are.
I have never been tested.

Good video from the site you found Colindo

[www.youtube.com]

Quote
colindo
High normal calcium maybe enough to effect afib. It would be interesting to know what afibbers levels are.
I have never been tested.

My calcium serum levels since 2014 are almost all mid-range (9.4) or lower. In 2007 was 9.3 mg/dL (range 8.5 to 10.6).

Quote
GeorgeN

High normal calcium maybe enough to effect afib. It would be interesting to know what afibbers levels are.
I have never been tested.

My calcium serum levels since 2014 are almost all mid-range (9.4) or lower. In 2007 was 9.3 mg/dL (range 8.5 to 10.6).

I have had mine tested abut 20 times since 2009. Always in range.

Hay NotLying,

Have you read this book? It was first posted by GeorgeN.
It's written by Hans Larsen

"Hans Larsen created and ran this afibbers.org for about 15 years. He just released The LAF Surveys: What we learned about the causes and treatment of lone atrial fibrillation This book is a collection of the surveys he ran during that time, as well as his analysis of the results. It is very complete and detailed"

[www.amazon.com]

I haven't but may. The thing that gives me pause is that most of us afibbers are multi-interventional - we'll do anything to try to stop AF so how to weight the information because it happens on both sides.

I'm a good example - there are dozens of suspects I can look at it when I first had AF event. Diet pill, adrenal pills, red bull I had a month earlier, coffee consumption, glycation, vitamin D, calcium, switch to keto diet, exposure to round up (yes) genetics and things I haven't thought of.

Same thing on the solution side - I've addressed everything I've thought of, taking taurine and mag and ginger and cranberry extract and multaq and still in AF - if it all of a sudden stops what did it?

Or if 2nd ECV holds what made that possible?

It's like this in life. Never one thing and always the tide.

If I can't solve this I am looking at an ablation.