Dirty words for most older people, real consistent exercises

When I talk to people even those very much younger than my 81 years I don't talk about exercise unless someone asks me. It offends people and sometimes it offends them after they have asked me because I haven't got the suggestion of doing practically nothing or some good pills

Of course you have to adapt to any problems you have and be sensible but for the great majority this means doing nothing or close to.

At the gym most people are less than half or a quarter my age. When I lie on the floor to do an exercise someone who doesn't know me may say ''I am a nurse. Am you okay''. We both laugh afterwards.

Ask yourself these questions. Are you at a very desirable weight[not just not as bad as some others]. Are you exercising vigorously and consistently within your limitations [don't expect a lot of models among your friends].

Exercise apart from not doing too much in your particular situation is a very rarely mentioned subject.

Close to two thirds of Americans are overweight or obese .Australia is not that far behind. People are getting fatter and fatter and the solutions are very simple but do demand some changes of habits.

It needs to be something that you think about and do something about now and not some other time in the future.
.

Alex

Hey Alex,

I've learned that it is very difficult to out exercise your mouth... Hence exercise is a great add on, but diet is 80-90% of the problem. In my case, chronic fitness was my ticket to afib. So the question to myself is always, "how much is too much." The answer for me is that I avoid steady state cardio training and minimize activities that mimic this. I focus on body weight training, HIIT (Tabatas) and my avocations (alpine skiing, rock climbing, hiking, mountaineering, snow shoeing, kayaking, bicycling & etc). I am very active, having to plan a day a week where I do no activity. Recently had a discussion with my son's girlfriend, an avid marathoner and Crossfitter, who has her Master's in Exercise Physiology. We concluded that the "minimum required dosage" is the optimal strategy. Figuring out what that is for me is the trick...

George

While "excessive" exercise may be a contributing factor to afib, I doubt that many would change behaviors just to possibly avoid afib down the road. I was a competitive swimmer for 14 years, which may have been a factor for me, but I would do the same thing again.

While I have nothing but personal experience as a resource, a good level of fitness meant that my afib was more of an inconvenience than an impediment. I chose an ablation 6 years ago (so far successful), because my wife and I wanted to go on extensive hiking trips in Europe and didn't want my afib to slow us down.

My fitness program and diet are nothing unusual, but they allow me to do all the active things I enjoy with little worry.

I completely agree about the importance of diet. I have mentioned my practice of a zero diet at various times previously with a lack of comments received.

It's very simple ,only eat a very wide variety of foods that are authoritatively recognised as very healthy. No demon sugar in the house for example.

My only weakness is an occasional rectangle of 90% chocolate.

No cheat days et cetera.

It has affected food based social life but I still have non-related friends ranging up from 20 years who seem to like seeing me even without food in our mouths. I only have two friends not quite as old as me The rest in my age category are all dead.

I may have narcissistic tendencies but being told without asking that I look much younger than my age, how do I keep so trim and fit helps to be sufficiently motivating for me to continue without regrets. Narcissism has its virtues. Passing my aviation medicals always involves some suspense but so far okay. It is another motivator.

I completely accept that excessive exercise can facilitate afib but that I don't think there are so many excessive exercisers amongst afibbers.

When my partner and I have been in New York we always order one meal for the two of us and sometimes have leftovers. Australia is catching up in the overweight and obese category which is regrettable.

At the gym in my role in the wise old man category I have often been told by a person that they eat well, exercise but don't lose weight so what is the best exercise?
My standard answer is push away the way the plate when there is a lot of food still left on it. And of course no evil foods especially sugar.

People kid themselves about what they eat. A more judgemental person would say lie to themselves about what they eat.

Alex

About all the over-weight people. I think it is a poorer food supply. I have heard they put chemicals in processed foods that make you hungrier, so that you eat more.

And alot of the food labelled as Healthy Food, is really not that great.

I go to the Gym also. The women had leaner figures 25 years ago than they do now on average.

Managing weight is not all the complex. A little information and commitment to a healthy lifestyle isn't that hard. It's calories (food) in and calories out (activity/exercise), plus a well functioning metabolism. Resistance exercise = increased muscle mass and a higher metabolism, 24 hrs. a day.

I don't see sugar as an enemy, just all things in moderation. Older people that eat out a lot have to have the smarts to share meals or they will put on the pounds. Serving sizes are ridiculous at most resturants, so shoving it away is hard to do, but splitting it in two is an easy solution as Alexe says.

I agree with Ken ''managing weight is not all that complex ''but moderation can be a problem as it is rubbery.

I have never been a smoker but I am told most people find it easier to give up rather than cut down a lot consistently.

Nancy Reagan had a drug solution "just say no".

That's my sugar solution .

Sharing meals and having a doggie bag reduces waste and helps the bank balance in a minor way as well.

Alex

Alex - at my gym, there are several of us 'seniors'... one woman is 89 and still lifting weights. She wins in competition because there is no one else competing in her age group. (smile) I haven't yet experience anyone checking to see if I'm okay if I'm on the floor mat.

On the topic of 'over-exercising' the following clip is worth noting and also remembering about what endurance exercise does to create the resultant cardiac fibrosis as a result of the ROS damage. Fortunately, with time and enough magnesium, the fibrosis is often reversible. (both website links elaborate on the risks)

Jackie


[fitness.mercola.com]

Endurance Training Can Produce Dangerous Arrhythmias, Myocardial Fibrosis, Hypertrophy and Atherosclerosis
Although researchers don't yet understand all of the factors in this process, they have theorized that high endurance exercise leads to cardiac fatigue, then a flood of catecholamines and adrenalin, which then triggers arrhythmias (abnormal heart rhythms). One common arrhythmia is atrial fibrillation, commonly known as "A-fib."12 A-fib is epidemic among endurance athletes, which sets them up for major increase in stroke risk. Marathoners above age 50 have a five-fold increase in A-fib rates.13

Arrhythmias can progress into full cardiac arrest. According to Dr. James O'Keefe, a research cardiologist and former elite athlete, 50 percent of marathon deaths occur in the final mile of the race, probably due to this cumulative stress on the heart. Dr. O'Keefe summarizes the entire phenomenon nicely in his Mayo Clinic Proceedings paper:14

"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."

Our Ancestors Did Not Run 20 Miles at a Time
Our Paleolithic ancestors did lots of walking, with occasional sprints, but not extended running. They would run long enough to escape the clutches of a tiger, but there were no marathons happening across the African savanna. One new study lends more credence to the benefits of walking versus running, finding that moderate intensity exercise (walking) produced equal health benefits as vigorous intensity exercise (running), with similar risk reductions for hypertension, hypercholesterolemia, diabetes and possibly coronary artery disease.15

Over the past 30 years, the number of people running marathons has increased 20-fold, while obesity has tripled. Phidippides was the first "marathoner," a Greek messenger who died suddenly after running more than 175 miles in two days. The changes being noted in the heart tissue of long-distance runners, especially in their right ventricles and both atria, have led some physicians to call the condition "Phidippides Cardiomyopathy."16

I want to be perfectly clear that I am not completely against running. If done appropriately, it can be an effective part of your overall fitness plan and may even help you to live longer.17 But you must keep it moderate, and find you own "Goldilocks Zone."

Dr. O'Keefe recommends running no more than 20 miles per week, spread out over three to four days, at a speed of about five miles per hour. If you run farther or faster than that, you may lose ALL benefits, and your health risks can rise to the magnitude of the couch potato—literally—according to the science. The statement written by Hippocrates 2,500 years ago hit the nail precisely on the head:

"The right amount of nourishment and exercise, not too little, not too much, is the safest way to health."

[fitness.mercola.com]

I previously said: "Resistance exercise = increased muscle mass and a higher metabolism, 24 hrs. a day."

I would also add that there are many other benefits to resistance exercise = stronger bones, joint protection, ability to manage daily routines with reduced risk of injury from lifting, and most importantly, less chance of falls and if you do fall, less chance of injury.

However, I see problems with many seniors that "work out" in my community clubhouse (over age 55 community of 1300 homes). This includes the weight room, pool and dance room. While I commend those that are making the effort, it's likely that most are not building muscle, and at best are just slowing the loss. WITH PROPER INSTRUCTION, most simply need more resistance to add muscle mass. It should be a lifetime commitment, so it's important to get the correct information early on to pave the way.

Two examples -

My now deceased (at age 97) Father had a couple of falls in his 90's and the only damage was to the sheet rock walls, not him.
My Mother-in-law in her mid 80's recently had a fall in her bedroom and broke a portion of the head off her humorous bone (upper arm bone connecting to the shoulder), but is managing pretty well in her recovery. Luckily it was her left arm - she is right handed.

Guess which one was superbly fit? No guarantees here, but I plan on having a very active lifestyle for as long as possible, and am willing to put in the effort to make it happen. My Father hiked to the bottom of the Grand Canyon and back out at age 88, the oldest to do that according to Rangers at Phantom Ranch at the bottom. Only one of his many feats.

Ken - How absolutely wonderful about your father's longevity and fitness.

I totally agree with your comments. My fitness center has numerous physical trainers available for hire to teach safe and appropriate targeted exercises. Resistance training has long been known and recommended to build or maintain muscle strength. One of my favorite books on the topic is "Strong Women Stay Young"...by Miriam Nelson, PhD. [www.library.tufts.edu] - pdf - 63 pages

I know from both personal experience and patient observations when I worked that the older we become, the more difficult it is to maintain muscle strength but we just can't afford to slack off.

Jackie

Quote
Jackie
On the topic of 'over-exercising' the following clip is worth noting and also remembering about what endurance exercise does to create the resultant cardiac fibrosis as a result of the ROS damage. Fortunately, with time and enough magnesium, the fibrosis is often reversible. (both website links elaborate on the risks)

Hi Jackie,
Do you have any URL's for the studies with details of how to implement cardiac fibrosis reversal, and/or info on the amount of reversal one might reasonably expect?

Thanks in advance,
-Ted

One thing to make clear Apache, I heard a lengthy discussion on this very question by Professor Jose Jalife and Dr Stanley Nattel at the recent AF Symposium 2016 in Orlando last week about using nutrients such as magnesium and other ions as well as proteolytic enzymes etc and what confidence does the science support as agents actual documented as reversal agents of cardiac fibrosis in humans ... These two research PhD and EPs are renowned as two of the leading lights in the world of research into core cellular causes and associated pathways contributing to arrhymogenesis in the heart.

Certainly everyone agrees fibrosis us often a major contributor to AFIB progression in many people ... But not always. They both emphasized fibrosis is as better looked at as a often a consequence or association with AFIB as it is causal for added degrees of fibrosis to be laid down once the process begins.

We are seeing now very direct evidence that the degree of cardiac fibrosis one might form as driven by core AFIB is mostly genetically determined. Mostly fibrosis does increase with increased progression and duration of AFIB/Flutter/ATachy ... But there are others in which even in long standing persistent AFIB, their hearts have very little to no fibrosis even in the face of decades long symptomatic AFIB!!

Furthermore, while preventing fibrosis will always be more effective than trying to remove existing fibrosis, especially fibrosis that has been there for a good which is highly resistant to reversal by any known means after crossing a tipping point in fibrotic progression and spread.. They are working on several agents that hold various degrees of promise for perhaps preventing the steady course of fibrosis from getting started if started early enough in ones AFIB career.

With regard to using magnesium and proteolytic enzymes specifically for pre-existing cardiac fibrosis removal, both classes of agents have been investigated and the evidence is very weak for both as reliable for removing already entrenched fibrotic scaring in the heart.

GAL-3 inhibitor is one promising agent when started in first months of AFIB and more work is underway looking at the hormone Relaxin-2 as well.

Again, while it may sound tempting to infer that since magnesium has some mild anti-fibrotic effects biochemically, what ever benefit it might have for direct fibrosis removal in the human heart is highly speculative and is not backed by strong or consistent evidence from any known reliable investigations
done and published. Rather a few papers look at the biochemistry of these ions and proteolytic enzymes in relation to fibrosis and see not much impact there at all.

Dr Jalife said any impact at all would need to be very early in the fibrotic process but they have looked at these agents throughly in the past and long ago moved on from them as not practical in efficacy for therapeutic removal of established fibrosis from on-going AFIB.

He did say Magnesium can have a transient ( meaning that if it has any impact at all in a given patient (which it well may I some cases), it would mainly be from its modulating effects on (intracellular calcium) CA2+ transport and similar biochemical pathways of action that are well understood in which magnesium sufficiency can contribute to a quieter heart. But not from any direct cardiac anti-fibrotic impact which is just too weak to be really effective at reducing existing mature cardiac fibrosis.

Anyway I'll touch on this talk a bit more in depth in the upcoming AFIB Report I'm working on now. And hope to have out by Feb 7th give or take a day or two.

Magnesium is good to take for most folks for multiple reasons, including helping to lower the cellular calcium load and its impact on quieting the heart. But also for numerous other health benefits too, but don't bank on it to reverse any well-entrenched AFIB-related fibrotic scarring.

Shannon

Hi Ted - Yes - give me time to find in my archives.

The best approach (obviously) is to avoid the formation of fibrosis in the first place (from the ROS implications) but as we know, often the only first related symptom is arrhythmia... ie, our canary in the coal mine that something is amiss in the body. Certainly, for endurance athletes, prevention deserves front and center attention and that speaks to the neglect to emphasize the importance of optimizing IC magnesium... testing, etc.

Jackie

Shannon,

It appears that similarly weak evidence supports Magnesium supplementation in general as a preventive or curative for AFIB. The most powered Framingham study only showed correlation for the lowest quartile of serum Magnesium levels, which would be characterized as deficient by standard lab measurements. This does not support more conservative intracellular Magnesium levels and/or higher thresholds.

Peter

Ted – Sorry this took a bit longer to find and organize than I thought... hope it's useful to you.

The following post was offered in 2004 which is described as a prelude to CR 24 on the fibrosis subject, titled: Cardiac Fibrotic Remodeling – The Role of Fibrosis in LAF (http://www.afibbers.org/conference/session24.pdf)

Since this posting 12 years ago, we’ve referenced the topic of fibrosis periodically and referred new readers to CR 24 and in 2012, an extensive update was posted as CR 75. Both 24 and 75 should be considered essential reading and should always be read with the understanding of the consequences of the inflammatory process that leads to fibrosis.
LAF and Cardiac Fibrosis - CR 75 [www.afibbers.org]

Another post was offered on the findings of William J Rowe, MD, and magnesium deficiency in the endurance runner Sy Mah. Reference link: [www.femsinspace.com] Dr. Rowe is well known for his research to help astronauts in space flight – maintaining their health, watching out for the detrimental effects such as advanced aging in space travel and as he indicates, it gives an important preview of what we might expect (eventually over time) in the aging body here on Earth. What’s useful is his emphasis on the importance of magnesium in the role of fibrosis and since magnesium is an antioxidant, correcting Mg deficiencies is equally important in controlling vicious cycles with catecholamines and (in turn) …. ischemia.

At this point in time, I remain disappointed that fibrosis presence or management thereof, is not emphasized or investigated when new afibbers seek medical attention. There is no mention of measuring intracellular stores of magnesium as a means of either helping to prevent arrhythmias or aggressive supplementing with either magnesium or fibrinolytic enzymes as a reversal method. In my 20-year history of consulting and treating for AF which includes three cardiologists, four EPs and three separate ER treatment facilities, the subject of preventing fibrosis formation or reversing it was never mentioned nor was measuring intracellular magnesium status. When I attended a local Atrial Fibrillation Summit sponsored by the Cleveland Clinic in 2004, I sat in on a session with Translational Researcher, David Van Wagoner, PhD, in which he explained his research on the role of fibrosis. That led to more research and the referenced fibrosis studies by Kuhmar & Shivakumar listed at the end of this report.

Understanding at least one cause of cardiac fibrosis formation – such as from intense endurance exercise and the resultant fibrotic response to the constant (and damaging) to free radical oxidative stress is important. With our own ‘poster boy example’ as in GeorgeN’s initial story, one can see that for him, tackling the afib problem with high dosing of magnesium, along with diet and other strategies has paid big dividends in that he was able to reverse the Afib trend and undoubtedly, with time, also the fibrosis or at least enough to lessen conduction interferences. As George states, he’s altered his exercise intensity.

This is an important topic.

Here’s the lead-in to that initial CR 24 post…(followed by other relevant study clips) for your reading enjoyment.

Jackie

Following also are a few links to relevant research reports and findings on cardiac fibrosis from my files and if you check those two Conference Room Sessions, there are other references as well.





2004 Consider this a prelude to the coming update on CR 24 – Cardiac Fibrosis.
Following are a few key points from my ongoing observations found in the literature. .
Specific details will be included in the final report.

Jackie


Consideration should be given to the use of systemic enzymes to eliminate fibrosis as it is a valid and effective treatment.

In CR 24 on cardiac fibrosis, reference was made to the explanation of the fibrosis connection as a substrate for atrial fibrillation by David Van Wagoner, PhD, researcher in Molecular Cardiology at the Cleveland Clinic. Fibrosis is a long-term response to injury, oxidative stress damage, inflammation and other influences as well. There is abundant support in the literature linking cardiac fibrosis and atrial fibrillation since fibrosis interferes with proper cardiac conduction. (A report as recent as June 2011, suggests that “targeting cardiac fibrosis has potential as a new frontier in anti-arrhythmic therapy”… indicating that cardiac fibrosis management is a logical consideration.) Yet, instead of developing drugs for this purpose, a safe, natural remedy already exists. Systemic enzymes.

The recommendation to reduce various types of fibrosis with systemic or proteolytic enzymes is not new. Practitioners of functional, regenerative or restorative and anti-aging medicine have been using these various enzyme combinations for many years safely and with great success; most importantly, without resorting to invasive surgical procedures.

When I researched the use of the fibrinolytic enzyme, nattokinase, I spent considerable time learning about managing fibrinogen as it relates to blood viscosity. Learning also about systemic enzymes was unavoidable as often they are combined in treatment plans. Audio podcast presentations explaining various applications to eliminate fibrosis by Dr.Wiliam Wong and Dr. Garry Gordon added to the material supplied by enzyme manufacturers along personal interviews with marketers of the Wobenzyme and Vitalzyme people. In one audio, Dr. Wong tells of his wife who had abdominal adhesions from surgery that began to contract so severely she was unable to stand completely upright. To avoid another surgery, he used the enzymes which allowed her to regain her full stature and functionality. He tells of many other patients who were severely impaired by various forms of fibrosis and who were restored to health with systemic enzymes.

I felt comfortable following the guidance of Dr. Wong. As covered in CR 24, and as it turned out, my choice of initially using Vitalzym for almost a year prior to my ablation, most likely helped improve my ablation success, although I was primarily concerned with blood viscosity issues and less aware of the fibrosis factor at the time. In hindsight, the enzymes along with my other heroics undoubtedly were very instrumental in enabling me to progress from having afib every day or every other day, often for 24 – 27 hours, down to zero events for several months prior to ablation.

Wobenzyme was introduced in 1960 in Europe and eventually, reached US practitioners. Wobenzyme Mucos Pharma of Germany provided some of the original data for my initial research as endorsed by Dr. Gordon. Wobenzym N is proven effective by over 160 clinical studies. [www.mucos.cz] For many years, Dr. Gordon (now in his mid 70’s) has successfully incorporated systemic enzymes into his own protocols and that of his patients.

Dr. Wong worked with World Nutrition (VitalZym) for a number of years and then formulated his own version of what he considers to be a highly effective product based on his hands-on treatment experience.

Dr. William Wong’s credentials:
Texas Complimentary and Alternative Medical Association professional member and World Sports Medicine Hall of Fame member, Dr. William Wong is a Classical Naturopath, a PhD. Exercise Physiologist, Certified Athletic Trainer (AATA), Certified Sports Medicine Trainer (ASMA), Old Rite Catholic Priest and Health/Fitness Consultant.

Dr. Wong has more than 27 years of professional experience in natural health as applied to sports medicine and rehabilitation. The last 8 years of which have been devoted to the application and teaching of Systemic Enzyme Therapy (SET). Studying SET techniques in both the US and Germany, Dr. Wong is widely acknowledged as one of the foremost experts in the field. In the 1990's, he taught Physical Medicine at the South West College of Naturopathic Medicine. In 1993, Dr. Wong was inducted into the Martial Arts Hall of Fame as Wing Chun Kung Fu Instructor of the Year and in 2004, after 37 years in the Martial Arts, he achieved the rank of Grand Master from the Soke (Grand Master's) Council and was awarded a Doctor of Philosophy in Martial Arts.

Dr. Wong has authored books on natural healing and on sports medicine. His shorter writings have appeared in such diverse magazines as G.Q., Black Belt, Survival Guide, The Townsend Letter for Doctors, Well Being Journal, BeautyWalk.com e-zine, and Healthy Options magazine in New Zealand. He has been a guest on over 1000 national and local radio programs, and has appeared on the nationally acclaimed PBS series Healthy Living hosted by Jane Seymour and Heartbeat of America hosted by William Shatner.

Continuing to lecture across the USA, Dr. Wong traveled to India in the Fall of 2005, where he conducted seven different lectures before hundreds of physicians teaching OBGYN's, Plactic Surgeons, Thoracic and General Surgeons, Cardiologists, General Practicioners and Dentists on how to integrate Systemic Enzyme use into Orthodox Medicine.

Currently, Dr. Wong writes books and lectures on anti-aging and pro-sexual topics. He also consults with individuals, specializing in the development of personalized programs for longevity and virility to help people overcome the effects of aging and the after effects of chronic debilitating conditions.

Dr. Gordon is a legend in his own right. One can get lost for days in his collection of audios and YouTube presentations. This article on cardiovascular use of enzymes is one of many.
[gordonresearch.com]

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

Dr. Gordon is an internationally recognized expert on chelation therapy and antiaging medicine. He is also a consultant for various supplement companies and the coauthor of The Chelation Answer. He lectures extensively on the topic, The End of Bypass Surgery is in Sight. He is on the board of the Homeopathic Medical Examiners for Arizona, is cofounder of ACAM (American College for Advancement in Medicine) and a board member of the International Oxidative Medicine Association. He received is Doctor of Osteopathy in 1958 from the Chicago College of Osteopathy in Illinois and completed his radiology residency at Mt Zion in San Francisco in 1964. He was the medical director of Mineral Lab in Hayward, CA, a leading laboratory for trace mineral analysis worldwide. He does telephone consultations for patients from around the world offering second opinions on any type of health issue from his offices in Arizona. Dr. Gordon is dedicated and passionate about educating doctors and patients about the harmful and devastating effects of environmental pollution and he provides documented alternatives for any health condition. He wants everyone to feel as good as he does at age seventy-six, having restored himself to optimal health in spite of suffering from serious illnesses for most of the first thirty years of his life including genetic heart disease.

About Vitalzym:

Systemic Enzymes Help You Feel Better, Look Better, and Live Longer
Vitalzym contains potent proteolytic enzymes designed to support health and promote healing and repair. It is an extremely effective systemic enzyme blend with a high Serrapeptase content.

Vitalzym works to break down fibrin in the body. Fibrin is a hard, sticky protein that has been associated with scar tissue, inflammation and pain, among other symptoms and conditions. Additionally, Vitalzym can help reduce viral load and regulate the immune system, reduce toxins and impurities in the blood, promote cellular detoxification, reduce internal inflammation, and promote overall better health.

Enzymes are said to be the “sparks of life.” They are considered keys that can unlock the door to a healthier you because they not only help improve digestion and nutrient absorption; they are also responsible for millions of bodily functions.

Vitalzym works synergistically to provide total system support. It contains protease, serrapeptase, papain, bromelain, amylase, lipase, rutin and amla. According to Dr. Peter Streichhan, a world-renowned enzyme researcher from Germany, "enzyme mixtures have a wider range of therapeutic advantages than do individual enzymes." 1
Continue: [www.energeticnutrition.com]

My thoughts are:
In light of the role cardiac fibrosis plays in causing arrhythmia, for those afibbers who have supplemented and tested for electrolytes, methylation issues, kidney, adrenal, thyroid, pH etc involvement and still seem unable to achieve NSR, treating with the systemic enzymes seems a reasonable adjunct. Emphasis on using systemic enzymes has not been included regularly or consistently but should be a definite consideration. This will be covered in detail in the fibrosis update report.

As mentioned in another post, the research by Dr. Shivakumar indicates that fibrosis is rooted in magnesium deficiency. Those afibbers who are refractory to magnesium repletion (who seem unable to achieve optimal or sustained intracellular magnesium levels in spite of heroics) are likely caught in the MgD/fibrosis generation web. Eliminating the fibrosis may enable magnesium repletion and/or help facilitate proper conduction without fibrosis interference.
Read more: [www.afibbers.org]


Magnes Res. 2002 Dec;15(3-4):307-15.
Pro-fibrogenic effects of magnesium deficiency in the cardiovascular system.

Shivakumar K.
Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram 695 011, India. shivak@sctimst.ker.nic.in

Magnesium deficiency is known to produce cardiovascular injury. A large body of experimental evidence supports the postulation that an immuno-inflammatory reaction and increased oxidative stress may damage the myocardium and vasculature in magnesium deficiency. Reparative/reactive fibrosis in response to the injury has, however, received little attention. Recent evidence from a rodent model of acute magnesium deficiency suggests that humoral factors may activate cardiac fibroblasts by a free radical-mediated mechanism and contribute to cardiac fibrogenesis. A similar mechanism may also promote cellular hyperplasia and increased matrix synthesis in the vasculature.


Abstract
Magnesium deficiency enhances oxidative stress and collagen synthesis in vivo in the aorta of rats.
Int J Biochem Cell Biol. 1997 Nov;29(11):1273-8.
Shivakumar K1, Kumar BP. [www.ncbi.nlm.nih.gov]


Antioxidants and Cardiovascular Disease
Ravindra Nath, M. Khullar, Pawan K. Singal
Alpha Science Int'l Ltd., 2004

Chapter Magnesium Deficiency and CV Disease:
Molecular Mechanisms and Recent Advances.
[books.google.com]

In 2001 Kumar & Shivakumar demonstrated that in hypomagnesia, serum factor may stimulate fibroblast proliferation and net collagen production (deposition) via superoxide-mediated mechanism and contribute to cardiac fibrosis. (clip from Antioxidants and Cardiovascular disease.. p 189)


Invited Review
Journal of Pathology J Pathol 2008; 214:199 – 210
Published online in Wiley InterScience (www.interscience.wiley.com) DOI: 10.1002/path.2277
[onlinelibrary.wiley.com]
Cellular and molecular mechanisms of fibrosis
TA Wynn*
Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and
Infectious Diseases, National Institutes of Health,
Bethesda, MD, USA
No conflicts of interest were declared.

Abstract
Fibrosis is defined by the overgrowth, harden ing, and/or scarring of various tissues and
is attributed to excess deposition of extracellular matrix components including collagen.
Fibrosis is the end result of chronic inflammatory reactions induced by a variety of stimuli
including persistent infections, autoimmune reactions, allergic responses, chemical insults,
radiation, and tissue injury. Although current treatments for fibrotic diseases such as idio-
pathic pulmonary fibrosis, liver cirrhosis, systemic sclerosis, progressive kidney disease,
and cardiovascular fibrosis typically target the inflammatory response, there is accumulat-
ing evidence that the mechanisms driving fibrogenesis are distinct from those regulating
inflammation. In fact, some studies have suggested that ongoing inflammation is needed
to reverse established and progressive fibrosis. The key cellular mediator of fibrosis is
the myofibroblast, which when activated serves as the primary collagen-producing cell.
Myofibroblasts are generated from a variety of sources including resident mesenchymal
cells, epithelial and endothelial cells in processes termed epithelial/endothelial-mesenchymal
(EMT/EndMT) transition, as well as from circulating fibroblast-like cells called fibrocytes
that are derived from bone-marrow stem cells. Myofibroblasts are activated by a variety
of mechanisms, including paracrine signals derived from lymphocytes and macrophages,
autocrine factors secreted by myofibroblasts, and pathogen-associated molecular patterns
(PAMPS) produced by pathogenic organisms that interact with pattern recognition recep-
tors (i.e. TLRs) on fibroblasts. Cytokines (IL-13, IL-21, TGF-β 1), chemokines (MCP-1,
MIP-1 β ), angiogenic factors (VEGF), growth factors (PDGF), peroxisome proliferator-
activated receptors (PPARs), acute phase proteins (SAP), caspases, and components of the
renin–angiotensin–aldosterone system (ANGII) have been identified as important regula-
tors of fibrosis and are being investigated as potential targets of antifibrotic drugs. This
review explores our current understanding of the cellular and molecular mechanisms of
fibrogenesis. Published in 2007 by John Wiley & Sons, Ltd.

See also : David Van Wagoner, PHD [my.clevelandclinic.org]

Quote
Jackie
With our own ‘poster boy example’ as in GeorgeN’s initial story, one can see that for him, tackling the afib problem with high dosing of magnesium, along with diet and other strategies has paid big dividends in that he was able to reverse the Afib trend and undoubtedly, with time, also the fibrosis or at least enough to lessen conduction interferences.

I don't know what I've done, except keep afib in remission. I doubt if I've had much regression in my system's propensity for afib, absent the high dose mag. Meaning I doubt if I've regressed whatever fibrosis I've had. At least I've not regressed it to the state it was prior to my first afib episode. I'll likely have to continue my protocol for life unless I get an ablation, which I've been able to avoid so far, and have no need for at this time.

Large doses of steady state cardio are what I do avoid, though I remain extremely active (and I do short high intensity intervals like Tabatas for training). There also seems to be a big difference between competing and pushing myself very hard versus doing "normal" activity (my wife says what is "normal" is not for others!). For example I went snowshoeing with my wife last week after skiing 26,000' vertical in the morning. We went out for a few hours and I was breaking trail in snow several feet deep. This is steady state cardio, but I was not particularly pushing myself, so from an afib perspective and me, no big deal. I alpine ski all the time but pushing myself to ski every run as hard and as fast as I can (on steep off-piste terrain) all day long is very different than skiing less aggressively. Even though if I'm skiing with my young friends (20's) or not skiing with others, I do ski nonstop all day (easily 30,000' to 50,000' vertical) - just not as fast and as hard as I can. For me, it is pushing myself as hard as I can for an extended period that puts me at risk for a delayed (hours to days) vagal triggered afib episode.

On limiter - I do everything breathing through my nose, including intervals, more here <[www.afibbers.org]

George



Edited 1 time(s). Last edit at 01/28/2016 07:59PM by GeorgeN.

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Jackie
Ted – Sorry this took a bit longer to find and organize than I thought... hope it's useful to you.

Thanks for taking the time to put that together Jackie - much appreciated!

It'll take me some time to go through all of that material, but what caught my eye right away was the section on Vitalzym. The name resembles Wobenzym (which I tried when I had a herniated disc). Googling "Vitalzym vs Wobenzym" turned up a very interesting 2006 article on the www.naturalproductsinsider.com web site. Apparently the maker of Wobenzym won a $5M lawsuit in Arizona against the maker of Vitalzym, for false claims. I haven't finished analyzing that article, but it did contain a few interesting sections...

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naturalproductsinsider
Marlyn is the exclusive U.S. distributor of Wobenzym, which is manufactured by Mucos Pharma in Germany.Wobenzym is one of the top selling enzyme products in the United States and second to aspirin as the top selling over-the-counter (OTC) product in Germany. In June 2001, the principal owner of Mucos, Dr. Karl Ransburger, died. After his death, and continuing through January 2002, Marlyn was negotiating with Mucos to extend its exclusive U.S. distributorship agreement for Wobenzym. The negotiations resulted in a temporary (few months) shortage of Wobenzym in the United States. At the same time, World Nutrition also tried to obtain the rights to Wobenzym. After World Nutrition learned Marlyn would retain the rights to Wobenzym and knowing of the Wobenzym shortage, World Nutrition introduced its product, Vitalzym, to the market. With the endorsement of William Wong—self-proclaimed “Dr. Wobenzym” who represented himself to be a Ph.D. and doctor—World Nutrition claimed its product, Vitalzym, was three times faster than Wobenzym, with much smaller doses
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Marlyn also showed there were no leading enzyme researchers involved in the development of Vitalzym and no basis for World Nutrition’s claims that Vitalzym worked three times faster than Wobenzym. In addition, Wong was not actually a doctor or physician and never graduated from any recognized medical school. In fact, the school where he obtained his diploma no longer exists. Wong never had a medical practice, never used systemic enzymes in any practice, and admitted he never saw or treated any patients in his life. Moreover, Wong’s doctorate was in martial arts.

Hi Ted - thanks for digging that info out about Dr. Wong. Back then in 2001, when I did the initial research on those enzymes, there wasn't much historical information on the internet about him....other than he worked initially with World Nutrition and then went off on his own to develop a newer, stronger enzyme product...or so he claimed.

I didn't venture into trying that because of cost, but found that a quality serrapeptase worked well on my fibrinogen which was elevated at the time. I have since learned that most likely, that was driven by the Lyme disease which was never diagnosed as such ...rather everyone said it was fibromyalgia. Thankfully, now, we have access to functional medicine practitioners who test for underlying stealth infections rather than just label everything with a catchall term such as fibromyalgia.

Later, I connected with Ralph O. Holsworth, D.O. who brought nattokinase (proteolytic enzyme) to the US for managing fibrinogen and from then on, I use mainly his brand to manage blood viscosity. So today, I use a combination product of both NK and serrapeptase for double coverage along with antioxidants and other antiinflammatories.

Be well,
Jackie