Remodelling? Or a reversible, age-progressive, metabolic and/or nutritional problem?

 

 

 

A prominent characteristic of paroxysmal atrial fibrillation, whether “lone” or otherwise, is the apparently relentless progression towards ever more frequent attacks, often of longer duration, until the attacks eventually merge into a state of continuous atrial fibrillation, termed permanent or chronic AF.

 

The common interpretation of this phenomenon is that it represents “remodelling” of the atrial substrate, that is: irreversible modification of the actual tissues of the heart’s atrium, at least partly caused by the atrial fibrillation itself.

 

However, an alternative and much less gloomy interpretation is that the phenomenon represents some underlying problem of whole-body metabolism or nutrition which the aging body is progressively less physiologically well equipped to deal with as various systems lose efficiency.

 

In this interpretation, if the underlying metabolic or nutritional problem can be corrected or if the physiology can be assisted to more effectively apply its natural mechanisms for dealing with the problem, then the apparently inevitable progression of the fibrillation attacks, in one direction only, can be halted or reversed.

 

A complete absence of AF for several years, and a complete absence of ectopic beats for several years except during two reductions in cranberry intake and one interval of hidden calcium intake, in an individual previously suffering very frequent occurrences of both, and seemingly well progressed on the “inevitable” one-way path, strongly suggests that the second, metabolic or nutritional, interpretation is correct. In addition, there are other reports on the internet of individuals greatly reducing their total atrial fibrillation burden without utilising medication or surgery but instead using large quantities of supplements or animal protein (discussed here -- Link K). So at least the possibility of reversibility, and that the problem is at least substantially metabolic or nutritional, both seem proven. Of course, documentation of this occurrence in numerous further individuals will be necessary before acceptance in mainstream medical literature.

 

This is not to say, regardless of the above, that “remodelling” is non-existent in situations where the cardiovasculature or the whole physiology is chronically held in some long-term adverse condition -- presumably mainly when held in the most adverse circumstances, which in this case would be during permanent AF. However, the existence of such processes would not preclude, and would probably tend to argue for, the existence of the reverse capability -- the eventual partial or complete reversion (remodelling) of the atrial substrate back towards its more original condition, at least in some respects, if the adverse condition(s) are removed. This is a hopeful thought. There are underlying issues too detailed to go into here, regarding fibrosis, the regenerative plasticity of cardiac tissues relative to other tissues, and the particular characteristics of stem cells in cardiac tissues, but it is not apparent that there are studies which rule out such a possibility or likelihood.