Curing Heart Disease

Curing Heart Disease

This post is off topic with a vengeance, but I beg your indulgence. I think that it is appropriate to share my thinking on the subject in the hope that it may assist others in the midst of similar inquiries.

To begin with, I suffered a major heart attack exactly three years ago. Let it be said that one day the lights went out. That explains the lack of fear of death after such an event. In the event, I was with a friend who was able to summon assistance and also apply CPR. This process is now understood as to consist of pressing the chest so as to slightly slosh the blood about. Since circulation has ended, blowing air into the lungs serve no purpose at all until the heart is restarted.

My heart was restarted after twenty minutes. This is important, because the actual physicalogical impact remained actually surprisingly slight. That was not the expectation. This was an actual confirmation of the efficiency of properly applied CPR and more recent CPR protocols reflect this. In any case, I remained here to annoy you all.

I have since used all the recovery protocols deemed useful by medical science to wrestle with my confirmed heart disease. This has included five stents and the expected battery of medication. None of these actually cures the disease and at best may retard the development of same.

This inspired me to do a literature search to see what has been done toward finding an actual cure. This provided some interesting information. First, though, several co-conditions appear to be part of the same disease pattern. These may or may not be directly linked as to unique cause, but they certainly reflect the same epidemiology of a typical endemic disease. These conditions are enlarged prostate, excess belly fat, morbid obesity, and type II diabetes, besides the general appearance of circulatory problems.

Unfortunately, as with the original chronic condition of stomach ulcers, the medical position has been to blame the patient. After all a person is fat because he eats too much and surely he has control over that. This is utter nonsense. However, persuading the patient to make a Herculean effort to reverse the damage generated by these conditions will at least ameliorate the problem and may succeed in bringing some control over the problem. It is still not a cure.

The strategy of either eliminating carbohydrates from the diet or nipping a piece of the duodenum out to short circuit the rapid uptake of sugar and starch appears to work best, but is still not quite a cure. But I would take it if I had to.

What we have learned is that the disease factors have similar epidemiological outputs regardless of patient inputs just as was discovered with stomach ulcers, now cured. This is an important finding, because as with other biological agents of disease, we have the lucky ten percent and the unlucky ten percent sitting there in the data. The rest of us just get the long version of disease process.

None of this would have done an ounce of good, had I not come across an article arguing the same thing. These thoughts had led to a conjecture that arterial disease at least, is a prime candidate for a biological causation. It was recognized that the potential agent was very small and that it must be living for two to four years, in view of the measured disease growth itself. It was also well known that plaques contained even visible amounts of calcium which has led to a parallel hypothesis in which chelating is used to attack these deposits. Premature attempts to name this Hypothetical Biological Agent (HBA) did not help anyone’s cause.

What I recognized though, was that the calcium explains the unusual life cycle of the HBA. A cell protects itself with a blocking layer of calcium carbonate by establishing a charge on the cell surface and accreting a molecule of calcium carbonate. This is how a sea shell or coral does the trick. It costs a lot of energy which is reflected in the long lives of these cells or animals. This also immediately means that our HBA will be quickly protected from attack and will likely be vulnerable only during reproduction.

As an aside, the paper that established this was written by the late Dr Wolf Hilbertz, a great grand nephew of David Hilbertz who was perhaps the last great mathematician who produced across the field. He and I became acquainted during the early eighties just after he published this insight.

What was done was an initial trial under the auspicious of the Mayo Clinic who conducted a trial attacking the HBA with a combination of chelation and a generic antibiotic that had already shown efficiency in this case. This trial was run for a period of about four months with a significant reversal of plaque damage. This had only been achieved to date with strong antioxidants with the best results reported on using an ounce of pomegranate juice daily. This was all done around 2005.

I recognized that this protocol had at least weakly confirmed the HBA idea but had also been badly flawed. A long lived and protected HBA needed a sustained attack that lasted through the full lifespan of the youngest likely HBA. What is also not obvious is that the maximum population will always be young and will not collapse until the end of the attack.

This also explains why chelation has always been shown to reduce the effect but never to terminate the problem. In fact, chelation is helpful but not nearly sufficient or perhaps even necessary to achieve a good outcome.

This all encouraged me to conduct an experiment on myself with an emulation of the Mayo experimental protocol using a reduced version of chelation to stimulate the mineral turn over and the appropriate antibiotic. I commenced around four months ago and expect to sustain the attack for at least a couple of years. It is all very safe of course. At worst, I am wasting a little coin in order to produce mineralized urine and all that.
I commenced the attack around four to five months ago and we can make an initial report. It is still far too early for best outcome results but not too early to identify beneficial improvements. I quickly noted that my urine flow ceased to be often suboptimal and now is rarely suboptimal. This surely reflects a loss of chronic inflammation in the prostate and is surely a good sign. This is good news since it also supports the continuance of the protocol with a tangible benefit.

The other observation is purely subjective and is thus currently meaningless. It is that I sense that my body may have switched over some how into a belly fat reduction regime. This is more a matter of going from easy to gain, hard to lose over to easy to lose and hard to gain. I am not banking the numbers yet and I do have twenty pounds of diet removal fat and twenty pounds of starvation removal fat to lose without a knock down fight. It is just that it now feels possible. The placebo effect is undoubtably at work.

My best outcome would be to easily lose most of forty pounds and to eliminate all signs of arterial plaques over the next two to four years. I will satisfy your curiosity by reporting on any progress every few months or so.

I also welcome any other new ideas on the subject. Who knows what is out there?

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