But if you can get it down to around 150, you’re VERY unlikely to have a heart attack.

Thanks for your feedback but I have already commented on the way this article was written. There are plenty of “likelys” “mays” and other words in the article that suggest I am just putting forth a well-reasoned hypothesis. I back everything I say with examples from the scientific literature or patient reports. The tone may be somewhat urgent, but looking at heart disease from alternate viewpoints is something the medical worlds needs very urgently to do.

I don’t know anything about Dr. Rath’s research and unfortunately do not have time to look into his work at this time as I am working hard on a presentation I will be giving at the World Conference of the Antibody in China.

Thanks for understanding,

Amy

Thanks for the great article. I see why you’re putting forward one single theory without spending too much time on alternatives or the missing parts of the puzzle… However, I also understand why others feel that a section dealing with the weaknesses of the theory, as well as a short overview of alternative theories might give more credibility to your writing.

A failure to acknowledge unclear areas or current lack of evidence would be a dangerous mistake to make, as it could lead to the precise sort of “consensus thinking” and the erroneous acceptance of unsubstantiated theories that you criticise so rightly.

I understand that you’re passionate about your claims and Dr. Marshall’s work. So am I: I have just started the Marshall Protocol for an undiagnosed chronic condition, and I cling onto hope that the Protocol actually works. If the MP is really the breakthrough that it seems to be, then news about it should be propagated tirelessly indeed, just the way you are doing it. Ever since first coming across this website, I have admired your work, and I hope you will continue to have the energy to keep it up.

Neither am I suggesting that you would be oblivious to the missing pieces of the puzzle. You are clearly aware of the areas where proof is lacking or where it is only available in silico. You actually do mention these areas in your articles.

However, since you’re fighting the erroneous acceptance of unsubstantiated theories, it may be even more conducive to the success of your work if you tried even more to even AVOID THE APPEARANCE of falling into the same trap.

Sorry to be so verbose, I’m not sure if my points (and my underlying SUPPORT) all come through… English is not my native language.

I would also like to ask a question concerning heart disease, if I may. I was wondering if you were familiar with Dr. Matthias Rath’s research and his theories linking vitamin C deficiency with atherosclerosis. I read about it several years ago, and found it very convincing (though that may not mean much to you, since I’m just a layman with heart disease in his family).

Even though Dr. Rath has been involved in several controversies and may have made unsubstantiated claims about other conditions, his theory linking heart disease and vitamin C may deserve an examination. If you could comment on it, I would appreciate it very much.

If you’re not familiar with his work, the following page may be a good place to start: http://www.drrathresearch.org/lab_research/heart_disease.html

Thanks,

Andy

That’s an interesting theory. I wouldn’t be surprised in bacteria were involved in the formation of advanced glycation endproducts, although I have no evidence to back that contention. This is certainly a questions our organization has not looked into. I will be seeing Dr. Marshall at a conference tomorrow and will try to pass the question by him. His answer though may very well be, “I don’t know.” Science is still at the stage where researchers are just identifying the bacteria in the human body let along figuring out exactly what many of the species are capable of. But it’s something to keep looking into.

I guess what we could do for some insight is to observe people who have been on the MP for several years and examine the state of their skin. Many people believe that their skin has become firmer or tighter on the MP. This would have to be confirmed more formally but could perhaps be observed in the trials of the MP that will soon begin at West China Hosptial.

I’ll let you know if Dr. Marshall has any insights.

Best,

Amy

Amy,

Is there any link between bacteria and the formation of advanced glycation end products (AGEs) that stiffen tissues? for example glucospane.

I have found some articles about e-coli growing on fructoselysine which seems to be a precursor to glucosepane.

We have alt-711 (Alagebrium chloride) for breaking certain crosslinks such as diketone and us (curing aging folk) are frantically trying to find something to cleave glucospane crosslinks.

Perhaps you can help us approach this problem from a fresh angle.

thank you,

Chris

Is there any link between bacteria and the formation of advanced glycation end products (AGEs) that stiffen tissues? for example glucospane.

I have found some articles about e-coli growing on fructoselysine which seems to be a precursor to glucosepane.

We have alt-711 (Alagebrium chloride) for breaking certain crosslinks such as diketone and us (curing aging folk) are frantically trying to find something to cleave glucospane crosslinks.

Perhaps you can help us approach this problem from a fresh angle.

thank you,

Chris

I’m so glad you’re finding the information on Bacteriality to be helpful!

Free radicals are common in many inflammatory diseases. Not surprisingly, they are tied to the presence of bacteria! Bacteria themselves are capable of secreting free radicals which can damage the surrounding tissues. Also, the immune system secretes free radicals in response to bacterial death. For example, the intracellular killing of bacteria by neutrophil granulocytes (special types of white blood cells) results in the production of free radicals.

So if a person is infected with a plethora of the intracellular bacteria and biofilm bacteria that cause inflammatory illnesses like cardiovascular disease, the bacteria they harbor create a free radical rich environment. By damaging the tissues the free radicals contribute to the disease process, but it is the presence of the bacteria in the first place that is the main problem.

So by getting rid of the bacteria, one gets rid of their free radical production. Another reason to do the MP!

Best,

Amy

THANK YOU! This all makes so much sense to me, but then again I am a complete layman with no medical training or scientific background at all. But I am intrigued by your information. I had a heart attack a few yrs ago and since then have been driven to get the scoop, find the real dope on this affliction. I have looked at a lot of theories, I find yours extremely compelling. Kudos and thank you again.

I have also read your “14 reasons” article on Vit D, the magic bullet de jour, fascinating and again seems to make a lot of sense.

The question I have is how does the bacterial theory tie in to the theory / evidence of free radicals causing heart disease. If you could point me to some info on this or perhaps provide a brief explanation I would be sincerely grateful.

Thank you very much.

David.

Thanks for writing. One of the points I made in the article is that obesity does not cause cardiovascular disease, or any other Th1 disease for that matter. Instead, obesity is a disease itself and results from a pathogenesis similar to that which drives the other Th1 diseases. So the fact that many people with cardiovascular disease are overweight is not because their obesity is contributing to or causing their heart problems. Instead, both the heart problems and the obesity result from the same cause – infection with a wide microbiota of intrphagocytic biofilm-like and L-form bacteria. There are many different species of these pathogens which employ myriad survival mechanisms.

However, it is becoming increasingly obvious that nearly all these pathogens are able to control our feedback pathways and receptors. We know that these bacteria (referred to as the Th1 pathogens) can disable the Vitamin D Receptor, but that is probably just the tip of the iceberg. There are almost certainly species that disable receptors involved in many of the body’s metabolic processes, many of which control weight gain.

A multitude of factors contribute to weight gain. Insulin helps regulate blood sugar, so if insulin levels are disrupted weight gain can result. It is now understood that the Vitamin D Receptor transcribes the insulin receptor, so image how VDR blockage by bacterial substances affects insulin regulation? There are other hormones that regulate weight gain. The ability of elevated 1,25-D ability to negatively impact the nuclear receptors that control our hormones could have affects on these pathways as well.

Then there’s the whole issue of the composition of bacteria in our guts. Like any of the bacteria that cause chronic disease, obesity-causing bacteria accumulate over a lifetime. There are over 3 trillion bacteria in the stomach alone, and restoring the balance of bacteria in the stomach and intestines to a population that does not promote weight gain is no small task.

For the most part, people who reach the later stages of the MP find it easier to regular their weight. Two of the first members to start the protocol each lost about forty pounds after about 5 years of treatment. But losing the weight and killing the bacteria that lead to weight gain takes time, particularly in people who have been heavy or obese for their entire lives. Reversing life-long obesity with the MP will take just as long as reversing any other life-long Th1 disease (sometimes life long symptom reversal takes well over 5 years).

Nevertheless, people on the MP continually report resolution of problems involving blood sugar or decreased carbohydrate cravings. Several patients are reporting recovery from diabetes. I think most people to reach the later years of the MP would tell you they find it easier to regulate their weight. Of course, after being ill for sometimes decades many don’t resume exercise right away, if at all, and weight loss is more gradual. Among those who exercise, I definitely know of some successful weight loss MP stories.

Why are some people who have been on the MP for several years still overweight? I would say they still have bacteria left to kill and that they are people who have probably struggled with lifelong obesity or have very serious bacterial dysregulation. It will be interesting to see how weight loss trends emerge as more and more people reach their later years of the treatment.

Benicar also helps people on the MP manage their weight. I’ll be writing a Newsflash soon about how ACE inhibitors that (just like Benicar) block the angiotensin receptor, are now being touted as diet drugs.

Best,

Amy