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Long-Term Antacid use causes Toxic Overload

From The Great Smokies Diagnostic Laboratory E-Newsletter

September 9, 1998--Volume 1, Number 13

HOW ONE PATIENT MISSPELLED "RELIEF"

Treating chronic gastrointestinal problems with antacids over long periods of time--even when following manufacturer's recommended dosages--can dramatically accelerate the body's toxic burden and trigger severe phosphate depletion, leading to a serious and painful softening of bone tissue known as osteomalacia.

A recent issue of Bone (June 1998;22[6]:695-698) presents a case study involving a pharmacist who self-treated her ulcer and gastritis symptoms with antacids over a period of 8 years. The antacids, like many other popular over-the-counter medications for stomach upset, contained both aluminum and magnesium hydroxide. So although the woman's dailyingestion of the antacid was just slightly above the maximum recommended daily dose, her cumulative intake of aluminum and magnesium hydroxide was estimated at 18 kg and 15 kg respectively. Thus, chronic antacid use triggered toxic accumulations of both of these elements in her body.

What's more, the antacids interfered with metabolism in her digestive tract, preventing the absorption of phosphate needed for the healthy formation of bone tissue.

Eventually, the woman sought medical attention for her symptoms of muscle weakness, back and limb pain, loose stools, and stress fracture.

Subsequent examination showed that aluminum had been highly absorbed into her bone tissue--even though her kidney was still functioning normally. The author noted that this finding contradicts a widely held assumption that aluminum toxicity from oral ingestion occurs only in cases of kidney dysfunction. Health care practitioners are thus advised to warn their patients about the potential danger of long-term antacid use posed by toxic accumulations, osteomalacia, and phosphate depletion.

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I do not know the orginal source for this, it was e-mailed to me by Bill Neall (Publisher and Editor of Macro Times -See Resources Page). All I can say is that this is a typical example of the amazing snowjob the medical system performs on the public. It seems these days when you get a degree in medicine it also qualifies as a degree in Spin Doctor. The question I have is, "Who is doing the snowjob on the medical profession"?

DEGENERATIVE DISEASES

At the turn of the century, our average life-span was 47 years, with the most common cause of death being infectious disease. Now we can expect to live more than 75 years, but the cause of death for the vast majority of us will be from degenerative diseases; Heart Disease, Cancer, Stroke, Diabetes, etc.

"heart disease, our number one killer, is a relatively new disease. The first modern cases of it were reported in 1912 and even then it was extremely rare. Only 3% of us died of cancer a hundred years ago. Today, almost 30% of us succumb to it. Same with stroke, which killed very few a hundred years ago. Today its the number three killer. Alzheimer's wasn't even diagnosed until1907. Today, 40% of those over 85 are suffering from it. And diabetes has increased 600% in just the last generation."

Robert G. Allen -"Your Life is in Danger!"

Of course, a part of the reason that we are now dying from degenerative disease is that modern medicine has conquered most of the deadly communicable and infectious diseases. Also, by living longer, we give these slowly progressing degenerative diseases more time to overcome our immune system and break down our body tissues. Our medical science has expanded our life-span but in the USA we have some frustrating problems.

97% of our health dollars are spent after our individual diseases are discovered. Despite the high cost and quality of our medical treatment system, we have dropped from 7th place to 18th place in life expectancy and rank last among industrialized nations in infant mortality rates. Japan proportionally spends about half of what we do on health care, and their life expectancy is 4 years longer.

Right, and they haven't been eating hamburgers, french fries and drinking soft drinks for as long as the US population. However, they'll join the US pretty soon, as our wonderful eating habits get more popular in Japan.

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Great Smokies Diagnostic Laboratory E-Newsletter

September 16, 1998--Volume 2, Number 1

BACTERIAL PATHOGEN MAY SPUR HEART DISEASE

Of course, there is no way the bacterial pathogen plays a causative role in this disease, or any other disease - refer to the Introduction for further discussion of this point, on Stage 5 of The Process of Disease. As I would like to remind everyone, micro-organisms attack diseased organs and tissues, they do not cause diseased organs and tissues.

A MINOR INFECTION WITH MAJOR CONSEQUENCES

Mounting evidence suggests that infection with a bacterial pathogen, Chlamydia pneumoniae, may act as the crucial early trigger for developing heart disease.

In a recent issue of Circulation (1998:628-633), investigators note that C. pneumoniae has been under suspicion by scientists for some time. Numerous studies have revealed the presence of this bacteria within fatty deposits of damaged arteries (but rarely in healthy arteries), and have established a significant association between infection and coronary heart disease. To explore its possible causative role more fully, a team of epidemiologists from Johns Hopkins and other universities tested for the presence of C. pneumoniae infection in a group of Alaska Natives--a population with a relatively low risk for developing heart disease--and, years later, compared these results with a forensic examination of each individual's cardiovascular system at the time of death.

The researchers found that early serological evidence of infection with C. pneumoniae was predictive of the presence of this bacteria in atherosclerotic tissue many years later, clearly supporting the notion of its pivotal role as an initiating trigger in the early stages CVD, rather than as an associated late-stage event. This strongly supports the use of C. pneumoniae as a powerful early warning indicator of CVD, even in young, low-risk individuals, and sheds a completely new light on the biomechanisms underlying the pathogenesis of cardiovascular disease.

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