Biomedical subjects

L Broxmeyer

Publications and source records attributed to L Broxmeyer.

5 recordsLinked to original sources

PubMed2004

Heart disease: the greatest 'risk' factor of them all.

By the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherogenesis; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious. Yet it was the very inability of 'established' risk factors such as hypercholesterolemia, hypertension and smoking to completely explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago. Today, half of US heart attack victims have acceptable cholesterol levels and 25% or more have none of the "risk factors" associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection. Even the case of the traditionalist's latest 2003 JAMA assault to 'debunk' what they call the "50% risk factor myth" falls woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl, a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and elevated cholesteriol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed to tuberculosis but do not get the disease. In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible role of infectious agents beyond the three infections which have in recent years been the focus of research: Cytomegalovirus (CMV) Chlamydia pneumoniae and Helicobactor pylori. Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking similarity to those of State and regional TB case rates. Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander-Jackson all saw clinical and laboratory evidence of a causative relationship between the mycobacteria and heart disease. And Xu showed that proteins of mycobacterial origin actually led to experimental atherosclerosis in laboratory animals Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein (CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis. It therefore behooves us to explore the link between heart disease and typical and atypical tuberculosis.

Comorbidity↗

PubMed2004

Is mad cow disease caused by a bacteria?

Transmissible spongioform enchephalopathies (TSE's), include bovine spongiform encephalopathy (also called BSE or "mad cow disease"), Creutzfeldt-Jakob disease (CJD) in humans, and scrapie in sheep. They remain a mystery, their cause hotly debated. But between 1994 and 1996, 12 people in England came down with CJD, the human form of mad cow, and all had eaten beef from suspect cows. Current mad cow diagnosis lies solely in the detection of late appearing "prions", an acronym for hypothesized, gene-less, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed the causative virus or bacteria. Therefore, even if samples appear to infect animals, it is impossible to prove that prions are causative. Manuelidis found viral-like particles, which even when separated from prions, were responsible for spongiform STE's. Subsequently, Lasmezas's study showed that 55% of mice injected with cattle BSE, and who came down with disease, had no detectable prions. Still, incredibly, prions, are held as existing TSE dogma and Heino Dringer, who did pioneer work on their nature, candidly predicts "it will turn out that the prion concept is wrong." Many animals that die of spongiform TSE's never show evidence of misfolded proteins, and Dr. Frank Bastian, of Tulane, an authority, thinks the disorder is caused by the bacterial DNA he found in this group of diseases. Recently, Roels and Walravens isolated Mycobacterium bovis it from the brain of a cow with the clinical and histopathological signs of mad cow. Moreover, epidemiologic maps of the origins and peak incidence of BSE in the UK, suggestively match those of England's areas of highest bovine tuberculosis, the Southwest, where Britain's mad cow epidemic began. The neurotoxic potential for cow tuberculosis was shown in pre-1960 England, where one quarter of all tuberculous meningitis victims suffered from Mycobacterium bovis infection. And Harley's study showed pathology identical to "mad cow" from systemic M. bovis in cattle, causing a tuberculous spongiform encephalitis. In addition to M. bovis, Mycobacterium avium subspecies paratuberculosis (fowl tuberculosis) causes Johne's disease, a problem known and neglected in cattle and sheep for almost a century, and rapidly emerging as the disease of the new millennium. Not only has M. paratuberculosis been found in human Crohn's disease, but both Crohn's and Johne's both cross-react with the antigens of cattle paratuberculosis. Furthermore, central neurologic manifestations of Crohn's disease are not unknown. There is no known disease which better fits into what is occurring in Mad Cow and the spongiform enchephalopathies than bovine tuberculosis and its blood-brain barrier penetrating, virus-like, cell-wall-deficient forms. It is for these reasons that future research needs to be aimed in this direction.

Animals↗

PubMed2004

Is cancer just an incurable infectious disease?

The word 'cancer' is of Latin derivation and means crab. By the turn of the 20th Century organized medicine had come to the conclusion that it was not a matter of whether infectious disease caused cancer, but which one. For over two hundred years a cancer germ had been discovered and rediscovered, named and renamed, each scientist adding to the knowledge, but to no avail. Then, in 1910, certain American medical powers did a 180-degree rotation, deciding that cancer was not caused by a microbe, and that anyone who thought otherwise was a heretic, a charlatan or a quack. But Dr. Virginia Livingston and her network were none of the above, their meticulous peer-reviewed research and publications, done at the height of US post World War II technology. And Dean Burk, Head of Cell Chemistry at the NCI went so far as to say that Livingston's cancer germ was as real and certain as anything known about cancer. Researcher, MD Alan Cantwell Jr. grew up thinking that all germs responsible for the important diseases were supposed to have already been discovered. But much to his dismay, he found one that was left out: the cancer germ. Cantwell already knew that for finding this, Livingston had already been branded by traditional medicine, leaving what he thought to be perhaps the major discovery of the 20th century largely discredited. The striking analogy between cancer and tuberculosis was noticed long before the tubercle bacillus was discovered. In 1877, Sir John Simon clearly pointed out the similarity and in fact argued very strongly in favor of a microbial origin for cancer. But Simon's vindication would have to wait for Livingston's germ, which although tuberculosis-like, was not tuberculosis but an atypical form of this mycobacterium, melded from the mycobacterium and other related Actinomycetales. Had medical science and the powers that be spent as much time in investigating and destroying Livingston's germ as they did in attacking her and those around her, cancer might be curable today.

Animals↗

PubMed2003

SARS: just another viral acronym?

Recent observations and experimental evidence have purported that a virus causes SARS, but such viruses have been isolated in only less than half of SARS patients in some studies and virologist Vincent Plummer of Winnipeg's National Microbiology Laboratory found that indeed 1 in 5 perfectly healthy Canadians with a history of recent travel to Asia had the virus. Therefore SARS microbiologic origins remain unclear. Outbreaks of multi-drug resistant (MDR) tuberculosis and the atypical mycobacteria simulate SARS on clinical, radiologic, epidemiologic, and diagnostic laboratory grounds and it is only logical then to include them in the differential to find a definitive cause and cure for SARS.

Diagnosis, Differential↗

PubMed2002

Parkinson's: another look.

Recent studies in the Parkinson's literature have cited a tuberculosis-like germ called Nocardia as being responsible for Parkinson's disease. Kohbata seemingly cemented a relationship between Nocardia and Parkinson's by finding serologic evidence in 20 of 20 Parkinson's patients, acknowledging that blood tests for Nocardia and the mycobacteria such as tuberculosis often cross-react, as they belong to the same order of bacteria, the Actinomycetales. Besides this difficulty in differentiation, a well-used medical school textbook of microbiology, Atlas, points out that even among experts, different observers may classify the same strain of bacteria as Nocardia or Mycobacterium tuberculosis. Parkinson's: another look is a theoretical article which presents compelling, well-documented evidence for an infectious cause for Parkinson's disease on historical, epidemiological, pharmacologic, microbiological, and biochemical levels.

Actinomycetales Infections↗