Burden of infection on Insulin Resistance, Metabolic Syndrome, Thyroid, Stress, and Inflammation

Rogue Bacteria Involved In Both Heart Disease And Infertility

But engrossed in his research, Azenabor is a shrewd and serious investigator who coaxes rogue bacteria to give up deadly secrets of how they cause several human illnesses.

Educated in Nigeria and Great Britain, Azenabor landed a fellowship sponsored by the World Health Organization soon after completing his doctorate on the bacteria Chlamydia. He was one of only two chosen worldwide.

Now an associate professor of health sciences at UW-Milwaukee, he has identified how two different kinds of Chlamydia can cause both coronary artery disease and miscarriages.

Solving one mystery gave him clues that he needed to figure out the other.

By focusing on the immune system mechanisms in Chlamydia infections, Azenabor has identified an important link in seemingly unrelated health problems.

The result could be new treatments and prevention strategies for both heart disease and infertility.

The first mystery

Chlamydia pneumoniae is a microbe that normally causes pneumonia and bronchitis, but it has long been associated with atherosclerosis, a cardiovascular disease also called "hardening of the arteries."

"It was a frightening prospect," says Azenabor, "that atherosclerosis could come from a bacterial infection." He decided to look for an explanation.

Chlamydiae are unusual, says the Nigerian-born scientist, because, unlike most other bacteria, they use the same form of cholesterol for metabolism that human cells use. Chlamydiae also are intracellular pathogens, meaning that they can only grow and reproduce inside of another cell.

But these bacteria have another peculiar ability.

Normally, when a pathogen invades human tissue, the immune response unleashes "killer cells" called macrophages, which stretch to engulf the attacker and destroy it with toxin-producing enzymes.

Chlamydiae fight back, says Azenabor, His work shows that, as they are ingested, these two species of Chlamydia can manipulate the functions of protective cells like macrophages in creative ways.

Cholesterol connection

One of the keys lies in the macrophages' cell walls, which store cholesterol and usually tightly control it.

But when it's infected with C. pneumoniae, the microbe traffics cholesterol from the macrophage cell membrane to its own, causing a change in the macrophage that makes it rigid and unable to move.

The bacterium also disturbs the macrophage's production of toxins in a process that transforms them into "signaling molecules," which support functions that keep the bacterium alive.

"C. pneumoniae really wants to hijack the cell functions for its own use, like a parasite would," he says. "The macrophage, though, wants to kill Chlamydia, but its killing ability has been converted to signaling."

This is the reason the infection becomes chronic, Azenabor says. "Because of signaling, everything else in the human cell is still fine except for the altered toxins, so the bacteria can reproduce in a short time."

As the macrophages become immobile, they accumulate in the blood vessel walls, setting the stage for atherosclerosis.

Infection and pregnancy

Armed with new information about how C. pneumoniae sabotages the immune response, Azenabor, who had also been studying the effects of estrogen on macrophages, turned his attention to another Chlamydia-related puzzle.

How is Chlamydia trachomatis, the species that causes a sexually transmitted disease, involved in the occurrence of spontaneous abortions or miscarriages?

He was immediately drawn to the protective cells in the placenta during early pregnancy -- the trophoblasts.

"It's not for nothing that trophoblasts are the early cells," says Azenabor. "They prevent any kind of infection that could threaten the fertilized egg. They produce toxic chemicals similar to those of macrophages."

Trophoblasts act like macrophages in many ways, and their functions are mediated by the hormones estrogen and progesterone. And cholesterol is the molecule used to produce those hormones.

Azenabor's research shows that, like its cousin, C. trachomatis does take cholesterol from the trophoblast, and it also reproduces once inside the cell.

"It's the same old story," says Azenabor. "Only this time the attacked cell is a trophoblast instead of a macrophage, and the depleted cholesterol hinders production of estrogen and progesterone instead of altering toxin production."

Azenabor's lab members are continuing their inquiry, and they then will need to test the theories with live animals.

But the scientist is optimistic. Already he has a patented process for blocking the effects of calcium signaling for C. pneumoniae.

"If we can prevent C. trachomatis from becoming chronic, we could apply this remedy to pregnancy," he says.

While conducting postdoctoral work at McMaster University in Ontario, he won the Canadian Distinguished Scientist Award in 1998, and moved to the University of Waterloo.

Azenabor joined the UWM faculty in 2001, after working as a scientist in a Chlamydia lab at UW--Madison. He jumped at the chance to start his own lab at UWM. Since arriving here he has won several honors, including the Shaw Distinguished Scientist Award from the James D. and Dorothy Shaw Fund in the Greater Milwaukee Foundation.

Although he didn't plan on working with Chlamydia for this long, he is now a leading researcher in the field. One attraction, he says, is the work is unpredictable.

"When you begin," he says, "you never know where you are going to go."

Infection and inflammation of the cardiovascular system are a frequent cause of cardiac and/or vascular disease, which represents an enormous clinical burden in adult medicine. Major advances have now occurred in understanding cellular and molecular bases of a wide variety of inflammatory cardiovascular diseases. Some of these (myocarditis) have been recognized as inflammatory disease for a long time. Of others (atherosclerosis), the inflammatory nature of disease and possible involvement of bacterial antigens therein has emerged only recently. In both cases however, new insights in inflammatory mechanisms will have great impact on clinical thinking and management. Therefore, Cardiovascular Research has decided to devote a spotlight issue to this topic. This issue contains 10 review articles that provide state-of-the-art knowledge and, in addition, 14 original papers with novel data on the intriguing relationship between infection/inflammation and cardiovascular disease.

As evidenced by the reviews as well as by the original articles of this special issue, many new insights have been made in the field of cardiovascular infection and inflammation. The application of molecular techniques on myocardial tissue has improved the sensitivity to detect viral inflammatory cardiomyopathy. Numerous studies of patients with myocarditis have demonstrated the usefulness of PCR analysis for etiologic diagnosis. These new diagnostic tools in the future will enable a tailored therapy. The molecular determinants of cardiac viral infections are now under intense investigation because an understanding of these determinants may lead to an explanation for the highly variable clinical course. In the modern molecular era the complex infective agents–host interaction will be clarified which will lead to a better knowledge of inflammatory cardiomyopathy and will significantly change our management of this disease in the near future.

Similarly, in vascular disease, more knowledge on the various mechanisms that play a role in atherogenesis and other types of vascular disorders will likely provide new therapeutic targets for prevention and treatment of disease. Since infection and inflammation are intricately involved in the pathogenesis of vascular disorders, it is likely that new therapeutic strategies, aimed at components or pathways of inflammatory responses will find a place in the therapeutic armoury to prevent or treat vascular disease.

Could Infection Accelerate Coronary Artery Disease?
Technology Spotlight

Murat V. Kalayoglu, M.D.
Contributing Editor

Established risk factors for coronary artery disease include high levels of low density lipoprotein, low levels of high density lipoprotein, hypertension, smoking, and a family history of early heart attacks. However, even when all of these risk factors are taken into account, over a third of patients with coronary artery disease have no identifiable risk factors. An old, intriguing hypothesis has been slowly revived over the last decade to explain why many individuals without the “classic” risk factors go on to develop heart disease. This hypothesis, originally proposed over a century ago, is that infectious agents contribute to the development of atherosclerosis.

One of the main reasons why the infection hypothesis has been revived is that atherosclerosis is now appreciated to be an inflammatory disease, a paradigm shift that also occurred over the last decade. If atherosclerosis is an inflammatory disease, then a trigger for inflammation also must be present to either initiate or accelerate the disease. Indeed, cardiologists are now well aware of the strong association between increased levels of C-reactive protein and coronary artery disease, an association that in many ways is stronger than that between increased levels of low density lipoprotein and coronary artery disease. C-reactive protein is a systemic marker for inflammation, and this link underscores the importance of chronic inflammation in the development of atherosclerosis.

So what could be the trigger? Since in many cases inflammation results from infection, then chronic infection of arteries could lead to inflammation with subsequent development of the atheroma. Persistent infection of the atheromatous lesions could lead to plaque destabilization, microemboli formation and ischemia.

In fact, several types of infectious agents have been identified in coronary artery plaques, including viruses such as cytomegalovirus and herpesviruses, as well as the bacterium Chlamydia pneumoniae. Cytomegalovirus has been found in both normal and atheromatous arteries, and the inflammatory response triggered by this infection is believed to be a major cause of restenosis after angioplasty; newer drug-coated stents may prevent CMV-induced restenosis by targeting the inflammatory response. In contrast, the bacterial pathogen Chlamydia pneumoniae is found almost exclusively in atheromatous tissues. Atherectomy specimens retrieved either post-mortem or during angioplasty show that this organism is present within atheromas in the majority of patients by either PCR, immunohistochemistry or even electron microscopy. Furthermore, patients with coronary artery disease are more likely to have antibodies to the viruses and to C. pneumoniae. In laboratory experiments, these pathogens have been shown to be capable of triggering many of the inflammatory events that occur in atherosclerotic lesions. Interestingly, infection of hyperlipidemic animals accelerates atherosclerosis; furthermore, since C. pneumoniae is a bacterial pathogen susceptible to certain antibiotics, those animals infected with C. pneumoniae and then treated with antibiotics show regression of their atheromas. Indeed, large-scale clinical treatment trials are currently underway to determine if giving antibiotics to heart disease patients can reduce the rate of heart attacks or other secondary coronary events.

Many cardiologists are hesitant to accept that infection could be another risk factor for heart disease. Indeed, the infection hypothesis in cardiovascular diseases is much less accepted than other infectious agent links, say the association between Helicobacter pylori and gastric ulcers. One of the reasons is because unlike gastric ulcers, atherosclerosis is a chronic disease that takes years or even decades to develop. Therefore, while ingesting H. pylori shortly leads to gastric ulcers and its treatment with appropriate antibiotics cures the ulcer, infection with C. pneumoniae or herpesviruses could take years to trigger the development of identifiable atheromatous lesions. Furthermore, treatment of C. pneumoniae infection is not as straightforward as treatment of H. pylori; in fact, circulating blood monocytes infected with C. pneumoniae appear to be resistant to treatment with traditional doses of Azithromycin.

The link between infection and atherosclerosis has been hampered by the lack of rapid and accurate diagnostic tests to detect which heart disease patients are infected. Improved diagnostics that determine if patients with coronary artery disease are infected could lead to cardiologists offering antibiotics to selected patients. Development of angioplasty devices that can perform in vivo biopsies for immediate diagnosis of infection could allow in situ drug delivery to eradicate infection. Innovations in medical devices and diagnostic tests are therefore necessary to move the infection hypothesis forward within the cardiology community.

Introduction:

Cardiovascular disease (CVD) is the leading cause of death in developed countries. The established risk factors associated with the disease are:

1) Lifestyle: smoking, diet, excessive alcohol consumption and physical inactivity.

2) Biochemical and physiological: elevated blood pressure and LDL cholesterol, hyperglycemia and diabetes, obesity

3) Personal: age, sex, family and personal history (1).

It has been noted, however that a fair proportion of people with CVD do not have the traditional risk factors. The search is on to find another factor (or factors) that would complete the etiological picture of cardiovascular disease.

One possibility currently being investigated is the association of infectious disease with CVD; either as a risk factor itself or an intensifier of other risk factors (2). This is not a new idea. Sir William Osler first proposed a causative role for infection in heart disease in 1908 (3).

Biochemical Basis:

The main pathological process underlying both cardiovascular and cerebrovascular diseases is atherosclerosis, or the accumulation of lipid-containing material within the blood vessels, causing arterial occlusion (2)
.
Various mechanisms have been offered to support the idea that infection and the inflammatory process affects the arteries and leads to disease onset. One scenario suggests that when bacteria attack the vessel wall the inflammatory response leads to an increase in lymphocytes and macrophages and in the production of cytokines and tissue growth factors. Tissue growth factors are within the clotting cascade. Lipid metabolism is also regulated during this response; lipoproteins are scavengers of foreign materials such as bacterial endotoxins. Cytokines are a mediator in this response and they also can increase very low-density lipoprotein levels, another risk factor for CVD (4)

Pesonen et al. (5) found an association between thickening of the inner coat of blood vessels and infectious disease based on autopsied children. They concluded that infections in general were associated with this thickening and suggested this association may predispose coronary arteries to atherosclerosis.

Repeated fibroproliferative events lead to atherosclerosis (6) Response-to-injury theory states that various factors, such as infection, can cause these events and damage endothelial cells.

Evidence:

The conditions or infectious agents most frequently studied include the Chamydia pneumoniae, Helicobacter pylori, cytomegalovirus, herpes simplex virus and periodontitis. The focus of current research is on the association of C. pneumoniae and atherosclerosis. Evidence for a possible association comes from two types of studies: seroepidemiology and the demonstration of the organism within atherosclerotic tissue.

Saikku et al. (7) found that chronic Chlamydia infection was higher in patients with acute myocardial infarction and chronic coronary heart disease than in controls. They concluded that chronic infections could be a factor in the pathogenicity of CVD. Further work by these investigators (8)showed elevated titers against C. pneumoniae were associated with an increased risk of developing a cardiac event six months later, again suggesting a risk role for Chlamydia in the development of CVD.


Other evidence for an association comes from the finding of the organism in the cells of atherosclerotic lesions (11). And in animal studies atherosclerotic-lesions have been found in the aorta of rabbits introduction of C. pneumoniae (12). Grayston (9) reported 44 studies finding the presence of this organism, 3 did not.


Leinonenn and Saikku (13) suggest that C. pneumoniae interacts with other risk factors of atherosclerosis. They found that the risk of a cardiac event was increased 4.6-fold when markers for atherosclerosis (obesity, elevated systolic blood pressure and blood glucose and lowered HDL cholesterol) were combined with markers of chronic C. pneumoniae infection.

Atherosclerosis is a complex, multifactorial disease. Recently, research has intensified to identify the role of various infections in the pathogenesis of atherosclerosis. Specific agents have been proposed as direct initiators or accelerators of atherosclerosis, while other infectious agents have been proposed as accelerators of atherosclerosis through nonspecific stimulation of the inflammatory cascade. Recently, the total pathogen burden concept has suggested that while each specific infection contributes only slightly to the pathogenesis of atherosclerosis, the cumulative effects of infectious agents contribute greatly. Several randomized trials evaluating antibiotic therapy in the prevention of cardiovascular events have now been completed, although results have been conflicting. This manuscript summarizes current understanding of the role of infectious agents as a trigger of inflammation, as a contributor to atherosclerosis, and the potential role of antibiotic therapy in the treatment of atherosclerosis.

Infectious agents, such as herpesviruses, have been hypothesized to be involved in development of atheromatous plaque. The study aim was to evaluate the possibility that HHV-8 infection could be an additional risk factor for the establishment of cardiovascular disease. HHV-8 seroprevalence was determined by immunofluorescence in a population of cardiovascular disease patients (n=50) as compared to an age- and sex-matched group of control subjects (n=47); HHV-8 genome was detected in DNA extracted from circulating PBMC and from atheromatous lesions by PCR with primers specific for the minor virus capsid gene (ORF 26). The seroprevalence of HHV-8 was significantly increased in the patients as compared to the control population, while the presence of HHV-8 genome was observed in PBMC from 2 patients and 1 control. Virus-specific DNA was found in 2 out of 4 atheromatous plaques. The higher seroprevalence in patients suffering from vascular diseases as compared to age-and sex-matched controls suggests that HHV-8 infection could be an additional risk factor for the establishment of cardiovascular disease, although the data on the persistence of viral DNA in PBMC or in the arterial lesions are too exiguous to definitively support this hypothesis. More extensive studies are needed to define the exact role of HHV-8 infection in the establishment and progression of atheromatous lesions.

"Total Pathogen Burden" and Atherosclerosis

Recently, the concept of a pathogen burden has been proposed.[4] While single infectious agents may increase the risk of atherosclerosis only slightly, the cumulative exposure to multiple atherogenic infectious agents might enhance the risk greatly. In an initial study of 233 subjects undergoing coronary angiography, IgG antibodies were measured to C. pneumoniae, CMV, hepatitis A, HSV-1, and HSV-2. The prevalence of CAD was 48%, 69%, and 85% for individuals with antibodies to ≤2, 3-4, or 5 pathogens. CRP increased with the number of infections, and the prediction of CAD by pathogen burden was limited to subjects with elevated CRP.[4]

To confirm and extend this association to secondary risk in a prospective trial, a cohort of patients with angiographically documented severe CAD was tested for antibodies to C. pneumoniae, H. pylori, CMV, HSV-1, HSV-2, and hepatitis A virus and followed for up to 5 years (Figure 1). After adjustment for traditional risk factors, the hazard ratio for death or MI was 2.0 for CMV, 1.6 for hepatitis A, and 1.5 for HSV-2 (p<0.05 for all). Notably, risk increased stepwise with the number of positive antibodies: relative hazard increased to 6.5 for seropositivity to five pathogens (p=0.0005 for trend).[37] Serologic risk was primarily driven by exposure to the viral pathogens (Figure 2).

The German AtheroGene study[38] of 1018 CAD patients correlated seropositivity to C. pneumoniae, H. pylori, Mycoplasma pneumoniae, Haemophilus influenzae, CMV, HSV-1, HSV-2, and Epstein-Barr virus with secondary risk. CV mortality increased with increasing infectious burden (Figure 1). Serologic infectious burden correlated somewhat with CRP, but it retained independent predictive value. Positive results also were driven primarily by exposures to herpesviridiae (Figure 2).

In a subgroup of 572 patients in the AtheroGene study,[39] the infectious burden correlated with the extent of atherosclerosis, determined by coronary angiography, carotid duplex sonography, and ankle-brachial index. The odds ratios for CAD were 1.8 for 4-5 positive serologies and 2.5 for 6-8 compared with 0-3 serologies (p<0.02). C. pneumoniae IgA, H. pylori IgG, CMV, and HSV-2 were individually associated with advanced atherosclerosis (≥2 vascular regions). Among patients with advanced atherosclerosis, CV mortality (at 3.2 years follow-up) was 7% in patients positive to 0-3 pathogens vs. 20% in those seropositive to 6-8 pathogens.

Other related studies of vascular disease have also suggested benefit of antibiotic therapy. Forty men with peripheral arterial disease and seropositivity for C. pneumoniae were randomized to 1 month of roxithromycin or placebo and followed for 2.7 years.[50] The treated group had fewer intervention procedures (20% vs. 45%; p=0.049), had less restriction in walking (20% vs. 65%; p=0.04), and had regression in carotid soft plaques compared with placebo. In a study of 272 patients with ischemic stroke,[51] C. pneumoniae seropositivity was associated with greater carotid intimal medial thickness progression compared to nonseropositivity. Those randomized to treatment with roxithromycin for 30 days showed reduction of rate of progression compared with those assigned placebo (0.07 vs. 0.11 mm/year; p<0.01). Finally, in a randomized trial[52] of azithromycin or placebo for 5 weeks, 40 patients with CAD were evaluated for endothelial function by flow-mediated dilation of the brachial artery. Azithromycin therapy resulted in improvements in endothelial function (change of 2.1% [p<0.005] vs. change of -0.02 [p=NS]) and a significant decrease in E-selectin and von Willebrand factor levels.

action reaction, your doing a really great job, I'm now convinced we should focus on killing pathogens, and frequencies seem to be the way to do it.

fredounet wrote:action reaction, your doing a really great job, I'm now convinced we should focus on killing pathogens, and frequencies seem to be the way to do it.

Thank you Fredounet, but you really should thank jdp, I'm just trying to get his work out there and into people's faces, standing on his shoulders if you will... haha, you can thank me when I develop that regeneration medium

Just want to add something in favor of rife, the squared statement say's a lot in terms of what electricity / frequency's can do.

In this article we will describe what Rife's frequency instrument was and how it could destroy a microbe without harming the host/patient.

Figure 1 shows a schematic view of the Rife frequency instrument in operation treating a patient. The frequency instrument consisted of an old style X-ray tube, which had been back filled with helium gas at very low pressure and had a current flow through the tube driven by a sine wave voltage oscillator. When the voltage polarity across the X-ray tube was such that the hot tungsten cathode was at a negative voltage as compared to the metal plate anode, an electron current would flow from the cathode to the anode. This electron current would collide with the helium atoms exciting them and thereby generating light. Since the polarity conditions for current flow through the X-ray tube were only met on one half the sine wave voltage cycle there was one pulse of light produced for each complete sine wave voltage oscillation cycle (see Figures 2 and 3). Another way to say this is, that if a million cycles per second of sine wave voltage is applied across the X-ray tube, the X-ray tube will produce one million pulses of light per second. As a practical example, Rife found that the common carcinoma breast cancer, (which is now reaching epidemic proportions among women), was killed by a light pulse of 11,780,000 light pulses per second.4,5

To that end I will now describe and illustrate how the Rife frequency instrument can destroy a virus. I will illustrate how a specific virus can be destroyed by a specific frequency of ultra sound. This ultra sound is generated by the Rife frequency instrument. Note that light carries linear momentum and that when the pulse of light from the Rife frequency instrument is absorbed by the patient's skin layer that skin layer must recoil in the direction of light flow to conserve linear momentum. When the light pulse has ended, the skin relaxes back toward its non light pulse exposure position. In other words, periodic light pulses generate periodic pressure pulses in the patient's skin layer which travel into the patient's body. The Rife frequency instrument converts the patient's entire exposed skin surface into an ultra sound transducer for the generation of ultra sound. Even though the efficiency of ultra sound production is exceedingly low by this method, it is still adequate to kill microbes

To see how the ultra sound generated by the Rife frequency instrument can destroy a virus we will examine the outer protein coat (capsid) structure of a virus. Most viruses of interest which cause diseases in plants and animals have an icosahedral capsid structure as illustrated in Figure 4A and B. A specific example of this icosahedral capsid structure is illustrated in Figure 5. Each dark circle represents a spherical protein molecule clump. When the virus capsid of Figure 5 is folded together as indicated in Figure 4A and B, a simple virus capsid model has been formed. Examination of this capsid model shows a large number of intersecting and overlapping closed rings of protein molecule clumps. These closed rings of periodically spaced protein clumps are illustrated in Figure 6A and B. In classical physics when studying standing wave phenomenon the periodically spaced protein clumps, as illustrated in Figure 6A and B, are known as the mass beads on a string problem with circular boundary conditions. Figures 7A, B and C, illustrate this classical physics problem. Figures 8A and B illustrate one of the standing wave motion modes which the closed periodically spaced protein clump rings of Figures 6A and B can sustain. Figure 8A shows a ten member protein clump ring linearized for ease of graphing wave motion displacement of the center of the protein clumps from their equilibrium position. Figure 8B shows the most stressful oscillation mode for the ten member protein clump ring. In this oscillation mode, adjacent protein molecule clumps are always going in opposite directions and therefore putting maximum stress on where they are bonded together. If this oscillation mode is raised to a high enough displacement amplitude the ring will rupture. If enough rings are ruptured, the virus capsid disintegrates. The Rife frequency instrument when set to the frequency which corresponds to the most stressful oscillation mode for the virus of interest, as illustrated in Figure 8B, will destroy that virus capsid coat and therefore destroy the virus.

The common virus capsid coat was chosen to show how the Rife frequency instrument can destroy a microbe which have closed on themselves periodically spaced protein clump structures. Bacteria, protozoa, rickettsias, and fungi all have these closed on themselves periodically spaced protein clump structures in their outer structure, which makes them susceptible to destruction by the Rife frequency instrument.

Advancements in electron technology have made a much more efficient and vastly more powerful replacement for the Rife frequency instrument. Namely, the piezo-electric transducer, driven by an appropriate signal function generator as can be purchased in any electronic test equipment store. In our present circumstances where antibiotic resistant bacteria are about to become rampant, anti-viral drugs are largely still just a bio-tech dream, and the war on cancer has been a dismal failure for the cancer patient, but not for the so-called cancer researcher. It is long since time for Rife's 1930's work to be implemented.

actionthe squared statement say's a lot in terms of what electricity / frequency's can do.

Would recommend to look into zeta potential here. Ormus appears to have most promise but many ways to increase zeta potential. Ormus is also good for DNA repair http://www.subtleenergies.com/ormus/tw/dna.htm

Regarding Rife and the Body Electric and zeta potential... kill enough pathogens and reverse these autoimmune disorders will normalize PH and "The most important factor that affects zeta potential is pH."

random quotes

"Zeta Potential" is expressed as voltage


Zeta Potential is a measure of the electrical force that exists between
atoms, molecules, particles, suspensoids, cells, etc., in a fluid.


Zeta Potential represents a basic law of Nature, and it plays a vital role in all forms of plant and animal life. It is the force that maintains the discreteness of the billions of circulating cells, which nourish the organism. The stability of simple inorganic man–made systems is governed by these same laws.

jdp701 wrote:

actionthe squared statement say's a lot in terms of what electricity / frequency's can do.

Would recommend to look into zeta potential here. Ormus appears to have most promise but many ways to increase zeta potential. Ormus is also good for DNA repair http://www.subtleenergies.com/ormus/tw/dna.htm

Regarding Rife and the Body Electric and zeta potential... kill enough pathogens and reverse these autoimmune disorders will normalize PH and "The most important factor that affects zeta potential is pH."

Hey jdp, I've looked into Zeta Potential and its ties with pH before, if I understand correctly this goes back to your remark regarding the body lowering pH to deal with pathogens.

Looking through your link now. Thanks!

Yes, that's correct.

If you remember back a youtube video that was posted months ago the guy was talking about low voltage = poor health. Believe the connection he's making is zeta potential. When I think of Body Electric think a lot goes back to zeta potential. Many stressors lower zeta potential. Many ways to raise zeta potential though.

Should also mention that very low voltage increases ATP.

Similiar way of studying some related info to this is biophotons.

Hey jdp.

I have a lot of notes saved on this subject as back when I was on that pH kick it was big part of what I was researching, I'll look into biophotons though, been meaning to.

Excellent studies ar. Now if only you can convince us of Rife as a useful treatment, haha.

Tobacco smoke induces a persistent, but recoverable state in Chlamydia pneumoniae infection of human endothelial cells

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WN6-4HGM77W-1&_user=10&_coverDate=12/31/2005&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1593305660&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=69dfbfa6fddf9f3bc2ec00db648731da&searchtype=a

We investigated the extent to which tobacco smoke could induce persistence of Chlamydia pneumoniae in human endothelial cells. Aortic and coronary artery endothelia were infected in the absence or presence of non-cytotoxic concentrations of tobacco smoke medium. Following exposure to smoke medium, chlamydial inclusions were smaller and demonstrated fewer genome copies as determined by real-time PCR. Enumeration of inclusion-forming units (IFU) established a significant smoke-mediated, dose-dependent inhibition of elementary bodies (EB). Host cell apoptosis did not contribute to the observed restriction of productive infection. Ultrastructure analysis demonstrated an arrest in chlamydial development following smoke-exposure, with a predominance of reticulate bodies (RB) observed inside inclusions. Recovery of viable IFU was achieved with removal of smokemedium and addition of l-tryptophan. In the presence of smoke, C. pneumoniae infection demonstrated all the characteristics of persistence in human endothelia cells. This is the first time that primary human arterial endothelial cells have been shown to support chlamydial persistence. Tobacco smoke is a well-characterized risk factor for progression of atherosclerosis, but a novel means of inducing chlamydial persistence in vascular cells. Thus, smoking may additionally contribute to atherosclerotic disease by inducing a persistent chlamydial infection in arterial endothelium.

crincrin wrote:Excellent studies ar. Now if only you can convince us of Rife as a useful treatment, haha.

Tobacco smoke induces a persistent, but recoverable state in Chlamydia pneumoniae infection of human endothelial cells

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WN6-4HGM77W-1&_user=10&_coverDate=12/31/2005&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1593305660&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=69dfbfa6fddf9f3bc2ec00db648731da&searchtype=a

We investigated the extent to which tobacco smoke could induce persistence of Chlamydia pneumoniae in human endothelial cells. Aortic and coronary artery endothelia were infected in the absence or presence of non-cytotoxic concentrations of tobacco smoke medium. Following exposure to smoke medium, chlamydial inclusions were smaller and demonstrated fewer genome copies as determined by real-time PCR. Enumeration of inclusion-forming units (IFU) established a significant smoke-mediated, dose-dependent inhibition of elementary bodies (EB). Host cell apoptosis did not contribute to the observed restriction of productive infection. Ultrastructure analysis demonstrated an arrest in chlamydial development following smoke-exposure, with a predominance of reticulate bodies (RB) observed inside inclusions. Recovery of viable IFU was achieved with removal of smokemedium and addition of l-tryptophan. In the presence of smoke, C. pneumoniae infection demonstrated all the characteristics of persistence in human endothelia cells. This is the first time that primary human arterial endothelial cells have been shown to support chlamydial persistence. Tobacco smoke is a well-characterized risk factor for progression of atherosclerosis, but a novel means of inducing chlamydial persistence in vascular cells. Thus, smoking may additionally contribute to atherosclerotic disease by inducing a persistent chlamydial infection in arterial endothelium.

Hahah, thanks Crincrin, I'm not too worried about the rife stuff yet, just about the basic pathology.
Thanks for posting!

Ohhh dear, happy new years too... hahahahaha.

Androgens and energy allocation: Quasi-experimental evidence for effects of influenza vaccination on men's testosterone

Androgens are proposed to allocate finite energetic resources away from immune function and toward anabolic processes related to reproductive effort. In situations of pathogen exposure, the significant energetic demands associated with mounting an immune response are expected to produce a decrease in androgen levels and commensurate redistribution of energy. We tested the hypothesis that even the mild immune challenge associated with vaccination may cause a decline in men's testosterone. As predicted, men who received an influenza vaccination exhibited a more negative change in testosterone over a 2-week period than did men in a nonequivalent control group who were not vaccinated. These results suggest that men's androgen concentrations may be finely calibrated to trade-offs between the energetic demands of immune responses and other life history problems. Am. J. Hum. Biol., 2009. © 2008 Wiley-Liss, Inc.




Would love to have the whole study on this.

Acute Chlamydia pneumoniae reinfection accelerates the development of insulin resistance and diabetes in obese C57BL/6 mice.

Wang C, Gao D, Kaltenboeck B.

Department of Pathobiology, Auburn University, Auburn, Alabama, USA.
Abstract

BACKGROUND: Epidemiological and pathological evidence links highly prevalent pathogens to chronic inflammatory diseases, such as type 2 diabetes. Animal models contribute critically to the mechanistic understanding of infectious enhancement of inflammatory diseases, which share insulin resistance as the central pathophysiological defect.

METHODS: With use of a mouse model, we examined insulin resistance progression and the influence of infection (Chlamydia pneumoniae-infected vs. uninfected control mice), genetic background (C57BL/6 vs. A/J mice), dietary fat concentration (27% vs. 5%), and time (2, 5, 9, or 15 weeks after inoculation).

RESULTS: In obese C57BL/6 mice, C. pneumoniae infection induced significantly increased insulin resistance that persisted long after bacterial clearance. Circulating tumor necrosis factor (TNF)-alpha produced in response to acute C. pneumoniae lung colonization exacerbated insulin resistance but not TNF-alpha released in situ during secondary chlamydial infection. Azithromycin or anti-TNF-alpha antibody prevented infection-exacerbated insulin resistance but significantly enhanced chlamydial dissemination to the heart. Azithromycin-treated mice did not eliminate C. pneumoniae from lungs by 3 weeks after inoculation but had significantly lower loads (42 genomes per 100 mg) than did control mice (219 genomes per 100 mg) or anti-TNF-alpha antibody-treated mice (3090 genomes per 100 mg).

CONCLUSIONS: Murine C. pneumoniae infection enhanced insulin resistance development in a genetically and nutritionally restricted manner via circulating mediators. The relevance for the current human diabetes epidemic remains to be determined, but this finding is potentially important because of the high prevalence of human C. pneumoniae infection worldwide.


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Background

The metabolic syndrome together with insulin resistance and their consequences are basic factors in pathogenesis of atherosclerosis. Chronic infections with herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), and Chlamydia pneumoniae are associated with the development of atherosclerosis and coronary heart disease. The infectious aspects of metabolic syndrome have not been investigated.
Methods

In a cross-sectional, population-based study, we used National Cholesterol Education Program (NCEP)-Adult Treatment Panel (ATP)-III criteria in 1791 subjects, aged 25 years and over, selected by cluster random sampling in three Iranian ports in the northern Persian Gulf. Sera were analyzed for IgG antibodies to Chlamydia pneumoniae, HSV-1, Helicobacter pylori (H. pylori) and CMV using ELISA.
Results

In multiple logistic regression analysis, of the infectious agents, CMV [OR = 1.81 (1.05–3.10); p = 0.03], H. pylori [OR = 1.50 (1.12–2.00); p = 0.007] and Chlamydia pneumoniae [OR = 1.69 (1.27–2.25); p < 0.0001] showed a significant association with the metabolic syndrome in men and HSV-1 [OR = 1.95 (1.22–3.11); p = 0.005], H. pylori [OR = 1.45 (1.09–1.94); 0.01] and Chlamydia pneumoniae [OR = 1.65 (1.23–2.21); p = 0.001] in women.
Conclusion

The metabolic syndrome, which occurs very frequently in the general population, has a significant association with prior infection with Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus and herpes simplex virus type 1. Hypothesis about participation of infection in pathogenesis of metabolic syndrome should be investigated.



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Chlamydia pneumoniae induces nitric oxide synthase and lipoxygenase-dependent production o

H Kälvegren, H Bylin, P Leanderson, A Richter, M Grenegård, T Bengtsson

There is increasing evidence that Chlamydia pneumoniae is linked to atherosclerosis and thrombosis. In this regard, we have recently shown that C. pneumoniae stimulates platelet aggregation and secretion, which may play an important role in the progress of atherosclerosis and in thrombotic vascular occlusion. The aims of the present study were to investigate the effects of C. pneumoniae on platelet-mediated formation of reactive oxygen species (ROS) and oxidation of low-density lipoprotein (LDL) in vitro. ROS production was registered as changes in 2',7'-dichlorofluorescin- fluorescence in platelets with flow cytometry. LDL-oxidation was determined by measuring thiobarbituric acid reactive substances (TBARs). We found that C. pneumoniae stimulated platelet production of ROS. Polymyxin B treatment of C. pneumoniae, but not elevated temperature, abolished the stimulatory effects on platelet ROS-production, which suggests that chlamydial lipopolysaccharide has an important role. Inhibition of nitric oxide synthase with nitro-L-arginine, lipoxygenase with 5,8,11-eicosatriynoic acid and protein kinase C with GF 109203X significantly lowered the production of radicals. In contrast, inhibition of NADPH-oxidase with di-phenyleneiodonium (DPI) did not affect the C. pneumoniae induced ROS-production. These findings suggest that the activities of nitric oxide synthase and lipoxygenase are the sources for ROS and that the generation is dependent of the activity of protein kinase C. The C. pneumoniae-induced ROS-production in platelets was associated with an extensive oxidation of LDL, which was significantly higher compared to the effect obtained by separate exposure of LDL to C. pneumoniae or platelets. In conclusion, C. pneumoniae interaction with platelets leading to aggregation, ROS-production and oxidative damage on LDL, may play a crucial role in the development of atherosclerotic cardiovascular disease.


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Effect of Helicobacter pylori Eradication on Insulin Resistance, Serum Lipids and Low-Grade Inflammation

* There is a close relationship between Helicobacter pylori (HP) infection and insulin resistance.
* Our study found that LDL and total cholesterol, triglyceride and C-reactive protein levels were significantly higher in patients with HP infection following treatment, while HDL cholesterol levels were significantly lower.
* HP eradication has a beneficial effect on insulin resistance, atherogenic lipid abnormalities and low-grade inflammation.
* This study suggests that HP eradication may help prevent coronary artery disease and metabolic syndrome.


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http://www.wjgnet.com/1948-9358/pdf/v1/i2/27.pdf <--------- Fantastic PDF if you're interested, very very good read. Not going to paste the whole thing as I think I've driven my point home and it's long.

anyone having trouble viewing this thread?

crincrin wrote:anyone having trouble viewing this thread?

I see it okay, then again I made it, what's up?

working now

here's that study

http://tinyurl.com/2784dmn

crincrin wrote:working now

here's that study

http://tinyurl.com/2784dmn

Thanks a bunch Crincrin, will check it out soon, deep into something else at the moment.