It sounds like Nanobacteria could be ANOTHER issue in our disease

Discussion in 'Fibromyalgia Main Forum' started by lilwren, Mar 26, 2003.

  1. lilwren

    lilwren New Member

    I’m awaiting my Nanobacteria test results. My doc thinks it is the culprit in my vascular blockage and consequent numbness in my arms. It seems the little nasties form a thick, slimy, calcium deposit inside the veins. I’ve been searching for info on-line and thought I would share some of what I found. I’m sorry, but I could not find the web site for this article. But, a search for Nanobacteria or nanobacterium should bring up articles.

    This is just the first part of the article I found – it is VERY long so I didn’t want to post it all.

    Love,

    Sharon L



    >>>>Nanobacterium sanguineum

    >>>>Nanobacterium sanguineum is a unique organism: there is no other like it on earth. N. sanguineum displays a helical cell wall ultrastructure, contains unique peptides, and its RNA and DNA have an unusual appearance. N. sanguineum is the smallest cell-walled organism yet described; it is smaller than the Vaccinia virus. N. sanguineum takes up amino acids from its environment, but produces biomass at just 1/10,000 the rate of E. coli. N. sanguineum divides only once every three to six days, also 1/10,000 the rate of common bacteria. Nanobacteria is the only mineral forming bacterial species to be isolated from mammalian blood. It is also the only bacteria that can create a calcific biomass at physiologic pH and mineral concentrations. N. sanguineum is pleomorphic, but all of its forms fix calcium and phosphorus to generate a carbonate apatite coating – the same stuff present in diseased arteries and kidney stones. Nanobacteria readily bind to mammalian cells, trick the cells into internalizing them, and then trigger target cell apoptosis - including killing those cells responsible for our natural defenses like T-Lymphocytes (fig1-Nanobacteria killing a T6 Lymphocyte). N. sanguineum demonstrates unique radioresistance, related to its unique nucleic acid makeup and low division rate. 16s ribosomal RNA analysis places N. sanguineum in the alpha-2 subgroup of Proteobacteria. Nanobacteria are sturdy organisms that are resistant to nearly all commonly employed anti-bacterial and anti-septic methodologies. N. sanguineum can be cultured from animal and human blood and diseased tissues. A closer look at N. sanguineum’s biology will help us understand its causative role in human disease.

    N. sanguineum is difficult to detect, difficult to exclude, and thus difficult to keep out of biological products. N. sanguineum is present in fetal bovine sera, human and animal blood, vaccines, and diseased human tissues. N. sanguineum is thus within us and within our field of vision, but we haven’t noticed it until now. Why?
    First of all, N. sanguineum is essentially too small to see. Apatite bearing Nanobacteria can be seen under microscopy using polarized light, but they don’t pick of standard stains, and are thus invisible under standard microscopy. With their small diameter, electron microscopy is absolutely required. Nanobacteria are coccoid to coccobacilar in shape, with a cell wall that varies between 20 to 200 nm in thickness. Divisional septa may occur in the central part of the cell, indicating binary fission (fig. 1), or at the end of the cell, suggesting a budding process (fig. 2, cell division by budding). Budding seems to start by formation of a capsule for a new cell, followed by transfer of cytoplasmic contents into this sheltered compartment.

    … a healthy immune system can try to wall off areas of limited Nanobacterial insult, but that if the blood borne Nanobacteria encounter a region of weakness or impaired local defense, they invade it and begin the process of colony growth; ie: areas of ischemia (ex: brain, cardiac or muscle), injury (ex: joint, infection or tumors) or if trapped (ex: kidney, prostate, cataract or gall bladder). Given that calcified Nanobacteria double only once every six days, calcific clinical disease will not show itself for decades. Consider the athlete who sustains knee damage. The joint heals up, normal function returns, and he returns to the playing field. At age 45, however, the joint is a little stiff. At age 50, he can tell when the weather is going to change (of interest, Nanobacteria grow more rapidly at decreased atmosphere and secrete more biofilm, causing increased inflammatory reaction). Some calcification can be seen on his X-Ray; this progresses (the growth rate of Nanobacterial calcific mass In Vitro is 44% per year, similar to the progression rate of coronary and kidney stone calcification), as do symptoms and functional impairment, leading to joint replacement at age 60. Something caused this joint to calcify over the years, and my hunch is (and NanobacLabs research supports this hunch) that it was Nanobacteria, that settled into the joint when it was damaged on the gridiron. Autopsy studies have demonstrated that early atherosclerosis is not uncommon in 20 year olds. The disease progresses ever so slowly, manifesting itself as clinical coronary disease at middle age, but then its clinical expression speeds up, with artery after artery plugging up. My hunch is that endothelial irritation or damage (e.g. smoking, local flow dynamics, vitamin C deficiency, elevated BP) at a young age allows transiently circulating Nanobacteria to gain a foothold within the artery wall. The bugs are ever so small and grow ever so slowly, so at first little macroscopic disease is seen within the vascular wall, or in the myocardium as ”heart sand”.

    However, with constant doubling, the Nanobacterial mass, now calcium generating, and the inflammation and fibrosis that represent the immune system’s frustrated attempt to contain it and wall it of, reaches size to become a visible plaque. Geometric growth continues; the 50% narrowing at age 45 becomes a 75% lesion at age 50, and you know what happens next. We know that unstable angina is a pan-vascular phenomenon. While the patient’s symptoms are typically related to the destabilization of one lesion in one artery, angioscopic study has demonstrated that plaques in other arteries are anatomically altered and activated (Nanobacterial biofilm stimulating the immune system cascade). In the circulation, inflammatory markers such as CPR will rise. Could it be that unstable angina is really acute Nanobacteremia? Unroofed Nanobacteria release biofilm, leading to an aggressive immediate and long-term immune response and inflammation. Inflammatory organ system dysfunction not infrequently accompanies CABG or major vascular surgery. Free radical stress related to ischemia/reperfusion injury certainly plays a role here, but just as likely it is that when the surgeon incises the diseased artery, he is releasing previously calcified Nanobacteria out into the circulation, precipitating aggressive Nanobacterial growth, biofilm elaboration, and endotoxin production.
  2. lilwren

    lilwren New Member

    and the mystery continues. It certainly sounded the doc was on the right track. We’ll just have to keep looking. I have a Doppler ultrasound of my carotid arteries scheduled for next week. Like having CFS isn’t bad enough - now I have the puzzle as to why my arteries are blocked. Hopefully something will give me some answers soon. Gosh I’m so tired of being a lab rat!

    I wish you all the best regarding your search for knowledge and better health.

    Love,
    sharon

  3. sandydo

    sandydo New Member

    Hi, I have CFS and was treated by Dr. Carol Ann Ryser in Kansas City, Missouri. A friend of mine also went to see the same doctor. She has the nanobacteria. You can check out Dr. Carol Ann Ryser site. Just type in Dr. Carol Ann Ryser and it should come up. Im getting better and Dr. Ryser is seeing all kinds of patients with Fibro and CFS. Hope this helps you. Take care.