Date:   11/16/2008 12:42:56 PM ( 16 y ago)
Hits:   6,616
URL:   https://www.curezone.org/forums/fm.asp?i=1300789

A couple of things it said in that post stood out for me too.

I've had the tiredness for some time, but thinking back on it, the severity of becoming ill was during a long period of an extremely stress-filled time of my life. I've always thought the stress triggered something. When the rash popped up on my face for no good reason, it was also during the time of dealing with a different stressful situtation.

>>>>Often mycoplasmal infections remain without symptoms until the victim suffers a traumatic event (stress, injury, accident, etc.). These stressing events enable the mycoplasma to begin consumption of cholesterol and symptoms may begin to present. The mechanism of this deterioration is thought to be suppression of the immune system secondary to stress.

Mycoplasma was discovered in 1898. These are living particles of bacterial nucleic acid which do not have a cell wall. In 1971 Rottem et al.3 learned that most species of mycoplasma were absolutely dependent for their growth on the consumption of pre-formed sterols including cholesterol obtained from animal and human host cells. These mycoplasmas live harmlessly in host cells until they are stimulated to activity by a stressing traumatic event (bullet wound, bad fall, injury from accident etc.). The growth of the mycoplasma consumes the cell’s cholesterol resulting in death of the affected cell. Mycoplasmas have been identified in ALS using high resolution blood morphology. In the November 9, 2001 issue of Science Dr. Daniel Mauch4 et al. revealed that the glial cells surrounding the motor neurone sully the extra cholesterol needed to repair and replace aging synapses. If the repair does not properly occur, the motor neurone cells proceed to die form overwork. Glial cells are also heavily involved in gathering, processing and storing glutamate. Elevations in glutamate have been found in brain tissue in ALS.

A mycoplasma species, probably fermentans, which was harmlessly sequestered in a glial cell, becomes aroused by some traumatic stressful event. This mycoplasma then consumes the glial cholesterol which makes up 40% of the glial cell membrane, causing rupture and death of the glial dell. The death of these glial cells releases large amounts of glutamate which becomes elevated in brain tissue. Within the neurone some of the excess glutamate accesses a urea molecule. The urea molecule gives up an ammonia ion which converts a glutamate molecule into less dangerous glutamine. This leaves the former urea molecule as a cyanate ion which damages the motor neurone’s mitochondria. One of the consequences of the damaged mitochondria is a decrease in the energy output available to the neurone. This produces the severe weakness and fatigue seen in patients with chronic fatigue syndrome. If the mitochondrial injury is severe the neurone dies. The death of motor neurone stops message delivery to muscle tissue – a universal finding in ALS.

This avid consumption of cholesterol may also contribute to the endocrine dysfunction seen in ALS because it decreases the amount of cholesterol available to produce estrogen, testosterone, progesterone, hydrocortisone, and aldosterone. Patients with ALS, fibromyalgia, and chronic fatigue syndrome often have hypothalamic dysfunction which may result in adrenal insufficiency, hypothyroidism, and gonadal failure.


 

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