What is the connection between diseases like 'MS' and Mitochondrial functions?
Is this a relationship of the dysregulation or dysfunction of the Mitochondria because of the environmental toxins and endo-toxins disrupting the Heme process which causes the secondary porphyria cascade (even more serious toxins) that leads to progressive symptoms and then disabilities?
It would appear that many if not most degenerative diseases are linked to Mitochondrial ATP production issues. Is the main cause of the ATP production disruption the incomplete 8 stage heme process and the additional toxins that occur?
Many researchers have a variety of theories why MS occurs and they list co-incidences or co-factors and yet they are unable to find a main link to join all the co-incidences. The list is long from Vascular to Diet and just as broad with Infection to Latitude. When I studied the papers I could find on infections such as Lyme and CPn mimicking MS, or vice-versa the link to Mitochondria production and Mitochondria dysfunction showed a cascade path of events that fitted MS symptoms because of the heme production disruption by secondary porphyria caused by these bacterial forms.
If environmental toxins for instance and bacterial endo-toxins (as the bacterial cells die) are producing health problems across the board it would also appear to link the secondary porphyria to the cause of a cascade form of disease progression, degenerative disease.
My personal experiences of being treated for CPn infection/MS have fitted hand in glove with the Mitochondria/porpyhria/symptoms link.
One of the reasons why I ask this question about Mitochondria and porphyria is because I found this piece of knowledge and it's link to degenerative disease and specifically MS;
Pathogenesis of Porphyria.
Both neurological and gastrointestinal symptoms are thought to result from neuronal dysfunction. Histological findings in peripheral
and autonomic nerves include oedema, irregularity of the myelin sheaths, thinned and
irregular axons, axonal vacuolisation, and
degeneration and cellular infiltration.'8
Electrophysiology shows muscle denervation
and decreased motor nerve conduction velocities.'9 The pathogenesis of the cerebral manifestations, however, remains unclear. The
main hypotheses are metabolic abnormalities,
ischaemia, demyelination, and oxidative stress.
Pathology of the CNS includes vacuolisation
of neurons, focal perivascular demyelination,
and reactive glial proliferation.40 Unfortunately, postmortem pathological findings
bear little relation to the clinical features in
life, supporting the theory that many of the
clinical features may be caused by profound