Mitochondrial Degenerative Disorders Support Protocol

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Problems That May Be Associated with Mitochondrial Cytopathies

Organ Systems Possible Problems
Brain developmental delays, mental retardation, dementia, seizures, neuro-psychiatric disturbances, atypical cerebral palsy, migraines, strokes
Nerves weakness (which may be intermittent), neuropathic pain, absent reflexes, dysautonomia, gastrointestinal problems (ge reflux, dysmotility, diarrhea, irritable bowel syndrome, constipation, pseudo-obstruction), fainting, absent or excessive sweating resulting in temperature regulation problems
Muscles weakness, hypotonia, cramping, muscle pain
Kidneys renal tubular acidosis or wasting resulting in loss of protein, magnesium, phosphorous, calcium and other electrolytes.
Heart cardiac conduction defects (heart blocks), cardiomyopathy
Liver hypoglycemia (low blood sugar), liver failure
Eyes visual loss and blindness
Ears hearing loss and deafness
Pancreas and Other Glands diabetes and exocrine pancreatic failure (inability to make digestive enzymes), parathyroid failure (low calcium)
Systemic failure to gain weight, short stature, fatigue, respiratory problems including intermittent air hunger, vomitting

Taken from Mitochondrial News, Fall 1997 Issue by Bruce H. Cohen, M.D.       When & Where to Get a Diagnosis

Diagnosis of mitochondrial myopathies has been done only since about 1988. Fortunately the situation has improved dramatically for diagnosis in a local hospital. In the past I recommended going to only three doctors: Dr. Richard Haas in San Diego; Dr. Bruce Cohen in Cleveland, Ohio; or Dr. John Shoffner in Atlanta, GA. They are still the top guys in the field, but are no longer the only ones who can accurately diagnosis mitochondrial disease through muscle biopsy. Most major medical centers can offer help. If you are looking for a doctor for diagnosis purposes, try the UMDF (linked on this page) or call and ask for a metabolic physician.   Actually, now there may not be a need for muscle biopsies in everyone, though that’s a matter for discussion with your doctors. Since we already knew that our kids had a confirmed mitochondrial disease because of the muscle biopsy done by Dr. Shoffner in the 90s, we’ve just been on the hunt for the error ever since. Two more muscle biopsies with Dr. Shoffner showed nothing wrong, one with a female sibling of Tim’s, and one with me. But a muscle biopsy done elsewhere with me showed the opposite, and that I did, in fact, have a mito disease. Along comes TRANSGENOMIC Clinical Reference Laboratory. They are able to take blood, and in a process that I don’t pretend to know how it works, read the whole mtDNA thing and tell what’s wrong. It worked in our family, and they were able to find 4 matching mutations in Tim and Danny (the two tested) plus 4 more mutations in Danny. Here is the info on this lab, direct from their result sheet:
TRANSGENOMIC Clinical Reference Laboratory

The discovery of Mendelian inherited genes has enhanced our understanding of the pathways that mediate neurodegeneration in Parkinson’s disease. One main pathway of cell toxicity arises through -synuclein, protein misfolding and aggregation. These proteins are ubiquitinated and initially degraded by the ubiquitin–proteasome system (UPS), in which parkin has a crucial role. However, there is accumulation and failure of clearance by the UPS over time, which leads to the formation of fibrillar aggregates and Lewy bodies. -Synuclein protofibrils can also be directly toxic, leading to the formation of oxidative stress that can further impair the UPS by reducing ATP levels, inhibiting the proteasome, and by oxidatively modifying parkin. This leads to accelerated accumulation of aggregates. Phosphorylation of -synuclein-containing or tau-containing aggregates might have a role in their pathogenicity and formation, but it is not known whether leucine-rich repeat kinase 2 (LRRK2) mediates this. Another main pathway is the mitochondrial pathway. There is accumulating evidence for impaired oxidative phosphorylation and decreased complex I activity in Parkinson’s disease, which leads to reactive oxygen species (ROS) formation and oxidative stress. In parallel, there is loss of the mitochondrial membrane potential. This leads to opening of the mitochondrial permeability transition pore (mPTP), release of cytochrome c from the intermembrane space to the cytosol, and activation of mitochondrial-dependent apoptosis resulting in caspase activation and cell death. There is evidence that recessive-inherited genes, such as phosphatase and tensin homologue (PTEN)-induced kinase 1 (PINK1), Parkinson’s disease (autosomal recessive, early onset) 7 (DJ1).

Disclaimer: These Wellness Protocols are not intended to replace the attention or advice of a physician or other qualified healthcare professional. These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease.

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