Multiple Sclerosis Reversed: Female, 43

Patient History: 

Patient was suffering from symptoms of MS.  An MRI confirmed 11 active scleroses in her brain.  Paragon’s research team did an analysis of the patient’s diet and lifestyle as well as other research to help determine the potential cause of the patient’s symptoms, and possible therapy. 

Initial Research and Analysis:

Previous blood tests and a detailed patient interview regarding dietary and lifestyle habits indicated:

Studies have shown cerebrospinal fluid levels of S-adenosylmethionine (SAM-e) to be low in patients with methyltetrahydrofolate reductase enzyme deficiency (folic acid, part of the b complex of vitamins), resulting in demyelination in the brain and degeneration of the spinal cord.  Trimethylglycine (TMG) has been shown to restore levels of SAM-e in the cerebrospinal fluid (CSF).

SAM-e deficiencies have been identified in individuals who have nerve damage from HIV/AIDS, multiple sclerosis, or spinal cord degeneration.  We needed to test this patient’s SAM-e related metabolism promptly.

Initial Intervention:

Prior to having comprehensive metabolic testing done, the patient immediately began essential fatty acid supplementation (essential to myelin synthesis) in conjunction with Interferon therapy (a derivative of vitamin C metabolism), and continued to take her own vitamin and minerals. 

Subsequent Metabolic Testing & Analysis:

The initial HTMA that came back showed potential calcium and copper toxicity; higher manganese levels (associated with neurological disorders); potassium and magnesium deficiency (impairing metabolism); as well as disturbed iron metabolism (which can both damage and prevent the repair of myelin).  Most importantly it  showed a problematic phosphorus deficiency – phosphorus is a critical component in the formation of myelin. 

Two months later the patient had Paragon’s PS3 Comprehensive Medical and Metabolic Testing and Analysis done, which confirmed: 

While each of the above test findings would potentially inhibit normal myelination, phosphorus and EFA deficiencies are particularly critical to impaired myelination, as these are the primary components of myelin.  

The patient’s HTMA, blood and urine results confirmed most of what we were expecting to see regarding the SAMe cycle and methylation blockages, very low anti-oxidant levels, impaired iron metabolism, low DHA levels, low B6 &12, as well as other vitamin & nutrient deficiencies necessary for enzyme synthesis of myelin.

Due to the factors cited above, which were further backed up by additional detailed research done, Paragon hypothesised that this patient’s degenerating myelin was caused by a biochemical chain reaction due to a primarily vegetarian diet, 56 months of pre and post-natal nutrient depletion, subsequent excess calcium supplementation, insufficient essential fatty acid intake, and a lack of B vitamins, zinc and other nutrients required for normal metabolism, as well as the proper synthesis of complex fatty fatty acids, all of which:

Final Intervention:

 Paragon designed a comprehensive targeted nutritional intervention meant to lower high homocysteine levels, restore normal SAM-e levels and B12 metabolism, enhance proper regulation of iron, increase plasma antioxidants, and restore other elements of her metabolism necessary for healthy nerve maintenance.

Methylcobalamin supports a healthy brain and spinal cord, and is the only form of vitamin B12 found in the brain.  When preparing the formulation we noted research showing that Methylcobalamin and that the liver can fall behind in converting synthetic cyanocobalamin (Cn/Cbl), into an ample supply of methylcobalamin (Met/Cbl).  Furthermore, not only is Cn/Cbl difficult to convert and slightly toxic, it requires adequate phosphorus, or alternatively SAMe, to be converted to Met/Cbl.  This patient was very low in both.  

All the factors discussed above were addressed with a mix of synergistic supplements, EFAs, and other dietary changes.  

Results

The patient’s symptoms went into remission once beginning EFA supplementation and Interferon.  6 months after beginning the comprehensive nutritional intervention determined by the metabolic research,  testing, and analysis, the patient’s next MRI showed no new scleroses, and no activity at the previous sites.  She has been taking a comprehensive formula since that time and continues to have no symptoms.  

To review the full report on the research, testing and analysis done for this patient see Sample Reports.