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:

• she was normally an extremely active person (indicating possible low B complex, magnesium), 
• she was vegetarian (indicating possible low B12, anemia, and protein deficiency), 
• she had very low dietary fat intake, no oil supplements (indicating probable essential fatty acid deficiency), 
• she had been through two recent pregnancies and breast feedings.  Babies require a large amount of essential fatty acids for their rapidly developing brains.  They also require zinc for the enzyme synthesis of more complex fatty acids in the brain.  These same nutrients are also required for the health and regeneration of the mother’s brain.  However, when pregnant or breast feeding, Nature provides these essential nutrients to the baby prior to mother.  Since this mother’s diet was deficient in essential fatty acids and other nutrients, and because she was a nurturing mother, her own body would have become depleted during two 9 month pregnancy  terms and two 12-18 month long periods of breast feeding, a total of 42-54 months (or 3.5- 4.5 years) in the past eight years.
• blood tests also showed high serum calcium, due to excessive calcium supplementation (indicating high intracellular calcium, which would cause lowered intracellular potassium, phosphorus, sodium, and magnesium uptake), 
• blood tests also showed high homocysteine (11.0 - which would have been damaging myelin and inhibiting its regeneration due to the lipid oxidation/degeneration it can cause).  This also usually indicates a deficiency in B vitamins necessary for healthy regeneration and detoxification.  High homocysteine, also leads to low levels of SAM-e, as homocysteine is not being converted to this molecule, as it normally is.   

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: 

•  low B6, low methylcobalamin (neuro B12), and low folic acid 
•  low SAM-e, required for synthesis of methylcobalamin
•  low anti-oxidants (especially ubiquinol), required to protect existing myelin.
•  extremely low retinol (0%), which is required for both antioxidant and regenerative roles, the decreased regenerative capability possibly being very serious in this case.  
• Despite adequate levels of ALA (since taking flax oil), her testing indicated no ability to synthesize DHA necessary for brain lipid formation (from ALA).  Indicated need for B3, B5, B6, 5P5, zinc, magnesium, insulin, Vit C, and biotin.  

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:

• caused a build-up of homocysteine, which led to a higher and damaging oxidation rate of lipids within her tissues, as well as a depletion of anti-oxidants stores,
• inhibited phosphorus uptake necessary for:
  • the normal regeneration of bi-lipid membrane from which myelin is formed;
  • the conversion of precursor metabolites to Methylcobalamin, necessary for proper brain and spinal cord function
• prevented the formation of DHA lipids necessary for brain function and myelin formation,
• interfered with iron metabolism within the brain necessary for oxygen utilization and normal regeneration & healing.

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.