The Methylation Priority PrincipleÂ©
Nutrients that support methylation are depleted. They clear stress markers nitric oxide and aldehydes and support recovery of active glutathione. Methylcobalamin does not scavenge for nitric oxide. The working hypothesis is that as less S-Adenosyl Methionine (SAMe) is generated over time, methylation functions are progressively sacrificed. In order for us to stay alive, we must all make adrenalin and turn it off, while less important functions are postponed until resources to make more SAMe become available. Functions may be delayed in this order: impaired healing (RNA, DNA and creatine synthesis), body systems malfunction (autonomic), failure to clear stressors (e.g. estrogen, histamine, metals and some toxins), and ultimately adrenalin metabolism.
Optimally the Autonomic Nervous System (ANS) responds quickly and briefly to stress. With help from the Adrenals, a quick response occurs (synthesis and inactivation of adrenalin). When chronically stressed, a patient experiences a dysfunctional ANS with rigid, inappropriate responses, paradoxical symptoms, and unpredictable outcomes. Parasympathetic Nervous System (PNS) usually becomes weaker as Sympathetic Nervous System (SNS) initially becomes dominant. Destabilization appears to occur, as methylation fails over time. This malfunction is predicted by the Accordion ReserveÂ© model, which describes the interaction of environmental stressors and energy.
More than 50 body functions require methylation (using SAMe to donate a methyl group in a chemical process).Many genetic SNPs (single-nucleotide polymorphisms) potentially complicate the ability to efficiently generate SAMe. Fifteen percent of SAMe is used to donate Methionine for nerve healing.
The same nutrients which clean up stress markers â€“hydroxocobalamin and folate, supported by glutathione â€“ are absolutely required to generate SAMe. As these are chronically depleted, less methylcobalamin is generated, less SAMe is created, and less methylation occurs. Increased SNS activity results, which requires increased PNS to compensate. In time PNS fails, and eventually SNS fails, as Adrenal function also fails.
Two steps are required to improve methylation (i.e. generate more SAMe). 1. Make all SAMe-generating loops currently available in the body work 'infinitely' well, 2. Make an 'infinite' number of loops work 'infinitely' well. Step 1 requires optimizing the primary six nutrients ('the Basic 6') to maximize
an individual's potential. There is also a third step (using the 2nd pathway) which incorporates trimethylgylcine,
zinc, and vitamin B6.
Muscle contraction requires adenosylcobalamin, which is created from hydroxocobalamin and glutathione, and contributes to the conversion of methylmalonic acid (MMA) to succinate. Methylcobalamin plays no role in muscle contraction. Isoleucine improves glucose transport into muscle but is invariably depleted in fatigue illness and diabetes. Isoleucine is a precursor to MMA, which may paradoxically account for normal MMA, with chronic B12 deficiency.