http://www.google.com/patents/US20120231089
Reversing autonomic nervous system dysfunction by potentiating methylation
Abstract
1. A method for reversing stress-induced dysfunctions of a human autonomic nervous system in accordance with Methylation Priority Principle comprising:
a first compound chosen from a group of compounds consisting of folic acid, folates, folinic acid, folinates, dihydrofolate, methyltetrahydrofolate and their mixtures and combinations; and
a second compound chosen from a group of compounds consisting of hydroxocobalamin, aquacobalamin, glutathionylcobalamin, adenosylcobalamin and their mixtures and combinations;
The ability to methylate via the methionine cycle is available in every cell . Methylation processes can be ranked according to the body's immediate needs for survival—alert for stress, rid the body of stressor(s), reverse the alert response when the stress is cleared, maintenance of bodily functions, repair and healing, and last, energy storage. When the resources for methylation are limited, those functions that are not immediately necessary for survival or stress reversal will be reduced or suspended.
The consequences of this principle account for the evolution of regional and generalized autonomic dysfunction. Acute and chronic medical conditions and symptoms then develop, resulting from inability to effectively regulate autonomic functions, failure to repair and heal, grow and store energy. In other words, less important methylations can and will be deferred until stress is resolved.
Ideally, the body's response to stress should be immediate, brief (but in no instance longer than necessary) and with the appropriate magnitude. Likewise, termination of the stress response should occur at the right time and with the appropriate magnitude. The end result of these interactions should be a return to the previous state of health. By definition, optimal health is that ideal state of ANS responsiveness to regulate stress responses.
Less than ideal immediate stress responses result in adaptive changes and metabolic consequences. These may include lipid peroxidatio, increased oxidised glutathione and the production of nitric oxide via the inducible nitric oxide synthase pathway. Sustained stress results in excess production of stress metabolites and depletion of necessary protective molecules.
Methylation (Table 1) is required in the body's generalized response to stress and its termination of the response. For example, heightened and sustained stress alerting requires adrenal responses to produce additional adrenalin and excess SNS activity. Adrenalin is activated by methylation. In turn, adrenalin must be inactivated by methylation. Increased PSNS activity to counterbalance SNS activity requires additional production of acetylcholine (Ach), which requires methylation for its production.
TABLE 1
Methylation Priority Principle—MPP.
FUNCTION METHYLATION FUNCTION
Alert for Stress Activate ADRENALIN, increase
sympathetic activity
Reverse the Alert for Stress Inactivate ADRENALIN. Increase
parasympathetic activity; make
choline for ACETYLCHOLINE
Remove the Stress or the response
to Stress
Allergy - Histamine release Inactivate HISTAMINE
Metals—mercury, arsenic, tin, Metabolize for excretion
selenium & others
Toxins Metabolize for excretion
Niacin Inactivate
Estrogen Metabolize
Maintenance of bodily functions Inactivate DOPAMINE,
(examples): NOREPINEPHRINE and
Blood pressure, pulse SEROTONIN,
Breathing depending on needs of
Bowel habits autonomic function
Urine habits Activate MELATONIN; inactivate
Mood, memory, concentration, NOREPINEPHRINE more and
balance, movement SEROTONIN less.
Sleep
Repair and Heal CREATE RNA for protein
synthesis. Proteins for
growth
remodeling (skin, bone, gut
lining)
enzymes for bodily functions
REPAIR DNA
Energy Storage Form CREATINE
The following symptoms are features of ANS dysfunction in its earliest stages of evolution: (1) localised or regional dysfunction—pain, temperature or vascular dysregulation; organ dysmotility, such as gastrointestinal and genitourinary; cardiovascular dysfunction—blood pressure alterations and pulse irregularities; neuro-motor, sensory, cognitive or psychosocial dysfunctions; hematologic, immunologic, dermatologic or secretory dysfunctions; (2) generalized dysfunction—multiple, regional dysfunctions occurring simultaneously, in stages, sequences or complex patterns.
Examples of regional dysfunction include so-called vasomotor rhinitis, palpitations, tics, constipation or urinary urgency. Generalized dysfunctions may include such end-stage autonomic dysfunction as syncope, and postural tachycardia. Well-recognized medical conditions often have autonomic neuropathy as a manifestation, such as diabetes, multiple sclerosis, and Parkinson syndrome.
Prolonged decompensated stress—intermittent or continuous—is frequently unrecognized. Those individuals with undetected stress may suddenly experience a serious morbidity, a life-threatening or life-ending event. They have undisclosed ANS dysfunction, just as those who present with ongoing symptoms.
The consequence of prolonged stress is failed or inadequate methylation, resulting in ANS dysfunction, and ultimately failure to repair, heal and store energy. Failure to repair and heal results in failed protein synthesis, furthering bodily malfunction, such as enzyme synthesis for complete digestion. Incomplete digestion results in reduced availability of essential amino acids, essential fats and carbohydrates, thereby exacerbating ANS decline.