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dysautonomia
Again, a page in progress; lots to cover here. Keep coming back as I build the page with much more info!
Dysautonomia is the improper functioning of the autonomic nervous system (ANS), which controls involuntary bodily functions such as breathing, heart rate, blood pressure, digestion, body temperature, hormonal function, bladder function, and sexual function among others. Under typical conditions, the autonomic nervous system increases cardiovascular sympathetic outflow and decreases parasympathetic outflow when an individual rises from sitting to standing. The increase in sympathetic response results in peripheral vasoconstriction of blood vessels, increased cardiac rate, and increased contractile force of heart muscle, which allows for maintained perfusion to the brain and other vital organs. When dysautonomia occurs, the body’s reflexive increase in sympathetic response and decrease in parasympathetic response does not happen properly. While dysautonomia generally involves failure of the autonomic nervous system to react, excessive or overactive ANS actions can also occur. LEARN MORE
My approach as a practitioner is to support the physiological processes that seem to be impacted, either as a result of an autonomic system disorder or processes that for some reason have been broken down and are more causative; I would say that in most cases it is a bit of both. Does mitochondrial dysfunction, for example, cause dysautonomia, or does dysautonomia cause mitochondrial dysfunction?
Either way, or both ways, I would look at those therapies we have in our biological/nutritional toolkit to support, in this case, mitochondrial energy production.
Here, for example, methylene blue is promising for that purpose.
Postural Orthostatic Tachycardia Syndrome (POTS): POTS is a form of dysautonomia characterized by symptoms such as orthostatic intolerance, tachycardia, dizziness, and fatigue. Mitochondrial dysfunction has been proposed as a potential mechanism underlying the pathophysiology of POTS, leading to abnormalities in autonomic nervous system function, energy metabolism, and vascular regulation, which contribute to the symptoms experienced by individuals with the condition.
Therapeutic Implications and Future Directions: The intricate interplay between mitochondrial dysfunction and neurological disorders underscores the potential therapeutic avenues for mitigating disease progression. Strategies aimed at enhancing mitochondrial function, reducing oxidative stress, and promoting mitochondrial quality control mechanisms hold promise for the treatment of various neurodegenerative conditions. Additionally, advancements in mitochondrial replacement therapies and gene editing techniques offer hope for addressing mitochondrial dysfunction at its root cause.
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