Dr. William Walsh's Comprehensive Theory (Explaining the Cause of Bipolar, the Reason For Switching From Mania to Depression & Treatment Implications) Shared at the Society of Neuroscience
What we know about photobiomodulation (PBM), especially 1070nm transcranial delivery, is that it can significantly increase ATP production and rapidly decrease ROS and NO levels. I would strongly suggest considering the inclusion of 1070nm continuous and pulsed photobiomodulation as a component of a treatment model seeking to address the root neurophysiological and bioenergetic causes of neuropsychiatric, neurodegenerative and neurodevelopmental disorders. Our research has confirmed the efficacy of a brief, self-administered transcranial 1070nm transcranial PBM stimulation protocol
Near-infrared photobiomodulation (NIR-PBM) impacts reactive oxygen species (ROS) and nitric oxide (NO) levels in the brain through mechanisms that involve mitochondrial function, redox signaling, and cellular metabolism. Here's a summary of its effects:
Reduction of Excess ROS:
NIR-PBM can reduce excessive ROS production by enhancing mitochondrial efficiency. Near-infrared light targets cytochrome c oxidase (CCO) in the mitochondrial electron transport chain, improving ATP production and reducing electron leakage that generates ROS.
By mitigating excessive ROS, NIR-PBM can decrease oxidative stress, which is implicated in neurodegeneration, inflammation, and apoptosis.
Modulation of Physiological ROS Levels:
Low levels of ROS serve as signaling molecules essential for cellular homeostasis and defense. NIR-PBM supports this physiological role by optimizing mitochondrial respiration and maintaining ROS at levels conducive to cellular signaling without tipping into oxidative damage.
NIR-PBM can displace NO bound to cytochrome c oxidase, allowing mitochondrial respiration to resume efficiently. This displacement alleviates NO-induced mitochondrial inhibition and supports energy production.
NO Production in Vasodilation and Neuroprotection:
NIR-PBM stimulates the activity of endothelial nitric oxide synthase (eNOS), increasing NO production. Enhanced NO levels improve cerebral blood flow through vasodilation, which is beneficial for oxygen and nutrient delivery to neural tissues.
NO generated through NIR-PBM can also play neuroprotective roles, such as modulating neurotransmitter release, reducing excitotoxicity, and enhancing synaptic plasticity.
Balancing NO Levels:
While NO is beneficial at physiological levels, excessive NO can contribute to nitrosative stress. NIR-PBM helps maintain NO within an optimal range, avoiding deleterious effects.
Therapeutic Implications:
Neuroprotection:
By reducing ROS overproduction and optimizing NO levels, NIR-PBM protects neurons from oxidative and nitrosative stress, both of which contribute to neurodegenerative diseases like Alzheimer's, Parkinson's, and multiple sclerosis.
Anti-inflammatory Effects:
ROS and NO are central mediators of neuroinflammation. NIR-PBM modulates their levels, reducing the activation of pro-inflammatory pathways and promoting a more anti-inflammatory environment in the brain.
Enhanced Cognitive Function:
Improved mitochondrial function, reduced oxidative stress, and increased cerebral blood flow due to balanced ROS and NO levels contribute to better cognitive and emotional performance.
These mechanisms make NIR-PBM a promising therapeutic tool for addressing oxidative stress, neuroinflammation, and mitochondrial dysfunction in various neurological conditions.
I am quite glad to offer this perspective and have someone with MD after their name actually appreciate it. Let me know if you have any further questions or wish to see associated publications.
She has chosen, rather than hypomania and depression, to identify as “cognitive vivacity” and “cognitive impairment”. This condition does indeed make for quite a ride!
How far back can you detect vulnerability at this time? At what age can you say a child might be at risk? And is it currently through behavioral or DNA analysis? Thanks 🙏
To my knowledge, genome-wide studies are not available outside of research. Once they are, however, the age won´t matter, as our genome doesn't change with age. The onset of bipolar disorder can be at any age, but the more typical onset is in the teens or early twenties. Other brain conditions, however, can also be due to high oxidative stress and may come before bipolar disorder. Thank you for this question.
What we know about photobiomodulation (PBM), especially 1070nm transcranial delivery, is that it can significantly increase ATP production and rapidly decrease ROS and NO levels. I would strongly suggest considering the inclusion of 1070nm continuous and pulsed photobiomodulation as a component of a treatment model seeking to address the root neurophysiological and bioenergetic causes of neuropsychiatric, neurodegenerative and neurodevelopmental disorders. Our research has confirmed the efficacy of a brief, self-administered transcranial 1070nm transcranial PBM stimulation protocol
Near-infrared photobiomodulation (NIR-PBM) impacts reactive oxygen species (ROS) and nitric oxide (NO) levels in the brain through mechanisms that involve mitochondrial function, redox signaling, and cellular metabolism. Here's a summary of its effects:
Reduction of Excess ROS:
NIR-PBM can reduce excessive ROS production by enhancing mitochondrial efficiency. Near-infrared light targets cytochrome c oxidase (CCO) in the mitochondrial electron transport chain, improving ATP production and reducing electron leakage that generates ROS.
By mitigating excessive ROS, NIR-PBM can decrease oxidative stress, which is implicated in neurodegeneration, inflammation, and apoptosis.
Modulation of Physiological ROS Levels:
Low levels of ROS serve as signaling molecules essential for cellular homeostasis and defense. NIR-PBM supports this physiological role by optimizing mitochondrial respiration and maintaining ROS at levels conducive to cellular signaling without tipping into oxidative damage.
Nitric Oxide (NO):
Marvin Berman PhD
Quietmindfdn.org
Release of Bound Nitric Oxide:
NIR-PBM can displace NO bound to cytochrome c oxidase, allowing mitochondrial respiration to resume efficiently. This displacement alleviates NO-induced mitochondrial inhibition and supports energy production.
NO Production in Vasodilation and Neuroprotection:
NIR-PBM stimulates the activity of endothelial nitric oxide synthase (eNOS), increasing NO production. Enhanced NO levels improve cerebral blood flow through vasodilation, which is beneficial for oxygen and nutrient delivery to neural tissues.
NO generated through NIR-PBM can also play neuroprotective roles, such as modulating neurotransmitter release, reducing excitotoxicity, and enhancing synaptic plasticity.
Balancing NO Levels:
While NO is beneficial at physiological levels, excessive NO can contribute to nitrosative stress. NIR-PBM helps maintain NO within an optimal range, avoiding deleterious effects.
Therapeutic Implications:
Neuroprotection:
By reducing ROS overproduction and optimizing NO levels, NIR-PBM protects neurons from oxidative and nitrosative stress, both of which contribute to neurodegenerative diseases like Alzheimer's, Parkinson's, and multiple sclerosis.
Anti-inflammatory Effects:
ROS and NO are central mediators of neuroinflammation. NIR-PBM modulates their levels, reducing the activation of pro-inflammatory pathways and promoting a more anti-inflammatory environment in the brain.
Enhanced Cognitive Function:
Improved mitochondrial function, reduced oxidative stress, and increased cerebral blood flow due to balanced ROS and NO levels contribute to better cognitive and emotional performance.
These mechanisms make NIR-PBM a promising therapeutic tool for addressing oxidative stress, neuroinflammation, and mitochondrial dysfunction in various neurological conditions.
Thank you for this.
I am quite glad to offer this perspective and have someone with MD after their name actually appreciate it. Let me know if you have any further questions or wish to see associated publications.
Best
Marvin Berman
Quietmindfdn.org
Thank you
Happy to inform other clinicians that a noninvasive option is available. We consult with providers and patients on the application of these resources.
Late onset with diagnosis - highly functioning senior, PhD, CPA - amazing ride for both of us. Medicated, chasing symptoms.
Thank you for sharing this. Hoping you´re seeing benefit from the treatment.
She has chosen, rather than hypomania and depression, to identify as “cognitive vivacity” and “cognitive impairment”. This condition does indeed make for quite a ride!
How far back can you detect vulnerability at this time? At what age can you say a child might be at risk? And is it currently through behavioral or DNA analysis? Thanks 🙏
To my knowledge, genome-wide studies are not available outside of research. Once they are, however, the age won´t matter, as our genome doesn't change with age. The onset of bipolar disorder can be at any age, but the more typical onset is in the teens or early twenties. Other brain conditions, however, can also be due to high oxidative stress and may come before bipolar disorder. Thank you for this question.
Hi, could you give me an authorization to translate this incredible article to Portuguese?