Among the many symptoms of vaccine adverse reactions is brain inflammation, often considered idiopathic or of unknown origins. There are a number of potential culprits underlying vaccine related brain inflammation, including the virus vectors, the neurotoxic adjuvants or the cocktail mistakenly presumed inert ingredients that accompany any vaccine. No matter the cause, however, once inflammation is unleashed within the central nervous system, the inflammatory response itself can become self-perpetuating, initiating secondary pathologies that are chronic, progressive and neurodegenerative.
Chronic brain inflammation, like inflammation in the rest of the body, is now considered one of the leading causes of disease. In the brain, chronic inflammation is believed to lead to Alzheimer’s, dementia and Parkinson’s, while chronic inflammation in the body is connected to heart disease, type 2 diabetes, depression and a myriad of autoimmune diseases. At the center of all inflammatory diseases are dysfunctional mitochondria that, as regulators of the cell survival and number of other functions, control immune reactions – inflammation. Mitochondria are highly susceptible to damage from pharmacological and environmental toxicants and inextricably dependent upon dietary nutrients for proper functioning. When toxicants attack mitochondrial pathways and/or nutrient depletion diminishes mitochondrial functioning, mitochondria activate the immune system and spur inflammatory cascades; cascades that can be stopped only if the exposures are removed and the nutrients restored.
In the brain, neural mitochondria and microglia (brain immune cells), regulate inflammation. Like the mitochondria, these microglia are highly dependent upon dietary nutrients. As we have written previously, the B vitamins are particularly important for central nervous system functioning. New research finds that vitamin B6 is a key regulator of brain inflammation.
Vitamin B6 and Brain Inflammation
Vitamin B6 (pyridoxine >peridoxal 5’ – phosphate) is a necessary co-factor in over 100 enzymes. It is critical for the catabolism (breakdown) of the essential amino acid tryptophan. Tryptophan is required for serotonin (well-being and GI motility) and melatonin (the sleep hormone) synthesis. Disturbances in tryptophan catabolism not only lead to disturbances in neurotransmitter activity, but also, can lead to cell death or apoptosis, in vital brain regions, like the hippocampus (learning and memory), basal ganglia (movement, motivation, intention) and in the cerebellum (motor control and balance).
When all is working well, tryptophan serves as a substrate for serotonin and melatonin. Excess tryptophan is degraded resulting in the by-products nictonic acid and nicotinamide adenine dinucleotide (NAD+) – or as most of us recognize, niacin, vitamin B3. Niacin is an essential nutrient in many physiological functions. Loss of niacin metabolism from this pathway can lead to significant disease, including, Pellagra, a disease characterized by scaly skin lesions, delusions and confusion. In addition to a loss of niacin synthesis, when vitamin B6 is deficient and the tryptophan pathway is disturbed, the incomplete degradation of tryptophan produces several metabolites that are neurotoxic, including one called quinolinic acid.
Quinolinic acid is a potent and self-perpetuating neurotoxin when unopposed in the brain. It generates ROS (reactive oxygen species indicative of mitochondrial oxidative stress and damage) and over-activates NMDA glutamate receptors (the brain’s primary excitatory neurotransmitter) to the point of apoptosis (cell death), all the while inhibiting brain astrocytes’ ability to clean up the excess glutamate. Once that cycle becomes initiated, quinolinic acid potentiates its own release and that of other neurotoxins, ensuring continued brain inflammation and damage.
With the appropriate vitamin B6, quinolinic acid is not the final product of tryptophan catabolism, NAD+ or niacin is, and any damage initiated by quinolinic acid as a natural by-product within this pathway is offset by two neuroprotective factors, kynurenine and picolinic acid. Vitamin B6 is critical for the kynurenine aminotransferase and kynurinase enzymes; enzymes that lead to neuroprotective compounds, kynurenine or picolinic acid. Kynurenine blocks the cytotoxic effects of quinolinic acid by blocking the NMDA receptor, making it unavailable to quinolinic acid, while picolinic acid is the primary metal chelator (remover) in the brain (likely critically important in post vaccine reactions). In other words, vitamin B6 controls the balance between inflammation and anti-inflammation within the brain and the body.
How do We Know Vitamin B6 is a Neuroprotectant?
Well, we’ve actually known this since the 1970s (perhaps earlier) when work on the kynurenine pathway began. Somehow though, it wasn’t recognized again until the 1990’s and has only recently become prominent over the last decade as connections between environmental and pharmaceutical toxicants and gut microbiota and mitochondrial damage are revealed.
Several studies have emerged over the last decade showing the importance of vitamin B6 (and other B vitamins) in systemic and brain inflammation. Defects in vitamin B6 metabolism are linked to seizure disorders resistant to traditional anticonvulsants but remediable with Vitamin B6. Vitamin B6 reduces brain atrophy in Alzheimer’s patients. Low vitamin B6 is believed to play a key role in the oxidative stress associated with Huntington’s disease. One of the more interesting studies involves preventing the hippocampal apoptosis associated with bacterial meningitis using vitamin B6.
Bacterial meningitis is a life threatening disease associated with high mortality and morbidity. Of those patients who survive, up to 50% suffer serious neurological impairment including: hearing loss, seizures, cognitive decrements and sensory-motor deficits. The bacteria attack cortical and hippocampal regions of the brain. Hippocampal cell death is associated with learning and memory deficits. In an experimental version of bacterial meningitis with rodents, researchers tested whether vitamin B6 supplementation could prevent the hippocampal apoptosis by moderating the tryptophan pathway towards the B6-dependent kynurenine and picolinic metabolites versus the neurotoxic quinolinic acid. They were successful. Vitamin B6 supplementation reduced brain inflammation and hippocampal apoptosis by up-regulating the neuroprotective factors controlled by the tryptophan – kynurenine pathway. An impressive result reached simply via vitamin supplementation.
Tryptophan metabolism and the kynurenine pathway are implicated in disease processes where inflammation is prominent. Vitamin B6 may be critical to maintaining the appropriate balance between inflammatory and anti-inflammatory immune reactions. With modern nutritional deficits (high calorie, low nutrient foods), commercial agricultural practices (glyphosate doused crops are nutrient poor), estrogenic medications and environmental exposures (estrogens inhibit vitamin B6), it entirely conceivable that many of us are vitamin B6 deficient and, as a result, functioning with a constant level of inflammation. Vitamin B6 supplementation, along with the other B vitamins might be warranted.
For those individuals suffering from brain inflammation mediated by disease, medication or vaccine adverse reactions, vitamin B6 might just reduce the inflammation cascades and improve quality of life. Given its direct impact on tryptophan metabolism, vitamin B6 ought to be considered critical for brain health.