Ninatoka
Migraine causes and counteractions
Here are some of the main pathways leading to migraine...
- Methylation issues. Methylation plays a crucial role in various bodily processes, including neurotransmitter metabolization and detoxification. Impairment in methylation can result from missing (co)factors like B12, B11, B6, and choline, or genetic variations such as SNPs on the MTHFR gene. Chronic stress can also strain methylation capacity due to increased metabolization of catecholamines (dopamine, adrenaline, noradrenaline). Additionally, an insulin-resistant liver can lead to methylation problems as the liver prioritizes gluconeogenesis over detoxification, affecting estrogen metabolism and leading to pro-inflammatory metabolites that may penetrate the blood-brain barrier and/or trigger the trigeminal nerve.
- Energy supply. The brain's dependency on glucose for energy makes it vulnerable to energy deficits when glucose levels drop. ATP shortage can activate the trigeminal nerve and initiate cortical spreading depression, leading to aura and migraine.
- Brain hyperexcitability. Early life stress can leave patients in a state of constant high alertness, leading to excess production of glutamate and increased consumption of salt through NMDA receptor activation. Elevated glutamate levels can cause oxidative stress and mitochondrial dysfunction. Certain dietary sources, such as MSG (often used in flavor enhancers), can also contribute to glutamate intake, making it a common trigger for migraineurs.
- Mitochondrial dysfunction. Mitochondrial dysfunction is closely related to brain hyperexcitability and energy supply issues. The combination of an overexcitable brain, heavy reliance on glucose, and insufficient antioxidants can result in oxidative stress and energy deficits.
- Leaky gut. Chronic inflammatory and oxidative and nitrosative stress is associated with the development of a 'leaky gut'. The pro-inflammatory cytokines associated with the inflammation can in turn cause increased blood-brain barrier permeability. With a leaky blood-brain barrier, more toxic substances can penetrate through the blood vessels into the brain and trigger more neuro-inflammation.
- Neuro-inflammation. Neuro-inflammation can be caused by a leaky blood-brain barrier and may further increase its permeability through the production of MMP-9. Activation of the trigeminal nerve, resulting in the production of substance K, can also trigger neuro-inflammation.
- Trigeminal inflammation and myelination issues. The trigeminal nerve can be activated from alarm systems from within the brain (like an ATP shortage, mineral disbalance, ...), but can also be activated peripheral. Chemicals reaching the nerve (e.g. topical face creams), insufficient barrier function in mouth or nose and/or insufficient myelination of the nerve can sensitize this nerve, resulting in the production of CGRP, directly resulting in a migraine.
conditionMigraine
Migraine is the most frequent type of recurrent headache that is brought to the attention of parents and primary care providers, but it remains underrecognized and undertreated, particularly in children and adolescents. Migraine is characterized by episodic attacks that may be moderate to severe in intensity, focal in location on the head, have a throbbing quality, and associated with nausea, vomiting, light sensitivity, and/or sound sensitivity. Compared with migraine in adults, pediatric migraine may be shorter in duration and has a bilateral, often bifrontal, location. Migraine can also be associated with an aura that may be typical (visual, sensory, or dysphasic) or atypical (hemiplegic, Alice in Wonderland syndrome) (Tables 613.2 to 613.6). In addition, a number of migraine variants have been described and, in children, include abdominally related symptoms without headache, and components of the periodic syndromes of childhood.
Ref:
May, Migraine, Editor(s): Harald Kristian (Kris) Heggenhougen, International Encyclopedia of Public Health, Academic Press, 2008, Pages 458-462, ISBN 9780123739605, https://doi.org/10.1016/B978-012373960-5.00023-X.
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