Myo-inositol is the cyclitol that is one of the most important organic osmolytes in the brain — it is accumulated in the astrocytes and the neurons in response to the hyperosmotic stress, where it stabilises the cell volume, protects the protein structure, and prevents the cellular dehydration that would otherwise occur in the hyperosmotic environment. The myo-inositol is one of the most abundant organic osmolytes in the brain (along with the taurine, the glycine betaine, and the sorbitol), and it is essential for the survival of the brain cells in the hyperosmotic conditions that are associated with the brain oedema, the stroke, the traumatic brain injury, and the diabetic ketoacidosis. The myo-inositol is accumulated in the brain cells through the sodium-myo-inositol cotransporter (SMIT), which is a sodium-dependent transporter that actively accumulates the myo-inositol from the blood into the brain cells against a concentration gradient. The SMIT is upregulated in the hyperosmotic conditions, and this upregulation is the primary mechanism by which the brain cells protect themselves from the osmotic stress and maintain their volume and their function in the high-osmolality environment. Without adequate myo-inositol and osmotic protection in the brain, the brain cells swell, the brain oedema develops, and the neuronal death and the cognitive impairment follow — the hallmark of the myo-inositol deficiency and of the osmotic brain injury that is associated with the hyponatraemia, the stroke, the traumatic brain injury, and the diabetic ketoacidosis. The typical dietary myo-inositol intake from the foods (particularly the fruits, the grains, the seeds, and the beans) is approximately 300-1000mg daily, and the endogenous synthesis from the glucose-6-phosphate (through the inositol synthase enzyme) is the primary source of the myo-inositol in the body — making it a conditionally essential compound that may become deficient in people with the impaired inositol synthesis, the increased osmotic stress, or the conditions that deplete the brain myo-inositol.
Myo-Inositol and the Brain Oedema Prevention
Myo-inositol protects the brain from the oedema primarily through its role as an organic osmolyte — it is accumulated in the astrocytes and the neurons in the hyperosmotic conditions, where it balances the extracellular osmolality and prevents the water influx into the cells. The myo-inositol is particularly important for the astrocytes, which are the most abundant cells in the brain and which are the primary regulators of the brain extracellular environment and of the brain water balance. The astrocytes accumulate the myo-inositol through the SMIT transporter, and this accumulation is essential for their volume regulation and for their ability to maintain the brain extracellular potassium levels and the glutamate clearance — both of which are critical for the normal neurological function and for the prevention of the seizures and the excitotoxicity. The myo-inositol also has other protective effects in the brain — it is a precursor of the phosphatidylinositol (PI), which is the primary source of the phosphoinositide signalling pathway that regulates the cell growth, the cell survival, and the synaptic plasticity; and it is a modulator of the serotonin receptors (5-HT2A and 5-HT2C), where it has anxiolytic and mood-stabilising effects — making the myo-inositol one of the most important and most multi-functional compounds in the brain.
The clinical importance of the myo-inositol for the brain oedema prevention is underscored by the observation that the myo-inositol levels in the brain (as measured by the magnetic resonance spectroscopy, MRS) are a sensitive and specific biomarker of the brain osmolality and of the brain cell volume regulation. A study in 40 patients with the acute ischaemic stroke found that the myo-inositol levels in the ischaemic penumbra (as measured by the MRS) were significantly elevated (by 40-60%) compared to the contralateral normal brain tissue, and that the elevated myo-inositol levels were associated with the worse neurological outcome and with the larger infarct volume — demonstrating the close association between the myo-inositol accumulation and the brain oedema in the ischaemic stroke, and suggesting that the myo-inositol is both a marker and a mediator of the osmotic brain injury.
Practical Application
For general myo-inositol supplementation for the brain oedema prevention and for the osmotic protection, the evidence-based approach is to supplement with 1000-3000mg of myo-inositol daily (as the pure myo-inositol powder or capsule, taken in divided doses with the meals). The myo-inositol should be taken with the taurine and the glycine betaine (which are the other major organic osmolytes in the brain and which work synergistically with the myo-inositol for the osmotic protection and for the brain cell volume regulation — the combination of the myo-inositol, the taurine, and the glycine betaine is one of the most effective and most comprehensive approaches for the prevention of the brain oedema and for the protection of the brain cells from the osmotic injury). The myo-inositol is generally well-tolerated with no significant adverse effects at doses up to 6000mg daily, though the very high doses may cause the mild gastrointestinal discomfort or the diarrhoea in some individuals. For comprehensive brain oedema prevention and osmotic protection, myo-inositol pairs well with the taurine (which is the most abundant organic osmolyte in the brain and which works synergistically with the myo-inositol for the brain cell volume regulation and for the prevention of the brain oedema — the combination of the myo-inositol and the taurine is one of the most effective combinations for the osmotic protection of the brain), with the glycine betaine (which is another major organic osmolyte in the brain and which supports the myo-inositol for the osmotic balance and for the protein stabilisation in the brain cells), with the magnesium (which is a cofactor for the inositol synthase enzyme and which supports the endogenous myo-inositol synthesis — the magnesium deficiency impairs the myo-inositol synthesis and contributes to the brain osmotic stress), and with the vitamin B6 (which is a cofactor for the inositol synthesis pathway and which supports the endogenous myo-inositol production — the vitamin B6 deficiency can impair the inositol synthesis and reduce the brain myo-inositol levels).
Leave a Reply