Evidence supporting the use of: Magnesium
For the body system: GABA

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Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Magnesium is primarily justified for use in supporting the GABA (gamma-aminobutyric acid) system based on scientific evidence, though the strength of this evidence is modest. Magnesium acts as a cofactor in many enzymatic reactions in the body, including those involved in neurotransmitter synthesis and regulation. Several studies have shown that magnesium can modulate the activity of GABA receptors, which are critical for inhibitory neurotransmission in the central nervous system. In vitro and animal studies indicate that magnesium may enhance GABAergic signaling by acting as a positive modulator of GABAA receptors and by antagonizing NMDA receptors, which counteract GABA's inhibitory effects. Clinical studies in humans are more limited but suggest that magnesium supplementation can have anxiolytic and calming effects, which are presumed to be mediated, at least in part, via the GABAergic system. Magnesium deficiency has been associated with increased anxiety and neurological hyperexcitability, further supporting a link. However, direct evidence in humans specifically detailing magnesium’s effects on GABA neurotransmission is sparse, and most clinical trials do not isolate GABAergic effects from other neurological impacts. In summary, there is some scientific basis for magnesium’s role in supporting the GABA system, but the evidence is not robust or highly specific to GABA. More research is needed to clarify the mechanisms and the therapeutic relevance in humans.

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