FYI
ms patients tend to have sub-optimal magnesium status. magnesium is known to help relax and sleep. it also has links to pineal health and melatonin production.
Dietary magnesium deficiency decreases plasma melatonin in rats
http://www.jle.com/en/revues/agro_biote ... article.md
It has been postulated that Mg depletion is associated with decreased melatonin. Exogenous magnesium (Mg) has been found to increase the activity of serotonin N-acetyltransferase, an enzyme in the pathway for melatonin synthesis\; but no data have been found on the effect of Mg deficiency on plasma melatonin. This pilot study examined the effect of a dietary Mg deficiency on plasma melatonin in male, Sprague-Dawley rats. Weanling rats were placed on a Mg-deficient (150 ppm) or a Mg-adequate (1000 ppm) diets for four weeks, after which they were sacrificed 4, 5 or 7 hours into the dark cycle. Plasma was assayed for melatonin concentrations. A significant decrease (p \= 0.0101) occurred in mean (± SEM) plasma melatonin levels of the Mg-deficient animals (50 ± 6.4 pg/mL) when compared to the Mg-adequate animals (75 ± 6.6 pg/mL). There was no obvious phase shift in the melatonin profile of the Mg-deficient animals when compared to the Mg-adequate animals.
Nocturnal Melatonin Secretion in Multiple Sclerosis Patients with Affective Disorders
a human study including ms patients
The pineal gland has been implicated recently in the pathogenesis of multiple sclerosis (MS), a chronic demyelinating disease of CNS. Since nocturnal melatonin secretion is low in some groups of patients with mental depression, we predicted lower melatonin secretion in MS patients with history of affective illness compared to those without psychiatric disorders. To test this hypothesis, we studied single nocturnal plasma melatonin levels and the incidence of pineal calcification (PC) on CT scan in a cohort of 25 MS patients (4 men, 21 women; mean age = 39.4 years, SD = 9.3), 15 of whom had a history of coexisting psychiatric disorders with predominant affective symptomatology. Other factors that may be related to depression such as vitamin B12, folic acid, zinc, magnesium, and homocysteine, were also included in the analysis. Neither any of the metabolic factors surveyed nor the incidence of PC distinguished the psychiatric from the control group. However, the mean melatonin level in the psychiatric patients was significantly lower than in the control group. Since low melatonin secretion in patients with depression may be related to a phase-advance of the circadian oscillator regulating the offset of melatonin secretion, we propose that the depression of MS likewise may reflect the presence of dampened circadian oscillators. Furthermore, since exacerbation of motor symptoms in MS patients may be temporally related to worsening of depression, we propose that circadian phase lability may also underlie the relapsing-remitting course of the disease. Consequently, pharmacological agents such as lithium or bright light therapy, which have been shown to phase-delay circadian rhythms, might be effective in the treatment of affective symptoms in MS as well as preventing motor exacerbation and hastening a remission from an acute attack.
'normal' serum range for magnesium is 0.70-1.10 mmol/L but to be optimal serum magnesium must be minimum 0.90 mmol/L. i strongly suspect that most or all ms patients (including the 'controls') in the above study had levels below 0.90, and that in some it manifested as poor pineal function, whereas others would have had pain or spasticity or something else from one of the other 300+ pathways in which magnesium is involved.
