Magnesium

Magnesium is a mineral cofactor for over 300 enzymes, and its retention in the body is fundamentally dependent on thyroid function and the production of ATP. 2 Peat observed that cells require good thyroid activity to synthesize ATP, which then binds magnesium intracellularly; when thyroid function is low, ATP levels fall, magnesium is released from cells, and calcium influx causes problems such as cramps, while the displaced magnesium is gradually lost in the urine. 1 This explains why a person with low thyroid cannot retain magnesium well and must replenish it frequently, whereas someone with robust thyroid and ATP levels retains it for a very long time. 1 Dinkov has elaborated that magnesium is a cofactor for pyruvate dehydrogenase, the rate-limiting enzyme for glucose metabolism, meaning a deficiency immediately shifts metabolism toward lactic acid accumulation and a diabetic or cancer-like state. 3

Peat described magnesium as the basic protective calcium blocker, noting that it is needed to form the phosphorylated ATPase that transfers a phosphate group to ADP, generating ATP while simultaneously subtracting excitatory inorganic phosphate from the cellular environment. 10 This intracellular role means that high serum magnesium is not a sign of sufficiency but rather indicates that cells are losing their magnesium content. 8 Magnesium suppresses parathyroid hormone (PTH), a stress-related hormone that rises when calcium is deficient and promotes inflammation, prolactin, and serotonin release. 2 Roddy has documented that magnesium deficiency precipitates hyperparathyroidism, while adequate intake promotes insulin sensitivity and decreases inflammatory messengers such as C-reactive protein, TNF-alpha, and interleukin-6. 2

Beyond its role in energy metabolism and mineral balance, magnesium acts as a functional antagonist to several catabolic stress hormones. Dinkov has stated that sufficient magnesium keeps estrogen relatively low while allowing protective hormones of youth—pregnenolone, progesterone, DHEA, and testosterone—to rise. 4 It also decreases the synthesis of cortisol and protects against muscle wasting in states of cortisol excess; in magnesium-deficient animals, elevated cortisol causes rapid tissue catabolism, and magnesium deficiency has been hypothesized as a contributor to the cachexia seen in cancer patients. 4 Magnesium is an antagonist of the NMDA receptor, similar to ketamine, which accounts for its sedative and brain-protective effects by increasing energy production in the brain. 7 In diabetics, doses of 1.5 to 2 grams daily have produced dramatic improvements, including lower blood glucose, accelerated wound healing, and prevention of kidney failure progression to the point of requiring dialysis. 7

Peat recommended obtaining magnesium primarily from foods rather than isolated supplements, citing coffee, fruit juices, and the green water from briefly boiled leafy greens such as kale or beet greens as concentrated, safe sources. 2 He cautioned that magnesium citrate supplements have other metabolic effects that could be harmful, while magnesium carbonate and glycinate are beneficial in themselves, though each carries its own impurities. 6 For therapeutic use alongside thyroid hormone, Peat advised approximately 100 mg of magnesium at a time with 1–2 micrograms of T3 (cytomel), which would be sufficient for the first few hours of response. 11 He noted that people with extremely high metabolic rates sometimes benefited temporarily from magnesium alone, but when magnesium was combined with a thyroid supplement, their metabolic rate returned stably to a normal, lower level. 12