Right you are :) About halfway down --
Magnesium deficiency, which is prevalent in the US population, results in increased levels of cytosolic free calcium.98 Intracellular free calcium levels above the normal range are cytotoxic causing calcification of mitochondria and cell death. The cell membrane possesses an ATP-dependant calcium pump that keeps intracellular levels of free ionized calcium within narrow limits. This calcium pump is magnesium-dependent for normal function. Magnesium deficiency results in a defective calcium pump and intracellular accumulation of ionized calcium. Inadequate iodine/iodide intake below orthoiodosupplementation results in decreased levels of delta-iodo-lactone. Combined magnesium and iodine/iodide deficiency based on the concept of orthoiodosupplementation are the basic factors involved in the oxidative damage caused by excess H2O2 and reactive oxygen species. If this proposed mechanism is valid, orthoiodosupplementation,30 combined with magnesium intake between 800-1,200 mg/day, a daily amount this author recommended 21 years ago 98 for magnesium sufficiency, should reverse autoimmune thyroiditis. This nutritional approach is also effective in Graves' autoimmune thyroiditis as previously discussed.
Don't know about needing more magnesium, but iodolactones are lipids with incorporated iodine.
Iodolipids are iodinated lipids -- i.e., lipids (fats) with incorporated iodine.
The requirements for the formation of iodolipids are (1) a peroxidase, (2) an elevated concentration of iodide and (3) hydrogen peroxide. These conditions can be met in various places in the body, including the thyroid, mammary gland, oviduct, and uterus.
Iodolactones consist of polyunsaturated fatty acids such as arachidonic acid (AA), eicosapentaenoic acid (EPA). and docosahexaenoic acid (DHA).
The delta-iodolactones of arachidonic acid inhibits the EGF (Epidermal Growth Factor) receptor. When the EGF receptor is inhibited, the metabolism of arachidonic acid induced by EGF (and TGF-a) is inhibited. This inhibition suppresses goiter formation and can induce involution (shrinking the goiter).
The delta-iodolactone of eicosapentaenoic acid exerts an antiproliferative effect in the nanomolar range.
Neither arachidonic acid by itself nor other iodolactones (besides delta-iodolactones) have this antiproliferative effect.
The synthesis of delta-iodolactone from arachidonic acid, iodine, and H2O2 is catalyzed by peroxidases. Thus, iodolactone formation is not limited to the thyroid gland but can occur in any organ that contains peroxidases (e.g., the breast).