Vitamin D

Vitamin D, specifically cholecalciferol (D3), is a secosteroid hormone-precursor whose primary evolutionary role is the regulation of calcium metabolism, a function so fundamental that it touches every cellular reaction in the body. 2 Peat argued that vitamin D is the most important immune-supporting nutrient for Americans, and its activity is as broad and complex as life itself. 2 The healthy human body produces cholecalciferol from cholesterol in the skin upon sunlight exposure; dietary sources from animals that have been in the sun, such as fish or dairy from pasture-raised cows, provide the identical molecule. 5 Once in the bloodstream, the liver hydroxylates cholecalciferol into 25-hydroxy vitamin D, the beneficial storage form measured in blood tests, which supports protective, immune-enhancing effects. 5

The metabolic pathway of vitamin D involves a critical distinction between its precursor forms and its terminal, activated hormone. Cholecalciferol is converted in the liver to 25-hydroxy vitamin D, and subsequently in the kidneys to calcitriol (1,25-dihydroxy vitamin D). 4 Peat explicitly warned that calcitriol is the toxic, dangerous last stage of vitamin D handling, which intensifies calcification of blood vessels and kidneys and impedes healing. 10 The production of calcitriol is driven by parathyroid hormone (PTH), which rises in response to a deficiency of calcium or vitamin D. 2 Therefore, a high calcitriol level is not a sign of vitamin D sufficiency but rather a marker of a deficiency state and physiological stress, paralleling the degenerative actions of PTH itself. 10 Supplementing cholecalciferol suppresses PTH, thereby lowering the dangerous active form, calcitriol. 2

Dinkov has extended this framework by outlining a clinical criterion for supplementation based on the negative feedback loop between calcitriol and PTH. If calcitriol is elevated but PTH is not suppressed into the bottom 25% of the normal range, it indicates a resistance to the hormone's action, and supplementing D3 is considered appropriate to re-establish the feedback mechanism. 3 Conversely, if calcitriol is high and PTH is already fully suppressed, further supplementation is unlikely to be beneficial. 3 Roddy has summarized the broad anti-stress profile of cholecalciferol, noting it is pro-thyroid, anti-cortisol, anti-prolactin, and anti-endotoxin, effectively framing it as a pro-mitochondrial energy substance that aligns with the protective actions of progesterone and thyroid hormone. 2 Peat also noted that a vitamin D and calcium deficiency, or a phosphate excess, increases both serotonin and calcitriol, linking the stress pathway directly to bone loss. 9

The therapeutic use of vitamin D3 is distinct from the dangers of its metabolites. Peat stated that the beneficial forms are cholecalciferol and its liver-modified 25-hydroxy version, which act as neurosteroids similarly to DHEA or pregnenolone, while topical or internal use of calcitriol is damaging. 10 Dinkov's formulation of a topical D3 supplement highlights its synergism with vitamin K in synthesizing osteocalcin, a hormone that reverses muscle aging and insulin resistance, and its interaction with the anti-aging gene Klotho. 12 Peat dismissed the idea that vitamin D3 could cause hypothermia, and he rejected the argument that one should avoid supplementation because it merely increases a "storage form," calling such a view "terribly confused." 2 The consensus from this perspective is that vitamin D2 is metabolized differently and lacks the full protective effects of D3, and that adequate calcium intake is foundational to the entire system, as demonstrated by cave fish that thrive without vitamin D in mineral-rich water. 2