More on Vitamin D…Friend or Foe?

Mushrooms are the >>>ONLY<<< vegetarian/produce based food that can make vitamin D. Actually, they contain a “pro-vitamin,” or precursor, called ergosterol that is converted into vitamin D when exposed to the sun’s ultraviolet (UV) radiation—similar to how your skin synthesizes the vitamin in response to sun exposure. -Berkeley Wellness

Ergosterol is a sterol found in cell membranes of fungi and protozoa, serving many of the same functions that cholesterol serves in animal cells. Because many fungi and protozoa cannot survive without ergosterol, the enzymes that synthesize it have become important targets for drug discovery. Ergosterol is a provitamin form of vitamin D2; exposure to ultraviolet (UV) light causes a chemical reaction that produces vitamin D2.

Ergosterol powder is an irritant to skin, eyes, and the respiratory tract. Ingestion of large amounts can cause hypercalcemia, which (if prolonged) can lead to calcium salt deposits in the soft tissues and, in particular, the kidneys. -Wikipedia

The Skin

Our body tries in many different ways to get rid of toxins. If liver, kidneys and lungs do not fulfill their tasks sufficiently, the body needs help from the skin.

The skin is the largest organ of protection and defense. It is a sensory organ. It serves for thermo regulation, secretion and excretion. The skin plays an important role in the elimination of toxins and can assist the kidneys in their work.

It evacuates the waste products that are classified as crystals. They are soluble in liquids and are evacuated in the form of sweat through the sweat glands. Crystals are the residues of the metabolism of food rich in protein, such as meat, fish, eggs, dairy products, legumes and cereals. Uric acid and urea are part of the group of crystals.

These may also result from an excess of refined sugar or very acidic food. Other types of waste products and toxins are excreted in the form of rashes. -Issels Immuno Oncology

Lipofuscin – Wikipedia

Liver Spots – Wikipedia

Vitamin D-Mediated Hypercalcemia: Mechanisms, Diagnosis, and Treatment

~Content Source-National Institutes for Health

Hypercalcemia occurs in up to 4% of the population in association with malignancy, primary hyperparathyroidism, ingestion of excessive calcium and/or vitamin D, ectopic production of 1,25-dihydroxyvitamin D [1,25(OH)2D], and impaired degradation of 1,25(OH)2D. The ingestion of excessive amounts of vitamin D3 (or vitamin D2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH)2D, and the formation of 5,6-trans 25(OH)D, which binds to the vitamin D receptor more tightly than 25(OH)D. In patients with granulomatous disease such as sarcoidosis or tuberculosis and tumors such as lymphomas, hypercalcemia occurs as a result of the activity of ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages or tumor cells and the formation of excessive amounts of 1,25(OH)2D. Recent work has identified a novel cause of non-PTH-mediated hypercalcemia that occurs when the degradation of 1,25(OH)2D is impaired as a result of mutations of the 1,25(OH)2D-24-hydroxylase cytochrome P450 (CYP24A1). Patients with biallelic and, in some instances, monoallelic mutations of the CYP24A1 gene have elevated serum calcium concentrations associated with elevated serum 1,25(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and on occasion, reduced bone density. Of interest, first-time calcium renal stone formers have elevated 1,25(OH)2D and evidence of impaired 24-hydroxylase-mediated 1,25(OH)2D degradation. We will describe the biochemical processes associated with the synthesis and degradation of various vitamin D metabolites, the clinical features of the vitamin D-mediated hypercalcemia, their biochemical diagnosis, and treatment.