Vitamin D and calcium

[Guest guest]

I was doing a little research on high Vitamin D and ran across this pieces.

Interesting note about high serum calcium levels being associated with toxic

D levels, as well as the part about too much D causing calcium to be drawn

from the bones! I think I'll be doing a little more research (even though my

D is back at normal levels!)

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http://www.merck.com/pubs/mmanual/section1/chapter3/3e.htm

Vitamin D Toxicity

Vitamin D 1000 µg (40,000 IU)/day produces toxicity within 1 to 4 mo in

infants, and as little as 75 µg (3000 IU)/day can produce toxicity over

years. Toxic effects have occurred in adults receiving 2500 µg (100,000

IU)/day for several months. Elevated serum calcium levels of 12 to 16 mg/dL

(3 to 4 mmol/L) are a constant finding when toxic symptoms occur; normal

levels are 8.5 to 10.5 mg/dL (2.12 to 2.62 mmol/L). Serum calcium should be

measured frequently (weekly at first, then monthly) in all patients receiving

large doses of vitamin D.

The first symptoms are anorexia, nausea, and vomiting, followed by polyuria,

polydipsia, weakness, nervousness, and pruritus. Renal function is impaired,

as evidenced by low sp gr urine, proteinuria, casts, and azotemia. Metastatic

calcifications may occur, particularly in the kidneys. Plasma 25(OH)D3 levels

are elevated as much as fifteenfold in vitamin D toxicity, whereas

1,25(OH)2D3 levels are usually within the normal range.

A history of excessive vitamin D intake is critical for differentiating this

condition from all other hypercalcemic states. Vitamin D toxicity occurs

commonly during the treatment of hypoparathyroidism (see http://www.merck.com/pubs/mmanual/section2/chapter12/12d.htm#A\

" >Hypocalcemia under http://www.merck.com/pubs/mmanual/section2/chapter12/12d.htm#A\

" >

Disorders of Calcium Metabolism in Ch. 12) and with the misguided use of

megavitamins. In Great Britain, so-called hypercalcemia in infancy with

failure to thrive has occurred with a daily vitamin D intake of 50 to 75 µg

(2000 to 3000 IU). syndrome consists of transient hypercalcemia in

infancy with the triad of supravalvular aortic stenosis, mental retardation,

and elfin facies. Plasma levels of 1,25(OH)2D3 during the hypercalcemic phase

are 8 to 10 times normal. Most cases are due to an unidentified defect in

vitamin D metabolism rather than to excessive intake.

1,25(OH)2D3 is 100 times more potent than vitamin D3. When it is used to

treat various disorders, possible toxic effects of long-term therapy must be

watched for.

Treatment consists of discontinuing the vitamin, providing a low-calcium

diet, keeping the urine acidic, and giving corticosteroids. Kidney damage or

metastatic calcification, if present, may be irreversible. Diuretics and

forced fluids are not helpful.

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http://www.ansci.cornell.edu/courses/as625/625vitd.html

Vitamin D Toxicity

Odd notes and high points... Natural vitamin D toxicities are limited to

ingestion of four known calcinogenic species: Cestrum diurnum,Trisetum

flavescens, Solanum malacoxylon and Solanum glaucophyllum.

Unfortunately, the existence of vitamin supplements have not only eliminated

rickets and other horrible consequences of vitamin D deficiency, but have

also made artificially-induced vitamin D toxicity possible. Animals with

access to sunlight usually do not need dietary vitamin D, because ultraviolet

light converts 7-dehydrocholesterol (abundant in skin) to the vitamin D3

cholecalciferol. Vitamin D2 (ergocalciferol) is created from the plant

steroid ergosterol. One International Unit of Vitamin D is 0.025 micrograms

of either D2 or D3. D2 is catabolized much sooner than D3 (at least in

chicks) and is not as readily converted to the 25OH form in overdose

situations. Perhaps that is why D3 is more than 10 times as toxic as D2. The

most active form of vitamin D is the 1,25 diOH form. The OH is added to the

25 position in the liver and to the 1 position mostly in the kidney. Once so

activated, vitamin D is a hormone that interacts with the DNA of target cells

(bone, gut, kidney, etc.) to promote the transcription of specific proteins

responsible for its actions. That 1-hydroxylation is promoted by low

phosphorus, low calcium (via parathyroid hormone) and calcitonin and

inhibited by the 1,25 diOH D itself.

Active vitamin D increases gut absorption of calcium and phosphorus,

resorption of calcium and phosphorus by the kidneys and increased bone

turnover (needed for proper bone formation and mineralization, but also

specifically promotes bone resorption). Dietary overdose of vitamin D results

in relatively successful shutdown of 1-hydroxylation, but 25OH D builds up to

such high levels that it begins to overwhelm and turn on 1,25 OH D receptors

around the body without being further hydroxylated. Ingestion of the toxic

calcinogenic plants causes even more severe toxicity because the active

compound is actually fully active 1,25 OH D3 form. That's right - the

" animal " form. In plants. Wierd, eh? Recommendations range from 2.5

micrograms (100IU) per day for adult Canadians to 10 micrograms per day for

Canadian infants (400 IU). USRDA is 5 micrograms per day. 2000 IU daily

poisons children, and especially sensitive kids have been intoxicated with

less than half of that. The principal direct toxic effects of vitamin D are

excessive absorption of calcium from the intestine and resorption of calcium

from bone. This results in deposition of calcium and phosphorus in soft

tissues all over the body, with particular damage to the heart, blood vessels

and kidneys. This a fairly reliable method for inducing high blood pressure

in model animals (such as dogs). This is presumably renal hypertension caused

by calcification of the renal arteries. Extreme toxicities caused by the

calcinogenic plants results in calcium deposition in and damage to lungs,

tendons, ligaments with attendent lameness.