All you ever wanted to know about Vitamin D (but were afraid to ask) LOL

[Guest guest]

Hey, everyone: There's a Hull wanna-be on the AMOS/morbid obesity

site! ROFL Look at this response! Whew! I thought someone might be

interested in the information -- I thought it was cool...

Just found it today in the Q & A section of that website

(www.obesityhelp.com/morbidobesity). Unfortunately, it doesn't address our

particular situation (being malapsorbers of vit D), but I found it

enlightening in it's own special way.

ps - emphasis is my own in the article below

all the best,

lap ds with gallbladder removal

January 25,2 001

Dr. Gagner/Mt. Sinai/NYC

10 months post-op and still feelin' fabu

preop: 307 lbs/bmi 45

now: 198 lbs/bmi 28/size sweet 16 but still squeezin' into a 14! LOL

Q: Is it possible to take too much Vitamin D?

[12/11]   Yes, but you're not going to. Each of those tablets probably has

400 IU of Vitamin D.

Vitamin D and its analogues are a group of sterol compounds that occur

naturally, chiefly in animals. It can also be found in plants and yeasts. The

D vitamins are generated from the provitamins ergosterol and

7-dehydrocholesterol, which are found in plants and animals.

Ultraviolet irridiation of a variety of this animal and plant sterols results

in the conversion of provitamins to compounds with vitamin D activity.

Ergosterol, which is derived from plants, can be converted into

ergocalciferol (vitamin D2) with the aid of ultraviolet irridiation. For

instance, vitamin D was once made available in commercial quantities when

vitamin D2 was manufactured by irridiation of ergosterol derived from yeast.

In animal tissues, 7-dehydrocholesterol, which occurs naturally in the

epidermal layers of the skin, can be converted by ultraviolet irridiation to

cholesterol (vitamin D3). Vitamin D3 is also present in fish oil. Both ergocal

ciferol and cholecalciferol are of equal biologic potency as D vitamins.

Basically, humans have two main sources of vitamin D. It can be obtained

through ingestion of appropriate foods in the diet and photolysis of

7-dehydrocholesterol in the skin. Once absorbed and bound to a specific

globulin. It is transported in the blood to the liver. The major storage form

of vitamin D in the body is 25-hydroxy vitamin D3. However, this is not the

active form of the vitamin. Instead, vitamin D3 undergoes several chemical

modifications before it is transported in its modified form to the target

tissue. The active compound is known as 125-dihydroxycholecalciferol. It is a

potent stimulator of calcium absorption in physiologic dosages. At above

physiologic levels, it stimulates reabsorption of bones.

Vitamin D has two important physiological functions. It is a fat-soluble

vitamin that promotes utilisation of calcium and phosphorus in the body by

enhancing absorption of these two minerals from the intestine. It is required

for normal mineralisation of bone and it plays an essential role in the

homeostatic regulation of plasma calcium concentration.

A deficiency of vitamin D results in inadequate absorption of calcium and

phosphate. Vitamin D deficiency results in osteomalacia or adult rickets,

which is likely to occur during times of increased calcium need, such as

pregnancy and lactation. The disease is characterised by a generalised

decrease in bone density. Demineralisation of bone may result in multiple

fractures.

Vitamin D deficiency is not simply due to malnutrition. More importantly, it

can be due to lack of exposure to the sun. This vitamin can be formed in the

skin when the skin is exposed to sunlight.

Vitamin D is present in substantial amounts in many vitamin formulations,

some calcium supplements and most milk products. It is also found in fish

oils and fortified foods such as margarine.

In adults, vitamin D deficiency is noted most frequently in pregnant women.

It appears as painful malformations of pelvis and femur. The average curative

dose of vitamin D in rickets is about 5,000IU daily. The administration of

the vitamin should be always accompanied by adequate calcium and phosphorus

intakes in the daily diet. Exposure to sunlight is also helpful.

The prescription of high doses of vitamin D in the absence of a deficiency

can result in hypercalcaemia - excessive calcium in blood. If this condition

is prolonged, it may lead to heart and kidney damage. Symptoms of vitamin D

toxicity include nausea, vomiting, anorexia, headache, weakness, apathy,

polyuria and bone pain. As vitamin plays an important role in mineralisation

and calcification of bones, the symptoms of excessive ingestion of vitamin D

are the result of abnormalities in calcium metabolism. These are largely due

to hypercalcaemia which cause calcification of soft tissue and produce renal

impairment.

Clinically, most cases of hypervitaminosis D seen in adults are the result of

large doses of the vitamin used for the treatment of conditions that are not

associated with vitamin D deficiency. Daily ingestion in excess of 2,000IU in

children or 75,000IU in adults may produce toxic symptoms related to

hypervitaminosis D. For example, most cases of vitamin D toxicity have been

reported to occur after the ingestion of greater than 50,000IU daily for

several years.

There is wide individual variation in the amount of vitamin D that causes

hypervitaminosis. The continued ingestion of 50,000IU or more daily by a

person with normal vitamin D sensitivity may result in poisoning. Doses of

60,000IU per day can cause hypercalcaemia, with muscle weakness, Proteinuria,

hypertension and irregular heartbeat. Symptoms and signs generally appear two

to eight days after acute intoxication with massive doses of vitamin D.

Chronic hypercalcaemia can lead to generalised vascular calcification with

high concentration of calcium salts in soft tissues, especially in the

kidney. This will exacerbate rapid deterioration of kidney functions. Other

sites of calcification may include blood vessels, heart, lungs and skin. The

stored vitamin in the body will be released slowly as it has a long plasma

half-life of three months.

Another potentially toxic action of vitamin D is the effect on fat

metabolism. There is some evidence that 700IU to 2,500IU daily in adults may

raise the plasma cholesterol level.

Massive doses of vitamin D up to a concentration of 10,000IU/kg during

pregnancy are teratogenic. Twenty per cent of normal adults receiving

100,000IU/day for several weeks or months develop hypercalcaemia.

Serious toxicity may result from excessive ingestion of the vitamin. The

supplemental requirements vary not only with age, pregnancy and lactation,

but also with the quality of the diet. It is clear therefore that any

recommendation for vitamin D supplementation must be made only after careful

scrutiny of the diet.     - Moseley Part4