VITAMIN D: Deficiency, Diversity and Dosage

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VITAMIN D: Deficiency, Diversity and Dosage

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Nov 13, 2006 10:10 PST

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by Andrew W. Saul

http://www.doctoryourself.com/dvitamin.htm

 

(Reprinted with permission from the Journal of Orthomolecular

Medicine, 2003; Vol. 18, Numbers 3 and 4, p. 194-204.)

 

" Vitamin D deficiency is a major unrecognized health problem. "

(Michael F. Holick, M.D., Boston University Medical Center)

 

There have been many papers published on vitamin D. A Medline search

for " vitamin D " will yield over 32,000 matches. It is well

established that insufficient quantities of the vitamin contribute

to osteopenia, osteomalacia, and osteoporosis. However, there is so

much new interest in " boneless " applications of vitamin D that the

topic was featured in the June, 2003 Reader's Digest. (1)

 

Vitamin D was first isolated from tuna fish oil in 1936, and

synthesized in 1952. It is a prohormone sterol which the body

manufactures, given sunlight, from 7-dehydrocholesterol. Vitamin D 3

(C27H44O,

cholecalciferol) is the form we and other animals make, and what is

found in fish liver oil. Oddly enough, fish cannot synthesize

vitamin D. They get theirs early in the food chain from planktonic

algae, and big fish eat little fish, and we eat them.

 

Vitamin D 2 (C28H44O) is made from ergosterol, not cholesterol, and

consequently is called ergocalciferol. This is the form that is

found in plants, and that is also man-made by ultraviolet

irradiation of ergosterol, and that is usually added to milk and

found in most American

supplements. Vitamin D3 is more commonly used as a supplement in

Europe. As a curiosity, reindeer lichen contains both vitamin D2

and D3.

 

Although D2 and D3 differ by a single carbon atom, there is evidence

that D3 is more efficiently utilized in chicks (4) and, more to the

point, in humans. " The assumption that vitamins D2 and D3 have equal

nutritional value is probably wrong and should be reconsidered. " (5)

 

There are two commercial sources of natural vitamin D3: fish liver

oil

and an oil extracted from wool. " If a label lists 'vitamin D3

(cholecalciferol)' then it is from wool oil. This is considered a

vegetarian source (the animal is not harmed, just sheared), but not

vegan. Fish liver oil will be in parentheses if it is the source. "

(6)

Animals can obtain vitamin D from licking their fur, and in humans,

rickets can be successfully treated by rubbing cod liver oil into

the

skin.

 

LONG-TERM SAFETY

 

As with all vitamins, there is ongoing and ever-protracted debate

about

vitamin D's safety and effectiveness. In the end, the issue really

boils

down to dosage. Because vitamin D can be made in the body, given

sufficient sunlight, it has been considered more of a hormone than a

vitamin. This terminology is likely to prejudice any consideration

of

megadoses, and that is unfortunate. Government-sponsored " tolerable "

or

" safe upper limits " (UL) for vitamin D have been established,

perhaps

based as much on speculation as on available facts. For babies under

one

year, that " upper limit " is 1,000 IU (25 mcg) per day. For everyone

else, including pregnant and nursing women, it is 2,000 IU (50 mcg)

per

day. (7) These " safe upper limits " may be excessively conservative.

Vieth et al write, " The 100-microg/d (4,000 IU/day) dosage of

vitamin D3

effectively increased 25(OH)D to high-normal concentrations in

practically all adults and serum 25(OH)D remained within the

physiologic

range; therefore, we consider 100 microg vitamin D3/d (4,000 IU/day)

to

be a safe intake. " (8)

 

Vitamin D has sometimes been regarded as the most potentially

dangerous

vitamin. In his 2001 article " Vitamin Toxicity, " Mark Rosenbloom,

MD,

writes that, for vitamin D, " Acute toxic dose is not established,

and

chronic toxic dose is more than 50,000 IU/day in adults. In

children,

400 IU/day is potentially toxic. A wide variance in potential

toxicity

exists. " There were no fatalities cited. (9)

 

The Merck Manual's assessment is somewhat different: " Vitamin D 1000

µg

(40,000 IU)/day produces toxicity within 1 to 4 months in infants,

and

as little as 75 µg (3,000 IU)/day can produce toxicity over years.

Toxic

effects have occurred in adults receiving 2,500 µg (100,000 IU)/day

for

several months. " (10)

 

The Merck Manual's lowest " toxicity " figure for " infants " of 3,000

IU is

substantially higher than Dr. Rosenbloom's " potentially toxic "

figure of

400 IU for presumably older and larger " children. " " Potentially

toxic "

is very different than " toxic. " Moreover, " toxic " is very different

than

" death. " The choice to use the word " toxic " may serve to convey a

false

impression of immediate and mortal danger. There are numerous

symptomatic warnings before serious toxic effects occur. Merck says,

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

polyuria, polydipsia, weakness, nervousness, and pruritus.

(Eventually)

renal function is impaired. . . Metastatic calcifications may occur,

particularly in the kidneys. 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). " (10) Though the details

and

duration of intake are not stated, a body-weight comparison suggests

that if an infant weighed 10 pounds, that would be the dose

equivalent

of approximately 32,000 to 48,000 IU per day for an average adult.

 

A widely-used nutrition textbook that I taught from (11) said that

2,000

IU daily for an adult is toxic (p 220-221). In this same textbook,

on

the same page, there was an error that, by the author's own

standard,

could likely be fatal to the reader's baby. A " Caution " statement on

page 221 indicated the daily vitamin D requirement for an infant as

10

MILLIGRAMS. This is 1,000 times the correct figure, which is 10

micrograms. 10 milligrams is 400,000 IU; 10 micrograms is 400 IU.

That

textbook typo is a far greater mistake than any health nut would

ever

make. By the next edition, the mistake had been corrected.

 

This is not an isolated instance. As recently as July, 2003, the

website

of a major university medical school (12) made the same mistake of

stating milligrams (mg) instead of micrograms (mcg). This

abbreviation

error, amounting to a difference of three orders of magnitude, was

present no fewer than six times in a single article. One of the

medical

school's statements read, " The upper limit of safety for vitamin D

established by the Food and Nutrition Board of the Institute of

Medicine

is 25 mg (1000 IU) daily for infants and 50 mg (2000 IU) for

children

and adults. " Actually, 25 mg would be one million IU/day, and 50 mg

is

two million IU/day. Mark Twain's advice comes to mind: " Be careful

in

reading health books. You may die of a misprint. " Perhaps it is a

testament to the safety of vitamin D that there has never been a

report

of any reader deaths from medical school-induced hypervitaminosis.

Additionally, if nutrition textbook and medical school proofreaders

can

confuse milligrams with micrograms, then certainly the public can.

This

may serve as a practical example of the advantage of using

International

Units in discussing and labeling the fat-soluble vitamins.

 

It is instructive to note that as far back as 1939, some truly

enormous

doses of vitamin D were in fact found to be far less deadly than one

might expect. In several countries, most infants, including

preemies,

survived 200,000 to as many as 600,000 units of vitamin D given in a

single injected or oral dose. These are incredibly high quantities,

especially when they are considered in relation to a premature

infant's

body weight. (13) Pregnant women have likewise been given two huge

oral

doses of vitamin D (600,000 IU) during the 7th and 8th months. (14)

 

In 2003, vitamin D's safety margins appear pretty much unchanged.

This

year, the British Medical Journal published a double-blind

controlled

trial of 100,000 IU vitamin D3 given orally to over 2,000 elderly

patients once every four months, for five years. The authors

reported,

in addition to greatly reduced fracture rates, that the high-dose

therapy was " without adverse effects in men and women. " (15)

 

It may be readily be conceded that huge but occasional doses are

insufficient to produce toxicity because vitamin D is fat-soluble,

stored by the body, and it takes many months of very high doses to

produce calcification of soft tissues, such as the lung and kidneys.

" Overdose, " " toxic, " and " fatal " are very strong, yet very different

terms that are often used interchangeably by critics of vitamin

supplementation. Most overdoses are not toxic, and most toxicities

are

not fatal.

 

Current US Daily Reference Intakes (DRI) for vitamin D are:

 

Infants 0-12 months, 200 IU (5 micrograms)

 

Males and females 1-50 years, 200 IU (5 mcg)

 

51-70 years, 400 IU (10 mcg)

 

71 years and older, 600 IU (15 mcg)

 

Pregnant or nursing women, 200 IU (5 mcg) (7)

 

Formerly, the US RDA for vitamin D was only 5 mcg (200 IU) for older

adults. The present recommendations are an improvement. However,

there

is evidence that even three times the DRI for an adult is inadequate

if

a person is not receiving adequate sunlight. (16) DRI or RDA levels

are

certainly not therapeutic levels, as the treatment of rickets

generally

requires a dose of 1,600 IU/day, and may require a daily dosage of

50,000 to as much as 300,000 IU in resistant cases. (17)

 

Current widely-publicized government recommendations are probably

inadequate for disease prevention. Reinhold Vieth, Ph.D.,

writes, " For

adults, the 5-microgram (200 IU) vitamin D recommended dietary

allowance

may prevent osteomalacia in the absence of sunlight, but more is

needed

to help prevent osteoporosis and secondary hyperparathyroidism.

Other

benefits of vitamin D supplementation are implicated

epidemiologically:

prevention of some cancers, osteoarthritis progression, multiple

sclerosis, and hypertension. Total-body sun exposure easily provides

the

equivalent of 250 microg (10,000 IU) vitamin D/day, suggesting that

this

is a physiologic limit. . . .Except in those with conditions causing

hypersensitivity, there is no evidence of adverse effects with serum

25(OH)D concentrations <140 nmol/L, which require a total vitamin D

supply of 250 microg (10,000 IU)/d to attain. Published cases of

vitamin

D toxicity with hypercalcemia, for which the 25(OH)D concentration

and

vitamin D dose are known, all involve intake of greater than or

equal to

1,000 microg (40,000 IU)/d. Because vitamin D is potentially toxic,

intake of >25 microg (1,000 IU)/d has been avoided even though the

weight of evidence shows that the currently accepted, no observed

adverse effect limit of 50 microg (2,000 IU)/d is too low by at

least

5-fold. " (18)

 

These figures, high though they may seem, may actually be fairly

conservative. The Nutrition Desk Reference, Second Edition (19)

states

that, for vitamin D, " The threshold for toxicity is 500 to 600

micrograms per kilogram body weight per day. " (p 40) " Toxic " in this

particular instance must mean " death, " as this figure is presumably

based on the US Environmental Protection Agency's published oral

LD50

for female rats of 619 mg/kg (20). 500 to 600 mcg is the equivalent

of

20,000 to 24,000 IU, per kilogram body weight per day. By

comparison,

this would mean that for an average (70 kg) adult human, toxicity

would

occur at an astounding 1,400,000 to 1,680,000 IU/day. In ducks, it

is

even higher: EPA's LD 50 for mallards is greater than 2000 mg/kg,

more

than three times that for female rats.

 

Even if such figures were not directly applicable to human beings,

vitamin D must remain one of the most non-toxic substances

imaginable.

It might be speculated that at least some of the recent increase of

interest in vitamin D analogs is due, in part, to patent- and

profit-driven attempts to chemically sidestep the presumed dangers

of

high doses of inexpensive, natural vitamin D. If the vitamin is

non-toxic, incentive to develop pharmaceutical analogs largely

disappears.

 

There are, of course, some reasonable cautions with its use. Persons

with hyperparathyroidism, lymphoma, lupus erythematosus,

tuberculosis,

sarcoidosis, kidney disease, or those taking digitalis, calcium

channel-blockers, or thiazide diuretics, should have physician

supervision before and while taking extra vitamin D.

Hyperparathyroidism

has been successfully managed with 50,000 to 200,000 IU of vitamin D

daily (21). When employing large doses of vitamin D, periodic

testing is

highly advisable.

 

DEFICIENCY

 

Vitamin D deficiency is, of course, to found in people who do not

take

supplements, who receive little sun exposure, and who do not drink

vitamin D fortified milk. A recent study (22) indicates that about a

quarter of supposedly bone-growing American adolescents are likely

vitamin D deficient. " Additionally, phenytoin (Dilantin), primidone

(Mysoline), and phenobarbital for seizures; corticosteroids;

cimetidine

(Tagamet) for ulcers; the blood-thinning drug heparin; and the

antituberculosis drugs isoniazid (INH) and rifampin may interfere

with

vitamin D absorption or activity. " (23) Cyclosporine and

carbamazepene

also negatively interfere with vitamin D. Vitamin D deficiency is

prevalent in the elderly, who all too commonly eat the worst diet,

take

the most medication, and get the least sunlight. Furthermore, the

normal

aging process itself decreases the body's ability to make vitamin D

from

what sunlight may be received. In any age group, even a relatively

wholesome-appearing diet heavy in cereal grains reduces the

availability

of vitamin D in the body. (24)

 

OSTEOPOROSIS

 

For decades, a milk-fed (and dairy industry-educated) public has had

its

attention focused on calcium and largely diverted from the " other "

important osteoporosis-preventing factor: vitamin D. Not only is

vitamin

D necessary for calcium deposition in the body, it is necessary for

getting calcium into the body in the first place. " (P)assive

diffusion

(dictated by calcium intake) is not the major mechanism by which

dietary

calcium is absorbed by normal adult humans. The vitamin D-dependent

processes are more important quantitatively and thus constitute a

major

determinant of calcium status. Individuals who are not exposed to

sunlight may be especially at risk. " (25)

 

Most persons with osteoporosis have low vitamin D levels. Along with

calcium, 800 IU of vitamin D daily has been shown in a double-blind

placebo-controlled study to increase bone density, and to reduce hip

fractures by an astounding 43%. (26) Fractures and their

complications

are a major cause of death in the elderly. Up to " 27% of all hip

fracture victims die within six months of their fall, usually of

complications following surgery or from infections. " (27) There are

over

250,000 hip fractures annually among persons over age 65, and

probably

" 90% of all fractures past age 60 are due to osteoporosis. " (28)

Vitamin

D therapy can save lives as well as bones. The fact that the DRI of

vitamin D is tripled for the elderly is an indication that this fact

is

not unknown. But 600 IU of vitamin D for a 71 year old is probably

too

little, and for some, too late.

 

Such was nearly the case for my mother, a grand mal epileptic who

took

phenytoin (Dilantin) for nearly 50 years. As she aged, she began to

fracture easily. This problem continued even after she was put on

calcium supplements accompanied by an RDA-level vitamin D

supplement.

But after her vitamin D intake was raised to 2,000 IU/day, she never

broke a bone again. This is true even though she still fell from

time to

time, sometimes so severely that she required inpatient care. But

there

were no more fractures. Epileptics may need as much as 4000 IU

daily.

(29) " Interestingly, vitamin D may offer another benefit for

osteoporosis: studies have found that when older individuals take

vitamin D supplements, they have less of a tendency to sway while

standing or walking, and may therefore be less likely to fall. " (23)

 

RICKETS

 

Childhood rickets remains a larger public health problem than might

be

expected. " Until recently, rickets secondary to vitamin D deficiency

was

considered a medical oddity rather than a clinical reality in

Catalonia

(Spain). However, recent data show a reemergence of the disease in

the

infancy. Nutritional rickets . . . mainly affects immigrant infants

and

children from Sub-Saharan Africa and Morocco, black or dark-skinned,

fed

with maternal milk alone, without vitamin D supplementation and with

little sun exposure. Systematic, preventive supplementation with

vitamin

D is essential in these populations. " (30)

 

Such is the case elsewhere as well, such as on the sunny island of

Crete, where " A full-term male infant presented with clinical and

biochemical findings consistent with the diagnosis of congenital

rickets: weak muscle tone, craniotabes, episodes of tremor,

hypocalcaemia, elevated serum alkaline phosphatase, secondary

hyperparathyroidism, decreased 25-hydroxyvitamin D and normal

1,25-dihydroxyvitamin D serum levels. The mother's history and

biochemical findings suggested nutritional vitamin D deficiency. . .

It

is surprising that this case occurred in an affluent setting, in the

Mediterranean island of Crete, with an abundance of sunlight

throughout

the year. " The authors assert that " a high index of suspicion is

required for prompt diagnosis and treatment, thus preventing

complications. " (31) Seizures may be a symptom of rickets. (32, 33,

34)

 

" A high index of suspicion " of vitamin D deficiency would be a good

policy for clinicians in the United States as well. Rickets has been

observed in Texas (35) and in North Carolina, where " Thirty patients

with nutritional rickets were first seen between 1990 and June of

1999.

Over half of the cases occurred in 1998 and the first half of 1999.

All

patients were African American children who were breast fed without

receiving supplemental vitamin D. . . Factors that may have

contributed

to the increase in referrals of children with nutritional rickets

include more African American women breast-feeding, fewer infants

receiving vitamin D supplements, and mothers and children exposed to

less sunlight. We recommend that all dark-skinned breast-fed infants

and

children receive vitamin D supplementation. " (36)

 

Heavily pigmented skin blocks up to 95% of UV radiation to the

deepest

skin layers. Additionally, now-widespread air pollution interferes

with

vitamin D synthesis in two almost paradoxical ways. Particulate

pollution reduces the amount of sunlight people may receive, and

ozone

depletion causes people to minimize exposure to what sunlight there

is.

As people are cover their skin to avoid skin cancer, they reduce

their

vitamin D.

 

On 4 August 2002, Reuters News Service reported that " the number of

cases of rickets in the United States has crept up in recent years.

Breast milk contains many valuable nutrients but not enough Vitamin

D to

meet the daily requirement of 200 International Units. Exposure to

the

sun's rays normally generates Vitamin D in the skin, but applying

sun

block stops that process. "

 

FOOD FORTIFICATION

 

With the exception of oily fish, foods do not contain a significant

amount of vitamin D. Because of concern over mercury levels, eating

the

flesh of fish may not be practical advice, and, while it contains no

mercury, there is widespread dislike for cod liver oil. Since the

1930's, vitamin D has been added to fluid milk but not to other milk

products. More recently, it has also been added to flour to reduce

rickets among immigrants to Britain. (10)

 

It is cheap and reliable for people to get their vitamin D from

enriched

foods. Iodine, iron and some of the B-vitamins are other examples of

nutrients that have been added to foods for decades. That action

should

be seen for what it is: a national policy effectively acknowledging

that

the masses eat so inadequately that they are otherwise unable to

avoid

the most obvious clinical ramifications of the most classic of

nutrient

deficiencies, including iodine-deficiency goiter, iron-deficiency

anemia, and pellagra. In the case of vitamin D, it is a tacit

statement

about safety as well. With 400 IU added per quart, it is easy for

many a

milk-drinking teenager to easily quadruple the DRI of 200 IU/day.

Few

dieticians appear worried that many people are routinely and

substantially exceeding government DRI's for vitamin D.

 

Adding fluoride to public water supplies is a similar, if less well

reasoned, application of government intervention. There has been

nearly

as much interest in trying to strengthen bones with fluoride as

there

has been in using vitamin D. But not only does fluoridation fail to

protect bones from fracture, it actually contributes to increased

fractures. (37, 38)

 

Additionally, both the National Toxicology Program and the National

Cancer Institute found a fluoride-related increase in osteosarcoma

in

young males. (39) Water fluoridation isn't particularly effective in

preventing dental caries, resulting in an average of one half of one

filling less per user per lifetime. (40)

 

OBESITY

 

Supplements, not sunlight, may be necessary for overweight persons

because they are less than half as able to utilize

cutaneously-synthesized vitamin D3 compared to lean persons. Since

approximately two-thirds of all Americans are overweight or obese,

this

is a very significant public health problem. " In the obese subjects

oral

vitamin D was more bioavailable than vitamin D from sunlight

exposure .

.. . The authors propose that vitamin D is being sequestered in body

fat

in obese persons, giving rise to a relative deficiency which could

be

corrected with oral administration of extra vitamin D. " (41)

 

DIVERSITY OF USES

 

Controversy over vitamin D therapy increases with the distance

research

moves away from the skeleton. There is growing evidence that the

" sunshine vitamin " may be vastly more important to human health than

previously thought and commonly taught. Vitamin D metabolite

(1,25-dihydroxyvitamin D) receptors (VDR), writes Michael F. Holick,

M.D., " are present not only in the intestine and bone, but in a wide

variety of other tissues, including the brain, heart, stomach,

pancreas,

activated T and B lymphocytes, skin, gonads, etc. 1,25(OH)(2)D is

one of

the most potent substances to inhibit proliferation of both normal

and

hyperproliferative cells and induce them to mature. . . Chronic

vitamin

D deficiency may have serious adverse consequences, including

increased

risk of hypertension, multiple sclerosis, cancers of the colon,

prostate, breast, and ovary, and type 1 diabetes. " (42)

 

It is noteworthy that skin cancer may actually be prevented by what

many

feel causes it: sunshine. (43, 44) Krispin Sullivan, author of Naked

at

Noon: Understanding Sunlight and Vitamin D, writes: " One of the

known

protectors of skin cells from pre-cancerous changes is vitamin D.

For

most Americans the primary source of vitamin D is sunlight. UV-B,

the

only band of light producing vitamin D, is significantly present

only

midday during summer months in most of the U.S., the exact time we

are

advised to avoid sunlight. UV-B is blocked by sunscreen. " (45)

Over-exposure to sunlight does not cause vitamin D toxicity.

Persisting

concerns over sun exposure are arguments in favor of its nutritional

equivalent: oral vitamin D supplementation.

 

MULTIPLE SCLEROSIS

 

Persons with multiple sclerosis typically are vitamin D deficient

and

demonstrate dramatically reduced bone mass. Unsurprisingly, such

bone

loss appears to be directly caused by insufficient vitamin D (46)

and

can " be safely and inexpensively corrected by the routine use of

vitamin

D supplements. " (47)

 

More importantly, vitamin D may have a key role in the progression

of

multiple sclerosis itself. Hayes et al write, " (E)xogenous

1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can

completely prevent experimental autoimmune encephalomyelitis (EAE),

a

widely accepted mouse model of human multiple sclerosis (MS) . . .

(T)he

hormonal form of vitamin D3 is a selective immune system regulator

inhibiting this autoimmune disease. Thus, under low-sunlight

conditions,

insufficient vitamin D3 is produced, limiting production of

1,25-dihydroxyvitamin D3, providing a risk for MS. . . This theory

can

explain the striking geographic distribution of MS, which is nearly

zero

in equatorial regions and increases dramatically with latitude in

both

hemispheres. . . MS may be preventable in genetically susceptible

individuals with early intervention strategies that provide adequate

levels of hormonally active 1,25-dihydroxyvitamin D3 or its

analogs. "

(48) Dr. Hayes adds that " Inheriting genetic risk factors for

multiple

sclerosis (MS) is not sufficient to cause this demyelinating disease

of

the central nervous system; exposure to environmental risk factors

is

also required. " (49)

 

In a review article, " Vitamin D Supplementation in the Fight Against

Multiple Sclerosis (50), Ashton F. Embry credits P. Goldberg (51,

52)

with being the first to propose that vitamin D is an important

factor in

the development of MS. Goldberg " postulated that such a close

correspondence between low sunlight and MS was due to low vitamin D

production in the population. Goldberg also showed that within areas

of

low sunlight (e.g. Norway) differences in MS prevalence could be

explained by dietary factors which affect vitamin D production. Such

factors include the amount of fish eaten (increases vitamin D) and

the

amount of grains consumed (reduces vitamin D levels due to the

action of

phytates). To explain how vitamin D levels were related to MS,

Goldberg

proposed that genetically susceptible individuals may need larger

than

normal amounts of vitamin D during myelin formation and that

insufficient vitamin D during childhood might result in defective

myelin

which would be susceptible to breakdown in later life. Goldberg's

ideas

were completely ignored by medical researchers. "

 

At least at the time they were. Eventually it was demonstrated that

vitamin D hormone could prevent or halt not only an animal form of

MS

(53, 54) but there had been a clinical study (55) showing that

vitamin

D, along with calcium and magnesium, reduced the relapse rate in

humans

with multiple sclerosis. Frederick R. Klenner, M.D., reported

success

using vitamin and mineral therapy for multiple sclerosis over thirty

years ago. (56, 57, 58)

 

HEART DISEASE AND OTHER CLINICAL USES

 

Vitamin D has an important role in cardiovascular health. (59, 60)

For

example, not only can it prevent hypertension, it can help treat it.

(61, 62) " Hypertension appears to improve with vitamin D

supplementation

whether or not the vitamin is deficient. " (63) This is an important

point.

 

Congestive heart failure (CHF) may be caused by vitamin D

deficiency.

" Low vitamin D status can explain alterations in mineral metabolism

as

well as myocardial dysfunction in the CHF patients, and it may

therefore

be a contributing factor in the pathogenesis of CHF. " (64) Not

surprisingly, bone loss is associated with congestive heart failure.

(65) Dilated cardiomyopathy has been linked with rickets, both of

which

" responded well to supplemental calcium and vitamin D. " (66)

 

Scleroderma has responded favorably to long-term oral vitamin D3

(1,25-dihydroxycholecalciferol) therapy (67) and psoriasis has been

successfully treated, not only with vitamin D analogues, but with

topical vitamin D3. (68) Vitamin D deficiency may be a contributing

cause of inflammatory bowel disease, and might be an effective

treatment. (69) Over 50 years ago, lupus vulgaris (tuberculosis of

the

skin) was reported successfully treated with 150,000 IU of vitamin D

daily for six to eight months. (70)

 

Colon cancer is clearly related to poor vitamin D nutrition (71, 72,

73). Inadequate vitamin D levels are also associated with ovarian

cancer

(74), polycystic ovary syndrome, (75) rheumatoid arthritis (76), and

lupus (77). Infants receiving vitamin D supplements show as much as

an

80% reduction in type I diabetes. (78, 79, 80, 81). A Medline search

will reveal nearly 300 papers on fighting prostate cancer with

vitamin D

and its derivatives, and nearly 400 in relation to D and breast

cancer.

 

DEFICIENCY AND DIVERSITY: A SUMMARY

 

Vitamin D deficiency is cause or contributor to a wide variety of

diseases, many of which appear unrelated to bone problems. So

important

is this vitamin for the entire population that it is necessary for

milk

to be enriched with it. Most persons do not get adequate vitamin D

from

sunlight, and the problem compounded for the obese and for the

elderly.

For those individuals, and for any person on any of a number of

commonly

prescribed medications, vitamin D supplementation is mandatory.

 

Government recommended dietary intakes of 200 to 600 IU/day are too

low,

according to the weight of clinical evidence. Government " tolerable "

or

" safe upper intake levels " (UL) of 1,000 to 2,000 IU/day are

likewise

too low, and largely unsupported by toxicological evidence. An

optimum

health recommendation of 1,000 to 4,000 IU/day, in total from all

sources, is not unreasonable for the vast majority of healthy

adults.

Effective therapeutic levels for illness may be far higher. When

high

doses are used, appropriate testing and monitoring is recommended.

It

would be unreasonable to deny a therapeutic trial of vitamin D in

cases

of multiple sclerosis, scleroderma, psoriasis, congestive heart

failure,

hypertension, and various forms of cancer.

 

Excessive avoidance of sunlight, and sensational but unscientific

dread

of relatively high-dose vitamin D side effects does more than merely

set

the stage for a population of rickety children and fracture-ridden

elderly. Overestimates and outright misstatements of vitamin D's

" potential toxicity " open new marketing avenues for the development

of

vitamin D-like drugs, a commercial opportunity that the

pharmaceutical

industry has not overlooked.

 

ON DANGERS AND DOSAGE: A CONCLUDING COMMENT

 

Hypervitaminosis articles are popular with the media, sometimes even

making it into the pages of the Wall Street Journal. On April 30,

1992,

David Stipp reported that between 1990 and 1992, " a series of

patients

with vitamin D overdoses began turning up at Boston hospitals. " One

of

these patients subsequently died from drug complications, and the

case

went to court. (82) " Essentially, this was a product liability

action

against the producer of dairy products, specifically milk which

contained excessive amounts of Vitamin D. The plaintiff's decedent

purportedly suffered from elevated levels of Vitamin D in her

bloodstream which required medication which in turn allegedly

compromised her immune system, leading to her death. " (83) This is

the

one and only vitamin D-related death I could find confirmation of

anywhere, and even this one was not directly due to the vitamin, but

rather to side effects of medication.

 

A physiology textbook later stated that " At least 19 cases of

vitamin D

toxicity were reported in the Boston area during 1992. Symptoms

included

fatigue, weight loss, and potentially severe damage to the kidneys

and

cardiovascular system. The problems resulted from drinking milk

fortified with vitamin D. Due to problems at one dairy, some of the

milk

sold had over 230,000 units of vitamin D per quart instead of the

usual

400 units per quart. The incident highlighted the need for quality

control in the production, and care in the consumption, of vitamin

supplements. " (84)

 

Such a conclusion is inaccurate. The incident might just as well be

taken to be an unintentional proof of vitamin safety, even in

ridiculously high overdosage situations. It is certainly noteworthy

that

580 times the normal amount of vitamin D produced, at most, one

alleged

fatality over a two-year period. Furthermore, there was a total of

fewer

than two dozen toxicity reports, for the entire Boston metropolitan

area, after large numbers of people had been ingesting close to a

quarter of a million units of vitamin D per liter of milk day after

day,

month after month, for up to two years. This borders on the

extraordinary. Events such as this demonstrate that the margin for

error

with vitamin D is very large indeed. Though the news reported about

the

vitamin's toxicity, the real story was the vitamin's safety. The

scientific literature confirms the vitamin's value.

 

References cited:

 

1. Freinkel S. The healing vitamin. Reader's Digest. June, 2003.

 

2. http://www.ibl-hamburg.com/prod/mg_11021_m.htm

 

3. Int J Circumpolar Health. 59: 26-32. 2000.

 

4. http://www.cyberlipid.org/vitd/vitd0001.htm

 

5. HM Trang, DE Cole, LA Rubin, A Pierratos, S Siu and R Vieth.

Evidence

that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently

than does vitamin D2. American Journal of Clinical Nutrition, Vol

68,

854-858, 1998.

 

JoAnn Guest

mrsjo-

www.geocities.com/mrsjoguest/Diets