VITAMIN D: Deficiency, Diversity and Dosage

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VITAMIN D: Deficiency, Diversity and Dosage

 

by Andrew W. Saul

 

(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. (2) As a curiosity, reindeer lichen

contains both vitamin D2 and D3. (3)

 

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. " (

 

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. " (1

 

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. " (2 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, 3

 

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. " (4 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, 5

 

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. (6 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.

 

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/CH25/html/ch25_8_4.html

 

 

 

 

Andrew Saul, PhD

 

 

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