NetNews Usenet Archive 1992 #31/NN_1992_31.iso/spool/sci/med/nutritio/1715

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From: [e-mail] (Ted Wayn Altar)
Subject: Re: Prof. Moon et al. on "vitamin" D
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Organization: Simon Fraser University, Burnaby, B.C., Canada
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Date: Thu, 31 Dec 1992 18:34:55 GMT
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For those who have not seen that earlier posting being referred
to here of late, I'll repost it now for your benefit.

As I earlier pointed out, the following was based upon
2 presentations at the university delivered by Professor
Moon and upon what was then a draft copy of his forthcoming
paper.  This paper has now been published:

     Moon, J. et al. 1992.  "Etiology of Atherosclerosis and
          Osteoporosis:Are Imbalances in the Calciferol Endocrine
          System Implicated?"  JOURNAL OF THE AMERICAN COLLEGE OF
          NUTRITION, 11:567-583.

Again, any errors then made, of course, are mine.  Professor
Moon (1) has presented some important evidence that calciferol
is maybe one of the most hazardous food additives so far
encountered.  It could well go down as one the biggest
nutritional mistakes of the modern era.  Also, you might want
to look for Dr. Moon's letter (see November, 1992 issue of the
CANADIAN MEDICAL ASSOC. J. on the detrimental effects of
calciferol on aluminum absorption.

First a summary of the highlights:

     i) this so-called "sunshine vitamin" is better classified
          not as a vitamin but as a potent and dangerous anabolic
          seco-steroid hormone.
     ii) it is not an essential dietary component for the vast
          majority and relatively small levels may be toxic
     iii) what we have is a toxic food additive to which the vast
          majority of people are needlessly ingesting unnecessary
          amounts, often even beyond RDA levels.
     iv)  there is disturbing evidence to seriously implicate
          this synthetic steroid hormone in the etiology of
          atherosclerosis, osteoporsis, and some other medical
          problems.


I.  THE SO-CALLED SUNSHINE VITAMIN

In the last decade, it has become generally accepted that vitamin
D's mode of action is similar to that of the steroid hormones (2)
In fact, it was strongly recommended for reclassification as
early as 1970 (ibid) as an steroid hormone rather than as a
vitamin, but this suggestion has unfortunately been slow to
disseminate and become adopted.  In 1980, Peng and Taylor (3)
further recommended that `vitamin D' be seriously considered "as
a potent, carefully controlled hormone".  Moon, Bandy & Davison's
important review (1992) of the prominent health risk implicated
in the usage of this substance have advised that:

     " to avoid confusion that might lead to excessive
     self-administration, the more correct hormone name,
     `calciferol', rather then the common name, `vitamin D',
     should be used for labelling purposes".

We should keep in mind that none of the known steroid hormones
are safe for use over prolonged periods and hence all are
restricted for use by prescription only, calciferol being
the sole exception.

This potent steroid hormone was ill-designated by Edward Mellanby
as a "vitamin" in 1921 when he suggested that the healing action
of animal fats in rickets is probably due to some fat-soluble
vitamin.  Calciferol, however, consists of a group of hormones,
one form of which is so toxic that it was appropriately called
"toxisterol".  Animal fats are used to manufacture vitamin D and
it is virtually impossible to manufacture a toxisterol-free form.
Another form called "ertron", that was claimed to be toxisterol
free, was extensively used in mega-vitamin therapy for arthritis
in the 1940's.  After several hundred arthritis patients were
poisoned by ertron it was withdrawn from the market.

When 1,25-dihydroxyvitamin D is now synthesized through 7-
dehydrocholesterol being treated with UV rays, there is also
produced a multiplicity of activation products (tachysterol,
lumisterol and some suprasterols).  It is virtually impossible to
remove the contaminating by-products (4)   Even if "pure" `D'
could be synthesized, thermal and photoinstability result in its
decomposition into other oxysterols. `D' in a tablets decomposes
at 40 degrees C within 3 days.

There are real differences between the body's dermally produced D
and this synthetic D.  As Moon et al.(1) noted, these
contaminating side-products of synthetic D are readily taken up
by the D carrier protein which has a great affinity for these
contaminating sterols.  This is not the case with the dermally
produced side-products.  We should further keep in mind this
steroid hormones also have a probable contamination by various
oxysterols, the potential side effects of these hormones being
cancer and cardiovascular diseases.

These assocations should, at the very least, lead us to suspect
and investigate whether calciferol might not, over a long period
of time, also have its health harzards at levels or uses formerly
thought safe.

Unfortunately, it may be that people have become too used to the
extant CONVENTION of grouping "D" along with the other vitamins
and therefore we may not see much change in this designation of
calciferol as a "vitamin" for some time.  We might have been
earlier alerted to the difference of "D" from the other vitamins
by noting that all the other `true' vitamins have common plant
sources.  The only known plant sources for calciferol are 2
plants found in South America (cattle grazing on these plants
routinely die of calciferol poisoning).


II.  CALCIFEROL IS NOT AN ESSENTIAL DIETARY COMPONENT FOR THE
VAST MAJORITY.

No evidence of vitamin deficiency based on serum levels of D
metabolites have been found in N.A. populations. (15, 16) Indeed,
no evidence for such deficiencies has been found in groups
thought most likely to develop vitamin D-deficiency osteomalacia,
such as East Indian immigrants to Canada (14).

The only situations that might justify calciferol replacement
therapy would be for infants under the age of two, and lactating
women, who do not get sufficient exposure to solar ultraviolet,
or people confined indoors, such as elderly invalids.  The better
therapy, of course, would simply be ultraviolet light.  An
infant, for instance, only needs about 15 mins. of exposure on an
area of skin the size of one facial cheek.  The body easily makes
and better regulates its own forms of calciferol.  Full spectrum
light, or glass that permits the entry of solar ultraviolet,
would be the better solution for those confined indoors than
their ingestion of the manufactured forms.  This would be in line
with Fraser's (5) recommendations reported in Lancet:

     The oral route as a means of supplying vitamin D is
     ineffective, unnatural, and potentially dangerous.  Yet, to
     achieve adequate exposure to the sun of whole populations such
     as those in large cities may well prove impractical.  Human
     ingenuity might therefore have to devise another way of
     providing vitamin D -- on which takes into account the
     natural physiology of its formation and processing in the
     body.


III)  HOW MUCH SYNTHETIC CALCIFEROL ARE WE CONSUMING?

   Authorities still inappropriately talk about the "recommended
nutrient intake" of this substance rather talk about its "maximum
permissible level".  Indeed, there are permitted overdosages of
these substances in milk by even current standards, to allow for
deterioration.  The question Moon would ask of health regulations
requiring calciferol additives, is, why should the vast majority
of the general population be subjected to this hormone by way of
their foodstuffs only to protect a small minority of people who
can easily be identified by an analysis of blood samples for 25-
hydroxycalciferol?  While Canada is now the only country in which
the addition of "D" to milk is mandatory it is still commonly
added elsewhere (85% of US milk, for instance, still has it
added).
Although the Nutrition Canada Survey never found a single case of
active rickets in the population surveyed, some infants were
getting less than 400 I.U. of "D" per day, and on this basis
calciferol additives were mandated for some foods, a measure
adopted merely to prevent what is only a HYPOTHETICAL
"deficiency".

      In order to protect the elderly from osteomalacia (a rare
disease in North America), "D" is also added to margarine in
Canada.  Yet, it was found by the 1970 B.C. nutrition Canada
survey that many women in B.C. were consuming excessive amounts
of "D", mostly in vitamin supplements.  Certainly, there is no
evidence to indicate any beneficial effect of calciferol hormones
in non-deficient people, but there is now evidence to indicate
harmful effects of chronic low-level consumption of this
substance.


IV)  THE IMPLICATION THIS SYNTHETIC STEROID HORMONE IN THE
     ETIOLOGY OF ATHEROSCLEROSIS AND OSTEOPORSIS.

According to Moon (1):

     "Ingestion of excess vitmin D can be dangerous, giving rise
     to withdrawal of Ca and Mg from the bone, and deposition of
     Ca, Mg, and Fe in a variety of soft tissues such as arteries
     and kidneys"

It is well known that with advancing age, levels of Ca in our
bones decreases while the deposition of Ca in soft tissue
increases.  Evidence for calciferol being a factor in this Ca
problem comes from a number of different sources.  For instance,
excess calciferol from megavitamin D therapy (6, 7), or with
infants receiving excess amount from fortified foods (8, 9), is
known to cause in a relatively short period of time
cardiovascular, renal, and skeletal damage.  The larger
population may also be consuming excess vitamin D (esp. compared
to RNI recommendations of 100 IU or RDA recommendations of 200
IU).  Multiple sources like milk (400 IU/quart in U.S.),
margarine (660 IU/100 g. in Canada), multivitamin supplements
(200-400 IU), some breakfast cereals (100 IU/serving), yogart,
eggs (50 IU/yolk), fish and meat (much of the vitamin D fed to
domestic animals as a growth hormone concentrates in their fat
stores). These multiple sources may result in consumption as high
as 800-1500 IU/daily.  When all these exogenous sources are added
to the variable amount from solar exposure, it is not surprising
that one study (10) found that 13% of infants had intakes over
1,000 IU/d and that 4.2% of adult women were in excess of 1,000
IU/d.

Now, what about chronic "low-level" ingestion over long periods?
It should be kept in mind that adults who are no longer growing
may be more sensitive to calciferol toxicity and that this
substance is not readily excreted but accumulates in our fat
stores.  Also, cofactors like nicotine along with low dietary MG
and high cholesterol/saturated fat intakes may also lower the
pathogenic levels of calciferol (the last two cofactors
characteristic of an omnivore diet).  Now, Dr. Moon claims that
when taken by non-deficient people, low level ingestion of
calciferol may still increase the aging of arteries, kidneys, and
bones.  Ingesting these manufactured forms may always result in a
calciferol substance that is readily absorbed into the blood but
which does not properly serve to best regulate the calcium
levels in the bone and blood.  Hence, Moon thinks that the
compulsory addition of calciferol in our milk (as required by
Canada Health regulation) and its routine addition to margarine,
baby foods, breakfast cereals, multiple vitamin supplements, and
animal feed, has substantially increased the risk factor towards
atherosclerosis, osteoporosis and kidney stones in the larger
population.

     There is, for instance, a direct correlation of incidence of
these diseases in various countries and the policy of those
countries to add calciferol to its foodstuffs.  The recent U. S.
and Canadian decrease, starting in the 1970's, in the death rate
from IHD (ischemic heart disease) parallels the new regulations
to decrease the delivery of exogenous calciferol in the foods.
(1)  This decline has not been explained by smoking status,
leisure time, physical activity, alcohol consumption, body mass
index, social support structures, education, preventive medical
care, number of physicians or greater availability of medical
care, etc.(11).  In countries where vitamin D was routinely added
to the food supply (U.S., Canada, Finland, Israel, Great
Britain), osteoporosis reaches its highest levels.


Country     vit D      Femur Fractures       heart disease
          additives     per/100,000          per/100,000
                        female male         female  male

Canada      ++++         200   50            650   200
USA         ++++         102   51            700   190
Sweden         +          87   38            340   100
UK             +          63   29            520   150
Neth           +          51   29            370   100
Finland        +          50   27            780   200
Israel         +          70   43            450   200
Yugo          no          39   38            320   200
Singapore     no          15   27            200   100
HongKong      no          31   27             83    37

  In addition, calciferol increases the retention of toxic metals
and radioactive nuclides.  Hence, it may be a cofactor in
childhood lead poisoning.  Calciferol also accentuates magnesium
deficiency and certain hypersensitive conditions (primary
hyperparathyroidism, sarcoidosis).  Finally, the relation of
calciferol and cancer is not a satisfactorily resolved question.

  The role of calciferol and atherosclerosis has been suggested
by a number of researchers (3, 12, 13)


V.  CONCLUSION:

   Now, if I may give a personal assessment of the above
information.  Here we have another reason to avoid meat and diary
products.  Keep in mind that the toxic effects of calciferol are
aggravated by saturated fats (which also contributes to the total
ingestion of exogenous calciferol). More importantly, we have
again an interesting case example where the complexity of whole
foods and our body's evolved means to handle those foods and
produce its own needed substances, like D, should be better
respected.  It is simply hubris at this point to suggest that the
atomistic biochemical approach to nutrition is sufficient to give
us just yet adequate synthetic substitutes in all cases.  Better,
in general, to still get your vitamins from whole foods than from
pills or food additives.

   While not unexpected, it is interesting to note that Moon has
been harassed by the dairy industry for doing this research.
For example, while serving as a professor of biochemical
toxicology for the Bioenergetics Research Laboratory in the
Kinesthesiology department at sfu, the dairy industry complained
to the administration.  The sfu president, however, backed Moon
informing this lobby that at sfu at least, the professors have
freedom of research.  It is curious that the dairy industry
should be so driven to contest this area of research.  You would
think it would be in the dairy industry's interest to improve
its product before the general public demands it, and also save
itself the costs of adding calciferol at the factory.  Maybe
they don't want to admit that anything whatsoever could be bad,
or ever was bad, with drinking milk and eating cheese.  After
all, they have been very successful in promoting these high
cholesterol foodstuffs as "health fostering foods".


A FEW REFERENCES FROM THE MANY IN THE PAPER:

(1) Dr. Jim Moon (biochemical Toxicology)
     School of Kinesiology
     Simon Fraser University
     Burnaby, B. C.
     V5A 1S6  Canada

     Moon, J. et al. 1992.  "Etiology of Atherosclerosis and
          Osteoporosis:Are Imbalances in the Calciferol Endocrine
          System Implicated?"  JOURNAL OF THE AMERICAN COLLEGE OF
          NUTRITION, 11:567-583.

(2) A. W. Norman, 1979, "VITAMIN D.  THE CALCIUM HOMEOSTATIC
     STEROID HORMONE".  New York: Academic Pr., 1979).

(3)  Peng & Taylor, 1980.  Probably role of excesses of vitamin D
      in genesis of arteriosclerosis. ARTERIAL WALL, VI: 63-68

(4)  Smith & Johnson, 1989, "Review article: biological
     activities of oxysterols.  Free radicals ... " in BIO. MED.
      7:285-332).

(5) Fraser, D.  (1983).  The physiological economy of vitamin D.
     LANCET 1:969-71.

(6) DeLangen, C. & donath, W. (1956).  Vitamin D sclerosis of the
     arteries and the danger of feeding extra vitamin D to older
     people, with a view on the development of different forms of
     arteriosclerosis.  ACTA MED. SCAND. 156:317-23

(7) Chaplin, H. et al.  Vitamin D intoxication. (1951)  AM. J.
     MED. SCI. 221:369-78.

(8) Seelig, M. (1969).  Vitamin D and cardiovascular, renal, and
     brain damage in infancy and childhood.  ANN. NY ACAD. SCI.
     147:537-82.

(9) Friedman, W. (1968).  Congenital cardiovascular anomalies and
     vitamin D.  HEART BULL. 17:101-5.

(10) (1974) Department of National Health and Welfare: Nutrition
      Canada.  National survey.  Information Canada.

(11)  Kaplan, g. et al. (1988).  The decline in ischemic heart
      disease mortality: prospective evidence from the Alameda
      County Study.  AM. J. EPIDEMIOL. 127:1131-42.

(12)  Holmes & Kummerow (1983).  The relationship of adequate and
        excessive intake of vitamin D to health and disease.
        J. AM.COLL. NUTR. 2:173-99.

(13).  Moon, J. (1972). Factors affecting arterial calcification
     associated with atherosclerosis.  ATHEROSCLEROSIS, 16:199-26.

(14)  Gibson, R. et al. (1987).  Vitamin D status of East Indian
      Punjabi immigrants to Canada.  BR. J. NUTR. 58:23-29.

(15)  Mazess, r. et al. (1985).  bone mineral and vitamin D in
      Aleutian Islanders.  M. J. Clin. Nutr. 42: 143-6.

(16)  Sowers, M. et al. (1986).  Parameters related to 25-OH-D
       levels in a population-based study of women.
         Am. J. Clin. Nutr. 43:621-8.