Nutritional vitamin defi ciency

In countries where diets are unbalanced and inadequate,
or where there are particular dietary customs,
certain typical disease patterns have been shown to
be due to vitamin defi ciency. Examples of the most
commonly observed diseases are xerophthalmia, rickets,
beriberi, pellagra and scurvy, which result from
defi ciencies of vitamin A, vitamin D, thiamin, niacin
and vitamin C, respectively. Defi ciency of a single
member of the vitamin B group is rare in humans
because these vitamins are largely found together in
nature, and foodstuffs lacking in one member of the
complex are likely to be poor in the others. Moreover,
the overt manifestations of defi ciency of this group
overlap to some extent.
Nutritional aspects of vitamins 9
Subclinical defi ciency and marginal defi ciency are
synonymous terms used to describe conditions in
individuals who are not clinically nutrient defi cient,
but who appear to be close to it. An alternative and
perhaps better term proposed by Victor Herbert in
1990 is ‘early negative nutrient balance’, which is
used when laboratory measurements indicate that an
individual is losing more of a nutrient than is being
absorbed.
By reference to the sequence of events in the development
of vitamin defi ciency, Pietrzik (1985)
emphasized the importance of preventing functional
metabolic disturbances that can evolve into overt
clinical symptoms. This sequence can be subdivided
into six stages as follows.
• Stage 1 Body stores of the vitamin are progressively
depleted. A decreased vitamin excretion in the
urine is often the fi rst sign. Normal blood levels are
maintained by homeostatic mechanisms in the very
early stages of defi ciency.
• Stage 2 The urinary excretion of the vitamin is further
decreased and vitamin concentrations in the
blood and other tissues are lowered. A diminished
concentration of vitamin metabolites might also be
observed.
• Stage 3 There are changes in biochemical parameters
such as low concentrations of the vitamin in
blood, urine and tissues, and a low activity of vitamin-
dependent enzymes or hormones. Immune
response might also be reduced. Non-specifi c subclinical
symptoms such as general malaise, loss of
appetite and other mental changes appear.
• Stage 4 The biochemical changes become more
severe and morphological or functional disturbances
are observed. These disturbances might
be corrected by vitamin dosing in therapeutic
amounts within a relatively short time or vitamin
supplementation in amounts of (or exceeding) the
recommended dietary allowances over a longer
period. Malformation of cells is reversible at this
stage.
• Stage 5 The classical clinical symptoms of vitamin
defi ciency will appear. Anatomical alterations characterized
by reversible damage of tissues might be
cured in general by hospitalization of the patient. In
most cases there are defi ciencies of several nutrients
and a complicated dietetic and therapeutic regimen
has to be followed.
• Stage 6 The morphological and functional disturbances
will become irreversible, fi nally leading to
death in extreme cases.
From the health point of view, Pietrzik (1985) proposed
that the borderline vitamin defi ciency is represented
by the transition from the third to the fourth
stage.

The causes of nutritional vitamin deficiency are
any one or combination of the following: inadequate
ingestion, poor absorption, inadequate utilization,
increased requirement, increased excretion and increased
destruction in the body. The capacity to store
vitamins in the body is another aspect to be considered:
humans can store thiamin for only about two
weeks, whereas vitamin B12 can be stored for several
years.

What is Rickets, History of Rickets

Rickets
Much of the pioneering work on the aetiology of
rickets should be accredited to the eminent French
physician Armand Trousseau during the 1830s.
Trousseau called attention to the experiments of Jules
Guérin, published in 1838. Weaned puppies were
placed in a dark basement and fed raw meat while
their litter mates were given a varied diet in a normal
environment. After a few weeks the meat-fed animals
exhibited all the classic signs of advanced rickets, in
contrast to the littermates which showed no signs of
rickets. A similar experiment conducted on young
pigs given no access to animal fats or to sunlight gave
analogous results. This led Trousseau to postulate that
rickets was due in part to defi cient diets. Trousseau
also postulated that cod-liver oil, which had been
demonstrated to cure rickets in children, was acting
as a fat containing unknown benefi cial dietary factors,
rather than acting as a specifi c drug. He recognized
that ‘good general alimentation’ is of prime importance
in the aetiology of rickets as well as the benefi cial
effects of sunshine. Unfortunately, these experiments
were ignored and forgotten by 1900. Most medical
authorities at the time advocated the development of
a vaccine in the belief that rickets was a chronic infectious
disease. They dismissed cod-liver oil as a useless
‘quack’ remedy.

In 1918, Sir Edward Mellanby in Great Britain undertook
the study of rickets, starting again at the same
point as Guérin 80 years before. Mellanby produced
rickets in puppies by raising them without the benefi t
of sunlight or UV radiation, and feeding them a highcereal,
low-fat diet in which white bread was replaced
by unrefi ned oatmeal. Mellanby further showed that
the addition of cod-liver oil or butterfat to the feed
prevented rickets. This clearly showed that rickets was
6 Vitamins: their role in the human body
a nutritional disease, and cod-liver oil or butterfat
contained a factor that prevented it.

In 1922 McCollum and associates published the results
of experiments designed to determine whether
the antirachitic factor in cod-liver oil was identical to
or distinct from the previously discovered vitamin A.
They found that cod-liver oil retained its antirachitic
properties after destruction of the vitamin A by heating
and aeration. Thus, in addition to vitamin A, codliver
oil contained a new fat-soluble vitamin, which
McCollum later (1925) called ‘vitamin D’. Zucker and
co-workers in 1922 found that vitamin D was present
in the unsaponifi able fraction of cod-liver oil, and
suggested that it was closely related to cholesterol.