Vitamin C deficiency

Defi ciency in humans
A defi ciency of vitamin C results in scurvy. Fully
developed scurvy is rarely seen nowadays, but clinical
signs of mild scurvy are found quite frequently in
alcoholics and drug addicts. The symptoms described
below have been observed in patients with scurvy
(Chazan & Mistilis, 1963) and in experimentally induced
scurvy (Hodges et al., 1971).
Early symptoms in adults are weakness, easy fatigue
and listlessness, followed by shortness of breath and
aching bones, joints and muscles. Progressive changes
in the skin then appear after about 4 months of complete
vitamin C deprivation. A horny material piles
up around the openings of hair follicles, and the hair
becomes fragmented and coiled. Red spots of pinpoint
to pinhead size caused by the rupture of small
blood vessels appear fi rst on the feet and ankles, and
then spread upwards. Thereafter, bruises appear over
large areas of skin, particularly on the legs. Bruising
is the manifestation of haemorrhages in subcutaneous
tissue, beneath the periosteum of bones and in
the synovia of joints. The gums become swollen and
bleeding, especially where there is advanced dental
caries. Haemorrhages are caused by rupture of capillaries,
which are fragile because of impaired ascorbic
acid-dependent synthesis of vascular basement
membrane (Priest, 1970). Wounds fail to heal and old
wounds reopen. The sufferer is visibly anaemic due in
part to haemolysis caused by peroxidative damage to
the erythrocyte plasma membrane (Goldberg, 1963).
Vitamin C defi ciency in adults may cause osteoporosis
due to a diminished production of organic matrix
in bones. The corresponding symptoms in infantile
scurvy are impaired ossifi cation and bone growth.
Kinsman & Hood (1971) studied the psychological
aspects of vitamin C defi ciency in healthy volunteers.
They measured four behavioural areas: physical fi tness
(strength, coordination and balance), mental
functions (memory, vigilance and problem solving),
psychomotor performance tasks (reaction time,
manipulative skills and hand–arm steadiness), and
personality. Three areas of change associated with
vitamin C deficiency were found: physical fitness involving
bending or twisting of the legs, psychomotor
tasks, and measures of personality. The changes in the
physical fitness could be accounted for by the pronounced
joint pain in the legs that occurred during
the deficiency period. The decrements in psychomotor
performance were attributed to a reduced motivational
level. The personality changes corresponded
to the classical ‘neurotic triad’ of the Minnesota Multiphasic
Personality Inventory, i.e. hypochondriasis,
depression and hysteria. Elevation of this triad is also
found in prolonged semi-starvation and defi ciencies
of B-complex vitamins.
In fully developed scurvy, as witnessed and recorded
at sea by James Lind in 1752, the body is covered with
spots and bruises, and the skin overlying the joints
becomes discoloured from the haemolysed blood in
and around them. There may be bleeding into the
peritoneal cavity and pericardial sac as well as into
joints. The gums become swollen, spongy and of a
livid blue-red colour. The swelling can develop to such
an extent that the gum tissue completely encases and
hides the teeth. The spongy gums bleed on the slightest
touch and become secondarily infected, leading to
loosening of the teeth and gangrene. Death preceded
by dyspnoea, cyanosis and convulsions is inevitable in
the continuing absence of vitamin C.
19.12.2 Rebound scurvy
Theoretically, the absorption of ascorbic acid could be
impaired on resumption of normal vitamin C inputs
following mega-dosing (>1 g per day), because of insuffi
cient carriers in the enterocyte cell membranes.
Based on experiments with guinea pigs, it is considered
likely that, in humans, renewed synthesis of
carriers will take place well before the onset of scurvy.
During mega-dosing, reduced ascorbate absorption is
accompanied by increased rates of ascorbate catabolism.
In adult guinea pigs, the accelerated catabolism
is not reversible after more than 2 months on subnormal
uptake of ascorbate (Sorensen et al., 1974). Guinea
pigs are thus susceptible to a systemic conditioning
effect known as rebound scurvy, caused by an induction
of ascorbic acid-metabolizing enzymes by high
dietary vitamin C. The body stores of vitamin C are
depleted more rapidly in juvenile guinea pigs than in
adults, increasing the likelihood of rebound scurvy in
juveniles. Solid evidence for the existence of rebound
scurvy in humans is tenuous (Gerster & Moser, 1988),
and reports by Schrauzer & Rhead (1973) and Siegel
et al. (1982) describe only single cases.