Agriculture Reference
In-Depth Information
In human diets, zinc accompanies protein; it is almost impossible to provide a
protein-deficient diet that is not zinc deficient (Golden and Golden 1981). Zinc is
highly available from breast milk and animal protein. Before the cause of acroder-
matitis enteropathica, an inherited defect of intestinal zinc absorption, was discov-
ered, it was treated effectively with breast milk.
In poverty, most of the monotonous plant-based diets contain little zinc but much
phytate, which further reduces intestinal absorption of zinc. Many millions of infants
and children grow less quickly than their genetic potential for many reasons. One
reason is zinc deficiency; the extent of its contribution is unclear but may be consid-
erable in, for example, rural India. When it limits growth, the children are smaller
and require less zinc. This is an example of reductive adaptation. Providing zinc as
a supplement allows growth to resume, but this can only continue while there is suf-
ficient energy and all other essential nutrients to sustain it. As the child grows, more
of everything is required.
The effects of zinc deficiency are, like zinc itself, ubiquitous. They appear first in
tissues with normally high turnover rates. Thus, intestinal mucosal function suffers:
Malabsorption is general and permeability is increased. Diarrhea, or
enteropathica
,
is the clinical outcome. Skin epithelium, the epidermis, thins, and it becomes less
effective as a barrier. Wound healing is also impaired. Minor trauma, which tends
to occur around orifices and on extremities, leads to chronic skin lesions, or
acro-
dermatitis
. These features manifest themselves late; before this, the child will have
“adapted” to a low-zinc diet by not growing and hence not requiring so much. There
are other costs of this adaptation. Not only are the barriers to infection reduced, but
also the ability to exhibit either nonspecific immunity, in the form of inflammation
or an acute-phase response, or specific immunity, especially cell-mediated immu-
nity, is reduced. Infections pass unnoticed because of the lack of clinical signs (of
the child's response); they are not treated, and the child suffers severe, prolonged
morbidity and much increased mortality from infections that were initially relatively
innocuous. Zinc deficiency is rarely diagnosed in such circumstances.
z
if in C
s
t a t u s
One of the most important and fascinating aspects of zinc in human health is that even
today, it is almost impossible to assess zinc status reliably “in the field.” It cannot be
done on clinical grounds because the effects of its deficiency are nonspecific, growth
failure, until very advanced. It cannot be done easily in the laboratory. Kinetic studies
using stable isotopes are probably the gold standard but are confined to the research
laboratory. Hair zinc analysis is fraught with methodological difficulties, and neither
plasma nor cell zinc concentrations inform zinc status reliably. A retrospective diag-
nosis of zinc deficiency can be made following a positive effect of a period of zinc
supplementation. This has led to large-scale zinc supplementation studies of infants
and children with various infections. In most, a positive effect has been demonstrated
(Umeta et al. 2000, Brooks et al. 2005). However, it is clear that, as with studies
of several other micronutrients, effects are seen if deficiencies are made good, but
not if the subjects are not deficient in the first place. Indeed, although zinc toxicity
