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EC number: 215-572-9
CAS number: 1332-65-6
In Chapter 1 we introduce the importance of copper as an essential
element to all aerobic life, including humans. The relevance to human
health is explained by the involvement of copper in many enzymes,
which are crucial to a wide range of physiological functions. Copper
is also involved in gene transcription and in the immune system. In
addition, copper deficiency is implicated in heart disease.
In Chapter 2 we examine the sources of dietary copper from food and
water. We include data on the copper content of foods and explain why
it varies. We consider the validity of dietary assessments and include
tables of dietary copper intake from many regions of the world. The
average adult dietary intake of copper is 1.5 mg/d in omnivores, and
2.5 mg/d in vegetarians. We report on copper in the water supply, and
the possibility of copper leaching from copper pipes and the risk of
adverse effects of drinking too much copper in solution.
Chapter 3 is an overview of copper metabolism that begins with whole
body physiology of copper and develops to look at some of the latest
research on intracellular transport and regulation. We note a
remarkable homeostasis at whole body, organ, and cellular level with
mechanisms to conserve copper when supply is limited and to reduce
uptake, sequester, or excrete it when supply is high.
Chapter 4 examines genetic disorders and other conditions that affect
copper metabolism. Menkes syndrome and Wilson's disease are
characterized by a defect in genes that control copper distribution to
the tissues. In Menkes patients we see the serious consequences of
copper deficiency with failure of the copper-containing enzymes to
function normally, resulting in early death. The Wilson's disease
defect causes accumulation of copper in the liver. The effects are
those of chronic copper toxicity, but treatments are available. Both
conditions have serious neurological consequences. These conditions
help our understanding of the normal control of copper transport and
metabolism and its relevance to health.
In Chapter 5 we consider pregnancy and fetal development. We describe
the remarkable adaptation of maternal metabolism with a rise of plasma
copper and ceruloplasmin concentrations that do not seem to require an
increase in maternal intake of copper. Copper deficiency in pregnancy
is rarely due to insufficient dietary intake, but may occur for a
variety of other reasons. There are considerable animal data, but
limited human data, to indicate that copper deficiency in pregnancy is
associated with birth defects and low birth weight. While overt
deficiency is rare, the possible widespread, mild, sub-clinical copper
deficiency is more likely. We found no data on toxic effects of copper
in human pregnancy. There is evidence that the placenta can regulate
the transfer of copper from the mother to the fetus, but the
mechanisms are not yet understood. Most of the copper in the fetus is
accumulated in the latter half of pregnancy and stored in the liver.
In Chapter 6 we discuss the needs of the newborn infant, the growing
child and adolescent. Premature and very-Iow-birth-weight infants are
particularly at risk of copper deficiency because of the small liver
and incomplete liver stores of copper. Copper absorption is higher
from breast milk than from infant formula, despite the low copper
concentration. Copper deficiency is rare in breast-fed pre-term
infants. Copper concentrations in human milk seem to be unrelated to
maternal dietary intakes of copper and unaffected by a range of other
variables. Maternal milk is a sufficient source of copper for about 4
months, but after that it is inadequate and weaning to a mixed diet
provides adequate copper. Cow's milk contains very little copper and
early weaning onto a diet of cow's milk or unsupplemented formula can
result in copper deficiency. Malnourished children, those with
infections, and those in a catchup growth spurt are at risk of severe
copper deficiency. Data suggest that most well-nourished children have
adequate copper intakes but there is some evidence that recommended
intakes are too low for rapid growth. Some adolescents may be at risk
of marginal copper deficiency as reports indicate an average
consumption below recommended intakes.
Chapter 7 examines some of the interactions that copper has with other
dietary factors, especially minerals and other nutrients. Some of
these factors, certain proteins, for example, enhance copper uptake,
but minerals, particularly iron and zinc, hinder uptake. Many infant
formulas, breakfast cereals, and prenatal vitamin and mineral
supplements are fortified with iron and zinc but do not have any
nutritionally Significant amount of copper. An inappropriate ratio of
iron or zinc to copper can interfere with copper availability.
Pregnant women and young children are particularly vulnerable. Those
who take over-the-counter zinc supplements may be at risk of copper
In Chapter 8 we compare the techniques for measuring copper status.
Severe deficiency can be detected by laboratory-based clinical
indicators, such as serum or plasma copper and ceruloplasmin
concentrations. Other techniques are based on the activity of the
copper-containing enzymes and the response of components of the immune
system. A different approach to measuring marginal copper status has
been suggested involving various functional tests, such as blood
pressure, cardiac function, and sleep patterns. There is a need for
specific and sensitive indicators of marginal copper intakes that are
clearly related to health effects. Only when these are available can
the extent and significance of marginal copper deficiency be
quantified. Research, using a variety of markers of status, indicates
that adults with intakes below 1 mg/d may be at some minor health risk.
Chapter 9 examines some of the existing recommendations and guidelines
concerning copper intake in humans, and explains the rationale behind
them. We compare various national and international dietary guidelines
for optimum intake, upper limits set to avoid toxicity from high
intakes, and regulations applying to the water supply. This chapter
summarizes the findings of earlier chapters on intakes and
requirements of our target groups in a format that allows comparison
with the guidelines and identifies those most at risk.
We did not consider any evidence strong enough to warrant changes to
present recommendations but we do suggest possible anomalies. We are
able to only partly answer the questions set out in the preface.
1. The amount of copper in the daily diet sufficient
for health is at least the lowest set out in the table of dietary
reference values. This is in the range of 20-60 j.Jg Cu/kg/day for most
children and adults. The needs of newborn infants are 40-150 j.Jg
Cu/kg/day; premature babies may need 150-400 j.Jg Cu/kg/day and
malnourished children may need over 500 j.Jg Cu/kg/day for recovery.
2. The question of how much copper is too much is more
difficult to answer.
The upper safe limit of around 200 j.Jg Cu/kg/day is safe for most
adults and children but formula-fed children may exceed this and the
needs of preterm and marasmic infants are much higher. Copper intakes of
800-900 j.Jg/kg/day are toxic to some adults and children. There is
uncertainty as to the risk of intakes in the range of 300-600 j.Jg
Cu/kg/day for healthy adults and children.
3. The margin between safe and adequate intakes and
intakes that are harmful is variable and not clear. For deficiency, it
may be only a factor of 2 or less. For toxicity it may be a factor
between 5 and 10.
Research questions. In the final section of this book we list questions
and possible areas for research identified from gaps in our knowledge.
It is to be hoped that the findings of any future research will aid our
understanding of copper requirements of the pregnant mother, her
developing fetus, and her children, so that in future we may be able to
answer the questions with more certainty and precision.
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