 |
One
of the advances
that changed the
way we look at
vitamins was the
discovery that
too little folate,
one of the eight
B vitamins, is
linked to birth
defects such as
spina bifida and
anencephaly.
Fifty years ago,
no one knew what
caused these birth
defects, which
occur when the
early development
of tissues that
eventually become
the spinal cord,
the tissues that
surround it, or
the brain goes
awry. More than
three decades
ago, British researchers
found that mothers
of children with
spina bifida had
low vitamin levels.
Eventually, two
large trials in
which women were
randomly assigned
to take folic
acid (the form
of folate added
to multivitamins
or fortified foods)
or a placebo showed
that getting too
little folate
increased a woman's
chances of having
a baby with spina
bifida or anencephaly
and that getting
enough folate
could prevent
these birth defects.
Timing of folate
is critical: For
folate to be effective,
it must be taken
in the first few
weeks after conception,
often before a
woman knows she
is pregnant.
Enough folate,
at least 400 micrograms
a day, isn't always
easy to get from
food. That's why
women of childbearing
age are urged
to take extra
folic acid as
a supplement.
It's also why
the US Food and
Drug Administration
now requires that
folic acid be
added to most
enriched breads,
flour, cornmeal,
pastas, rice,
and other grain
products, along
with the iron
and other micronutrients
that have been
added for years.
Since the advent
of mandatory folate
fortification
in 1998, neural
tube birth defects
have dropped by
20 to 30 percent,
and studies have
shown that far
fewer people have
low levels of
folate in their
blood.
The other exciting
discovery about
folate and two
other B vitamins,
vitamin B6 and
vitamin B12, is
that they may
help fight heart
disease and some
types of cancer.
It's too early
to tell if there's
merely an association
between increased
intake of folate,
vitamin B6, and
vitamin B12 and
heart disease
or cancer, or
if high intakes
prevent these
chronic diseases. |
In
1968, a Boston
pathologist investigated
the deaths of
two children from
massive strokes.
Both had inherited
conditions that
caused them to
have extremely
high levels of
a protein breakdown
product in their
blood, and both
had arteries as
clogged with cholesterol
as those of a
65-year-old fast-food
addict. Putting
one and one together,
he hypothesized
that lower, but
still elevated
levels of homocysteine
would contribute
to the artery-clogging
process of atherosclerosis.
Since then, most—but
not all—studies
have linked high
levels of this
breakdown product,
called homocysteine,
with increased
risks of heart
disease and stroke.
However, linking
higher levels
of homocysteine
with heart disease
risk does not
necessarily mean
that lowering
homocysteine levels
will lower risk.
That requires
testing in randomized
trials. |
