pector@ihuxw.UUCP (Scott W. Pector) (03/20/84)
This is in response to your request for info on folic acid requirements
and supplementation during pregnancy. I asked my wife (who is just about
to graduate from the U. of Chicago School of Medicine) and she submits
the following. (Note that folic acid = folate and mcg = micrograms and
and mg = milligrams throughout this article.)
Part I:
In regard to requirements, 150 to 300 mcg per day are required during
pregnancy and 60 mcg per day during breast feeding
to maintain a positive folate balance, 100 to 300 mcg supplementation
is normally suggested for pregnancy, and post partum (after the baby is
born) for mothers who elect to breast feed.
This is in contrast to nonpregnant daily requirements of 50 mcg per day.
So, you see that the developing fetus does markedly increase folate
requirements.
A vegetarian cookbook I own mentions the legal restriction of folate
in a single vitamin pill to 0.1 mg, and adds that synthetic folate is
four times more potent than dietary folate (the RDA they mention is
400 mcg dietary folate per day in normal nonpregnant adults).
A little background information in addition to the above should persuade
you that large folate doses are unnecessary in an otherwise healthy
pregnant woman. (800 mcg certainly would be more than adequate.)
Folate is a key co-factor in synthesis of DNA in cells. Quickly
dividing cells, especially red blood cell precursors in bone marrow
and cells lining the gastrointestinal tract, thus have high folate
requirements. 5 to 20 mg of folate are stored in the body, which would
be used up within a matter of months if dietary intake or intestinal
absorption of folate were abruptly halted. Most folate comes from
plant (fruit and vegetable) sources in the diet, especially dark green
leafy vegetables, orange juice, legumes, brewers and torula yeast.
Cooking temperatures can destroy up to 65% of folate in vegetables
and 3 days storage at room temperature can destroy up to 70%.
Folate deficiency states can occur in three ways:
1. Inadequate intake - most common in alcoholics, drug addicts,
and other malnourished groups (poor, elderly, or "Coke-
and-potato chip-diet" in teenagers).
2. Increased demand - pregnancy, growth spurts (in infancy and
adolescence), chronic hemolytic anemias with high
turnover rate of red blood cells (i.e., sickle cell anemia).
3. Malabsorption - small intestinal disorders that interfere with
folate absorption from the gut.
Various medications can interfere with folic acid use, including cancer
chemotherapeutic agents, anti-parasite drugs, anti-seizure medicines
(Dilantin, phenobarbital), estrogens, colchicine (used to treat gout),
and neomycin (an antibiotic). Symptoms of folate deficiency are mainly
from anemia and gastrointestinal symptoms (red, beefy tongue, diarrhea).
Supplements for DEFICIENT patients are usually 1-5 mg per day.
Part II:
Vitamin B12 exists in two active forms in the body. One of these (adeno-
sylcobalamin) is required for a reaction in metabolism of fatty acids. If
B12 is deficient, methylmalonyl coA and its precursor, propionyl coA, build
up in large amounts and are incorporated into abnormal fatty acids with an
odd number of carbon atoms. (Normal fatty acids have an even number of
carbon atoms.) These in turn are incorporated into abnormal lipids (fats)
in nerve cells and this abnormality may be the reason for development of
neurologic abnormalities in B12 deficiency. Folic acid has no role in this
biochemical process.
However, the second form of B12 (methylcobalamin) is a co-factor required
for another reaction, conversion of homocysteine to methionine (an amino
acid). This reaction is important in folic acid metabolism, which becomes
disrupted if the reaction can't occur. An ineffective form of folic acid
builds up in the tissues and gradually leaks out of the cell unusable.
Thus B12 deficiency leads to a deficiency of *usable* folate in tissues,
even though folic acid itself might be present in normal or even high
bloodstream levels. Defective DNA synthesis results, leading to anemia
and gastrointestinal problems similar to those seen with folic acid
deficiency alone.
In patients with B12 deficiency, high doses of folic acid can partially
correct the anemia and gastrointestinal symptoms associated with methyl-
cobalamin deficiency, masking the anemia of B12 deficiency. However,
folic acid has no effect on the neurologic symptoms due to adenosyl-
cobalamin deficiency, and some authorities feel it can *aggravate* neurologic
symptoms (numbness and tingling in extremities, defective position
sense, unsteady gait, dementia or psychosis). Thus in
patients with megaloblastic anemia (due to defective DNA synthesis and
characterized by abnormally large red blood cells) which can be due to
*either* B12 or folate deficiency, both deficiencies are checked for prior
to starting treatment.
B12 deficiency is very unlikely in young women unless they are strict
vegetarians ("vegans" who abstain from all animal products including
dairy and eggs), have had total stomach removal or extensive gastric
damage, or have terminal ileum damage (damage or removal of the very end
of the small bowel before the colon starts). Overgrowth of bacteria
elsewhere in the small intestine in certain illnesses can also lead to
B12 deficiency. There are rare hereditary forms as well. I assume that
your wife has none of these problems.
Folic acid is a water soluble vitamin, so in a healthy person without
B12 deficiency, "overdosage" of folic acid would not be harmful. However,
there is no real need for large doses above the standard doses recom-
mended for pregnancy unless your wife has an underlying condition affecting
folic acid metabolism.
In elderly people (over age 60), B12 deficiency occurs most commonly as
pernicious anemia, which is a disease of very gradual onset. It is thought
to be due to the patient's production of antibodies against his/her own
parietal cells in the stomach, which secrete intrinsic factor (necessary
for B12 absorption in the terminal ileum). Parietal cells are gradually
destroyed and B12 absorptive capability in the GI tract is lost. The
important point is that it has a very insidious onset and elderly patients
who took massive doses of folate could well mask the anemia until
irreversible neurologic changes occurred. This sort of
reasoning probably underlies the regulation regarding folate dosage.
B12 replacement is usually given intramuscularly; oral replacement is
exceedingly expensive, requiring very large doses and close medical
surveillance to prevent relapse. Thus "reasonable amounts of B12" in
a multi-vitamin don't exist for B12 deficient patients who would unknowingly
mask their anemia with high multi-vitamin folate.
By the way, iron is very important during pregnancy, and I assume your wife
has probably been given a prescription for iron supplements. A well-balanced
high-protein diet (60-80 grams per day) with adequate calories and not too
much refined sugar or fat is the most important nutritional factor, as well
as reasonable vitamin and iron supplements.
Good luck to you both with this pregnancy and I hope to hear of a happy
healthy baby in the future!
(Soon to be) Dr. Beth Pector
I echo her sentiments.
Scott Pector