Dfvieira09 2014-07-26 20:01:17
I’m 34 and was diagnosed with hypothyroidism in October, at which
point I was 5 months post-partum. My TSH at that point was 36 and my
Free T4 was .7. I was originally prescribed 50 mcg Levoxyl, but I’ve
been on 88 mcg for the past month. I finally feel almost back to
normal. I am pregnant again (4.5 weeks), and I had my TSH and T4
levels tested on Monday. My TSH level is now 1.74 (it was 2.1 a month
ago), and my Free T4 is 1.1. I talked to my Endo today, and she said
that she was a little concerned about my Free T4, that she’d prefer it
to be in the higher end of the range (around 1.7). So, she recommends
that I continue on my current Levoxyl dosage (88 mcg), except I should
take an extra half tablet (44 mcg) once a week, until I have repeat
tests done in 4 weeks.
After talking with my endo, I did research about Free T4 and
pregnancy, and I’m concerned that just increasing my dosage by 44 mcg
a week isn’t going to do much good, and may ultimately result in
developmental delay for the baby, or even miscarriage.
I also tested high for antithyroid antibodies, and in the past I have
had a high ANA (along with joint stiffness and pain)as well as 1
positive and 1 negative test for antiphospholipid antibodies (I’ve
never officially been diagnosed with Lupus, but after seeing 3
Rheumatologists, the consensus was that I MAY have mild lupus).
What do you think about my Endo’s recommendation to just increase it
by 44 mcg a week? Since I’m already in the lower end of the normal
Free T4 range, and since thyroid levels often fluctuate in early
pregnancy, I’m concerned that this dosage won’t be enough and that my
pregnancy or the baby will be at risk.
Cavaliers 2014-07-26 20:01:32
You don’t give the ranges – are you still within range? Is the 1.7 you
refer to below the top of the range of where the endo wants you to be? Did
you discuss the research you located with the endo? If it is a reliable
source this might be a good idea if you think she is being too cautious.
Your endo is obviously keeping a very close eye on things. IMHO I would
suggest that you NOT change any medications without discussing fully with
her. It’s good that you are being tested every four weeks, which is about
the time for the meds to kick in. Small increments are the best way to go.
Clearly, your endo wouldn’t want to go hyper. It is not always easy to
obtain the delicate balance of ‘normal’ and perhaps this is more difficult
when a person is preggie.
Skipperbeers 2014-07-26 20:02:05
It’s a good sign you’re feeling back to normal. You’re T4 does seem a bit low,
but it would greatly surprise me if adding 1/2 tablet only once a week would
significantly increase your level.
Below are a couple of things regarding hypo and pregnancy. One if from a
doctor who practiced thyroid treatment for many years. He thinks T3 is
important, and if you are not turning the T4 you are getting into T3, then he’s
right. Your T4 is down, if you are actually producing rT3 which implies your
not producing as much active T3, then you are being undertreated.
If you have hashimoto’s, it’s not unusual for it to go into remission during
pregnancy, and stay away until a couple months after childbirth. My wife was
hypothyroid and untreated during three pregnancies and she generally felt
better at that time. She hasn’t tested positive for antibodies, but then 10%
of Hashi’s cases don’t, but the damage the antiboides do can be seen on
ultrasound, but even if she didn’t feel better because of Hashi’s remission, it
may be as the doctor below says the fetus supplements the mother’s thyroid.
All I know, is during her second pregnancy she was eating well, drinking lots
of chocolate milk and losing weight so that we didn’t actually know she was
pregnant until five months along. (Many pregnancy tests over the years before
that because of irregular cycle, it wasn’t unusual.)
Below, Alford thinks most hypothyroidism might start in the womb because mother
is hypothyroid. I don’t know if that’s valid. On the other hand, all 3 of my
children are hypo. (But if I didn’t come to an undrestanding of all the
problems hypothyroidism could cause, none of them would have been treated, and
one was very severe. But, childhood symptoms are different than adult, and
just because children don’t have the same symptoms as you doesn’t mean their
health problems aren’t caused just the same by the thyroid. For example,
anorexia and a skeletal thin appearance can be caused by hypothyroidism. If
our severe child had been fat, we might have suspected and not been persuaded
otherwise by the excellent TSH level.)
The Etiology, Diagnosis and Treatment of Hypothyroidism.
R. M. Alford, MD
What is low metabolism or hypothyroidism?
Hypothyroidism results from the insufficient production of the active thyroid
hormone, triiodothyronine (T3). The insufficient production of thyroid result
from one of two causes.
1. The failure of the thyroid gland to produce a sufficient reservoir of
thyroxine (T4), the precursor of T3
2. The production of an excessive amount of an aberrant isomer of T3,
reverse T3 (rT3), that prevents the production of sufficient T3 for a normal
Triiodothyronine is produced by an enzymatic removal of a specific iodine
radical from the thyroxine molecule. When there is an aberrant form of that
enzyme, another of the iodine radicals is removed resulting in the inactive
isomer of T3, reverse T3 (rT3).
What is the one normal condition in life is most threatened most by rT3
hypothyroidism? Pregnancy. Here it is well established, along with liver
disease and chronic illness, that considerable amounts of r T3 are produced in
a high percentage of seemingly normal women. It is also very evident in the
vast majority of pregnancies that they are clinically hypothyroid by the fact
they almost always have cold hand, the sure sign of core hypothermia. when
mother is hypothyroid, she is unable to maintain the incubator at an optimal
developmental temperature and fetal development suffers, probably also being
the cause for many of the spontaneous early abortions as well as some
congenital defects. As the pregnancy progresses, the fetal thyroid gland comes
on board functionally at about five months and its temperature control center
stimulates its thyroid gland to produce more hormone to increase the incubator
temperature. As a result of this excessive stimulation, two thing happen.
Mother feels better with the boost to her metabolic rate and the child ends up
hypothyroid to the same relative degree that mother is. The deficiency is also
the cause of a very high percentage of premature deliveries.
What is the etiology/cause of hypothyroidism?
Essentially all hypothyroidism is the result of failure to treat maternal
hypothyroidism during pregnancy, most often as the result of increased rT3
production. Using the above guide lines as early as possible in the pregnancy,
particularly before the fetal thyroid begins to supplement the maternal
deficiency at about the fifth month, maternal hypothyroidism can be corrected
to prevent or minimize the level of hypothyroidism in the child at birth. It is
the relative degree to which the fetal thyroid has to supplement the maternal
deficiency that determines the relative degree of the child s deficiency.
Supplementation is especially important in the ectomorphic female because of
their greater heat loss coefficient. This problem is most deleterious when
their last trimester of pregnancy occurs during the coldest months of the year.
When a patient already on thyroid becomes pregnant, especially when being
treated with T4, changes usually have to be made to compensate for the
increased production of rT3.
What is the mechanism for newborn thyroid deficiency? The critical factor
overall is the temperature level in the incubator. By the time the fetal
thyroid becomes functional, the fetal temperature control mechanism is also
functional. The fetal temperature control center is set for an optimal fetal
developmental temperature, about 99+ degrees. When the incubator temperature is
below that level, it signals the fetal thyroid to produce an additional amount
of thyroid to raise the incubator temperature through calorogenesis. That
increased heat in the incubator also heats the surround maternal structures and
thus her entire body. Some of that thyroid production also defuses through the
placenta increasing the level of maternal heat production. This is why so many
mothers feel their best during the last trimester of pregnancy. Thus, the
maternal level of hypothermia dictates the relative amount of hormone the fetal
thyroid is forced to produce. When that relatively optimal environment cannot
be achieved, there is an increased potential for fetal abnormalities/anomalies.
Again, the greater the demand put on the fetal thyroid to attain that optimal
level, the greater the level of thyroid deficiency that will be finally
manifest in both mother and child following delivery. Because thyroid hormone
does cross the placenta barrier, as is evidenced by the fact that the
athyreotic child appears to have essentially normal function at birth, testing
for fetal hypothyroidism would be better done after six weeks of age.
How is the above rational confirmed outside the human specie? If the poultry
farmer does not keep his incubators within a very narrow temperature range, he
is out of business. At a regional steelhead hatchery, they have found that when
the water temperature throughout the cycle of egg to smolt maturation is kept
very near the determined optimal temperature, they are able to release the
smolt back to the ocean after one year. Stream reared smolt require two years
to mature to the same point. Even the lowly one-cell organisms when cultured
are afforded a constant 98.6 degree temperature for their most rapid growth.
(This might be evidence why such organisms do not thrive as well in those
humans maintaining a 99 plus degree core temperature.) In general, the children
born of T3 supported pregnancies have matured faster in every aspect.
Some obvious benefits of thyroid supplementation.
With the use of T3 in about four hundred pregnancies starting in 1972, using
only clinical judgment in its prescription, there were only two births under
five pounds. One was a case of missed incompetent cervix and the other a
primipara/first pregnancy with a deep bicornate uterus, conditions in which
pre-maturity is usually inevitable. The usual rate of pre-maturity is more in
the range of 6%. Additionally, there were ten sets of twins born over a span of
about 800 deliveries. One set of twins was born before the beginning use of
supplemental thyroid. The first twins were below five pounds with only one twin
in the remaining sets weighing in at less than five pounds. The supplemented
pregnancy is better able to produce sufficient progesterone to prevent
premature labor. Additionally, after beginning the use of T3 prenatal
supplementation, there were no cases of postpartum depression, toxemia,
essentially no subsequent uterine fibroids nor cases of excessive weight gain.
Supplemental thyroid used appropriately will make a significant difference in
fertility, spontaneous abortion, breast, ovarian and uterine cancer and
possibly some genetic defects, such as Down s syndrome.
Synthroid Information. I’ve heard that it’s not unusual to increase dosages by
as much as 50% during pregnancy, and obviously levels should be checked
periodically and dosages kept as high as needed.
Pregnancy Category A
Studies in pregnant women have not shown that levothyroxine sodium increases
the risk of fetal abnormalities if administered during pregnancy. If
levothyroxine sodium is used during pregnancy, the possibility of fetal harm
appears remote. Because the studies cannot rule out the possibility of harm,
levothyroxine sodium should be used during pregnancy only if clearly needed.
Thyroid hormones cross the placental barrier to some extent. T4 levels in the
cord blood of athyroid fetuses have been shown to be about one-third of
maternal levels. Nevertheless, maternal-fetal transfer of T4 may not prevent in
Hypothyroidism during pregnancy is associated with a higher rate of
complications, including spontaneous abortion and preeclampsia, and has been
reported to have an adverse effect on fetal and childhood development. On the
basis of current knowledge, levothyroxine sodium should therefore not be
discontinued during pregnancy, and hypothyroidism diagnosed during pregnancy
should be treated. Studies have shown that during pregnancy T4 concentrations
may decrease and TSH concentrations may increase to values outside normal
ranges. Postpartum values are similar to preconception values. Elevations in
TSH may occur as early as at 4 weeks gestation.
Pregnant women who are maintained on levothyroxine sodium should have their TSH
measured periodically. An elevated TSH should be corrected by an increase in
levothyroxine sodium dose. After pregnancy, the dose can be decreased to the
optimal preconception dose.
Dfvieira09 2014-08-04 01:45:03
Thank you so much Diana and Skipper for your feedback and information.
I really appreciate it!
Skipper–at what age were your children diagnosed with Hypo, and what
were their main symptoms?
Is there anyone else out there who has been pregnant with Hypo and
willing to share your advice? I’m particularly interested in how low
your TSH and Free T4 levels were kept throughout the pregnancy, how
often you had dose adjustments, whether T3 should also be tested, etc.