----- Original Message -----
From: "Laurel" <[log in to unmask]>
>
> Given that I seem to need an unusual amount of t-3 I wonder how this
> affects the fetus and then the infant with breastfeeding - or is
> placenta crossover different from breast milk crossover?

Us all,

The fetal thyroid starts to function at around 10 weeks of pregnancy,
and starts to absorb and use the bloodstream iodine as it passes the
thyroid. Thyroxine (T4) and fetal TSH becomes detectable in the blood
and the presence of TSH (progressively increasing) indicates development
of the fetal hypothalamic-pituitary-thyroid axis. The maternal TRH
(Thyrotropin Releasing Hormone) crosses the placenta while the maternal
TSH does not. so, while the fetal thyroid axis is developing (at around
the second trimester), thyroid regulation is handled by the fetal TSH,
while the TRH stimulation of the fetal pituitary is handled by the
mother's TRH. This is so because the fetal hypothalamus has not yet
reached it's maturity and it has to depend from the mother's. As the
fetal hypothalamus matures it starts it's own regulation and the fetal
thyroid increases its thyroid secretion and the fetal blood starts
increasing it's carrier proteins (thyroglobulin). There is a difference
in the value of thyroxine between the fetus and the mother at this
point, and this is indicated by an elevated Reverse T3 in the fetal
blood. Fetal Reverse T3 in elevated because the main thyroid hormone
available to the fetus is T4. Reverse T3 is a pathway for diverting
excess T4 in a regulatory manner (gets flawed in some -- not perfect).
There is very minimal transfer of maternal T3 and T4 to the fetus
because the fetal thyroid axis is fully functioning at this point.

Ref: Harrison's Principle of Internal Medicine 14th Ed
Part 13 - Endocrinology and Metabolism, Diseases of the Thyroid -- Leon
Wartofsky

Here's an excerpt from the CYTOMEL (LIOTHYRONINE, T3) PRESCRIBING
INFORMATION

Pregnancy­ Category A. Thyroid hormones do not readily cross the
placental barrier. The clinical experience to date does not indicate any
adverse effect on fetuses when thyroid hormones are administered to
pregnant women. On the basis of current knowledge, thyroid replacement
therapy to hypothyroid women should not be discontinued during
pregnancy.

Nursing Mothers­ Minimal amounts of thyroid hormones are excreted in
human milk. Thyroid is not associated with serious adverse reactions and
does not have a known tumorigenic potential. However, caution should be
exercised when thyroid is administered to a nursing woman.

Pediatric Use­ Pregnant mothers provide little or no thyroid hormone to
the fetus. The incidence of congenital hypothyroidism is relatively high
(1:4000) and the hypothyroid fetus would not derive any benefit from the
small amounts of hormone crossing the placental barrier. Routine
determinations of serum T4 and/or TSH is strongly advised in neonates in
view of the deleterious effects of thyroid deficiency on growth and
development.
Treatment should be initiated immediately upon diagnosis and maintained
for life, unless transient hypothyroidism is suspected, in which case,
therapy may be interrupted for 2 to 8 weeks after the age of 3 years to
reassess the condition. Cessation of therapy is justified in patients
who have maintained a normal TSH during those 2 to 8 weeks.
_________

Hope this helps.


Greg

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