[Rice Catalyst Issue 14]

explain the findings by Haddow et al. (1999) on
IQ score discrepancies. [11-12] These IQ
discrepancies are further explained by
research performed by Moog et al. (2015)
which demonstrates that THs are fundamental
in the proper development of the fetal cortex
which is involved in memory, thinking,
learning, and reasoning [6, 22]. Additionally,
Moog et al. (2015) also identifies that both T3
and T4 have significant effects on neuronal
proliferation, migration, differentiation,
synaptogenesis, and myelination. [6] With so
many biochemical cascades building off of
[l]ndividuals untreated
for clinical
hypothyroidism present
with explicit symptoms,
including, but not
limited to, menstrual
disturbances, abnormal
weight gain, hair loss,
and excessive fatigue.
neurological abnormalities due to the
synergistic nature of neurological activity.
Ultimately, such perturbations in brain activity
on a biochemical level could be a leading
factor in the lower IQ scores observed in
human fetuses by Haddow et al. (1999). [8]
Severity of neurocognitive implications, such
as lowered IQ scores, are believed to be
dependent on the extent of TH imbalance. [14-
17] Specifically, though a study conducted by
Akintola et al. (2015) identified potential
cognitive impairments linked to subclinical
hypothyroidism, characterized by moderately
elevated TSH levels of 4.6-8.0 mlU/mL and
normal T4 levels, through a systematic
literature search, the study acknowledged that
the data was conflicting and could not
confidently establish a connection between
altered neurocognition and subclinical
hypothyroidism. [14-15] However, the same is
not upheld with clinical hypothyroidism,
classified with raised TSH serum levels greater
than 12mU/L and low T 4 levels, where
researchers have established a clear
Euthyroid
state
Subclinical
hypothyroidism
connection between clinical hypothyroidism
and disturbances to neurocognitive function.
[16-17] These studies demonstrate that the
extent of deviation from normal THs and TSH
serum levels corresponds to the severity of
clinical symptoms because while individuals
suffering from subclinical hypothyroidism are
often asymptomatic and present with
nonspecific symptoms suggestive of early
abnormal thyroid function, individuals
untreated for clinical hypothyroidism present
with explicit symptoms, including, but not
limited to, menstrual disturbances, abnormal
weight gain, hair loss, and excessive fatigue.
[1, 18] Studies by Stasiolek (2015) and Akintola
et al. (2015) similarly suggest that severity of
TH deficiency correlates to severity of
symptoms because subclinical hypothyroidism
is not correlated with significant
neurocognitive decline, but clinical
hypothyroidism is strongly associated with
mood and cognitive disturbances and in
severe cases, myxoedema coma. [14, 16] This
trend is also reflected in fetuses whose
mothers had varying severities of
Overt
hypothyroidism
TSH
each other during fetal development, even
subtle changes in TH levels can accumulate
and begin to manifest as neurocognitive
problems, likely amounting to a lower IQ in
human fetuses in later stages of life. [6]
Altogether, the fetal consequences of maternal
hypothyroidism observed through lower IQ
scores establishes a near definite link between
T3 and T4 levels and neurocognitive function.
Beyond research focusing solely on
connections between THs and IQ scores,
studies unrelated to hypothyroidism by
Oommen (2014) and Marsman et al. (2017)
identify that lower IQ is associated with
abnormalities in total brain gray matter, cortex
thickness, magnitude of blood and
biochemical activity, frontal lobe integrity, and
neurological excitatory-inhibitory balance. [12-
13] Hence, it is possible that lowT3 and T4
levels during pregnancy can result in any one
or a combination of the following
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Normal range
Figure 2. Illustrates differences between the Euthyroid state, Subclinical hypothyroidism, and
Overt hypothyroidism. T4 levels are still in the normal range in subclinical hypothyroidism, and
below normal T4 levels is a defining criteria for overt hypothyroidism. [18]
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