Iodine and thyroid hormones (TH) transport in the placenta are essential for fetal growth and development, but there is little research focus on the human placenta. The research aimed to investigate iodine and TH transport mechanisms in the human placenta. The placenta was collected from sixty healthy pregnant women. Urinary iodine concentration (UIC), serum iodine concentration (SIC), placenta iodine storage (PIS) and the concentration of serum and placenta TH were examined. Five pregnant women were selected as insufficient intake (II), adequate intake (AI) and above requirements intake (ARI) groups. Localisation/expression of placental sodium/iodide symporter (NIS) and Pendrin were also studied. Results showed that PIS positively correlated with the UIC (R = 0·58, P < 0·001) and SIC (R = 0·55, P < 0·001), and PIS was higher in the ARI group than that in the AI group (P = 0·017). NIS in the ARI group was higher than that in the AI group on the maternal side of the placenta (P < 0·05). NIS in the II group was higher than that in the AI group on the fetal side (P < 0·05). In the II group, NIS on the fetal side was higher than on the maternal side (P < 0·05). Pendrin was higher in the II group than in the AI group on the maternal side (P < 0·05). Free triiodothyronine (r = 0·44, P = 0·0067) and thyroid-stimulating hormone (r = 0·75, P < 0·001) between maternal and fetal side is positively correlated. This study suggests that maternal iodine intake changes the expression of NIS and Pendrin, thereby affecting PIS. Serum TH levels were not correlated with placental TH levels.

Iodine is an important element in thyroid hormone biosynthesis. Thyroid function is regulated by the hypothalamic–pituitary–thyroid axis. Excessive iodine leads to elevated thyroid-stimulating hormone (TSH) levels, but the mechanism is not yet clear. Type 2 deiodinase (Dio2) is a Se-containing protease that plays a vital role in thyroid function. The purpose of this study was to explore the role of hypothalamus Dio2 in regulating TSH increase caused by excessive iodine and to determine the effects of iodine excess on thyrotropin-releasing hormone (TRH) levels. Male Wistar rats were randomised into five groups and administered different iodine dosages (folds of physiological dose): normal iodine, 3-fold iodine, 6-fold iodine, 10-fold iodine and 50-fold iodine. Rats were euthanised at 4, 8, 12 or 24 weeks after iodine administration. Serum TRH, TSH, total thyroxine (TT4) and total triiodothyronine (TT3) were determined. Hypothalamus tissues were frozen and sectioned to evaluate the expression of Dio2, Dio2 activity and monocarboxylate transporter 8 (MCT8). Prolonged high iodine intake significantly increased TSH expression (P < 0·05) but did not affect TT3 and TT4 levels. Prolonged high iodine intake decreased serum TRH levels in the hypothalamus (P < 0·05). Dio2 expression and activity in the hypothalamus exhibited an increasing trend compared at each time point with increasing iodine intake (P < 0·05). Hypothalamic MCT8 expression was increased in rats with prolonged high iodine intake (P < 0·05). These results indicate that iodine excess affects the levels of Dio2, TRH and MCT8 in the hypothalamus.

The present study reports on first-trimester reference ranges of plasma mineral Se/Zn/Cu concentration in relation to free thyroxine (FT4), thyrotropin (TSH) and thyroid peroxidase antibodies (TPO-Ab), assessed at 12 weeks’ gestation in 2041 pregnant women, including 544 women not taking supplements containing Se/Zn/Cu. The reference range (2·5th–97·5th percentiles) in these 544 women was 0·72–1·25 µmol/l for Se, 17·15–35·98 µmol/l for Cu and 9·57–16·41 µmol/l for Zn. These women had significantly lower mean plasma Se concentration (0·94 (sd 0·12) µmol/l) than those (n 1479) taking Se/Zn/Cu supplements (1·03 (sd 0·14) µmol/l; P < 0·001), while the mean Cu (26·25 µmol/l) and Zn (12·55 µmol/l) concentrations were almost identical in these sub-groups. Women with hypothyroxinaemia (FT4 below reference range with normal TSH) had significantly lower plasma Zn concentrations than euthyroid women. After adjusting for covariates including supplement intake, plasma Se (negatively), Zn and Cu (positively) concentrations were significantly related to logFT4; Se and Cu (but not Zn) were positively and significantly related to logTSH. Women taking additional Se/Zn/Cu supplements were 1·46 (95 % CI 1·09, 2·04) times less likely to have elevated titres of TPO-Ab at 12 weeks of gestation. We conclude that first-trimester Se reference ranges are influenced by Se-supplement intake, while Cu and Zn ranges are not. Plasma mineral Se/Zn/Cu concentrations are associated with thyroid FT4 and TSH concentrations. Se/Zn/Cu supplement intake affects TPO-Ab status. Future research should focus on the impact of trace mineral status during gestation on thyroid function.

Intensive selection of broilers for faster growth and better feed efficiency resulted in greater susceptibility to metabolic disorders such as ascites syndrome, which is one of the major causes of mortality and economic loss in broiler industry. Whereas cool temperature is one of the primary triggers for ascites, early feed restriction (FDR) significantly alleviates its incidence and mortality. However, little is known about effects of FDR, cold environmental temperature and their interaction on physiological responses in broiler chickens. For this purpose, 320 one-day-old male broilers were divided into two treatment groups of Ad libitum (Ad) and feed restricted (FR) with eight pen replicates each. Chickens in FR group underwent feed access limitation from days 7 to 14 of age. On day 21 half of the birds (four pens) in each group exposed to the cold temperature (CT) and the other half (four pens) continued at normal temperature (NT). Average daily feed intake, average daily weight gain and feed conversion ratio (FCR) were measured at days 7, 14, 21, 28 and 42. At 39 and 46 days of age two chicks with a BW around the pen average were selected from each pen and slaughtered after collecting blood samples. Then, relative weight of internal organs and right ventricle weight per total ventricle weight (RV : TV) ratio were calculated. Compared with NT group, CT birds had higher daily feed intake and FCR (P<0.05) from day 28 to 42. Cumulative ascites mortality in CT chickens was higher (P<0.001) than NT chicks. Within the CT group, ascites mortality in FR chickens was reduced (P<0.001) to 1.25% compared with 8.75% in Ad chicks. Birds in CT group had significantly (P<0.05) thicker right ventricle and greater relative weight of heart, hematocrit and triiodothyronine concentration. However, none of these parameters were affected by FDR. Under cold stress conditions, FDR reduced activity of alanine aminotransferase and aspartate aminotransferase (P<0.05). Serum triglyceride, cholesterol, high-density lipoprotein and total protein were not influenced by either temperature or feeding regimen. In conclusion, these findings suggest that FDR reduces ascites incidence mainly by allowing better development of internal organs, which helps them to cope with the high metabolic pressure and suffer less damage.

The writers of this paper made an inventory of the studies on the use of thyroid hormone in the treatment of depression. Fifteen clinical trials (353 patients), published between 1969 and 1987. were found, that can be described, as to their design, in two seperate groups:

One group (7 studies) administers thyroid hormone simultaneously with a tricyclic antidepressant to reach a faster effect of the antidepressant. The other group (8 studies) adds thyroid hormone to a tricyclic antidepressant in patients who fail to respond to this treatment, with the aim to convert therapeutic failure to success. After studying the literature we think we are able to conclude that it can be usefull to combine the antidepressant with thyroid hormone in view of the fact that, in a number of depressed patients, it shortens the duration of the illness. The augmentation of tricyclics by thyroid hormone needs further study.

The present study aimed to investigate the possible changes in anthropometric and biochemical parameters in low-income women living in the outskirts of Maceió (northeast Brazil), and to explore the possible role of dietary intake and physical activity in these changes. A prospective longitudinal study was conducted in a cohort of mothers of malnourished children who attended the Center for Nutritional Recovery and Education, an outreach programme of the Federal University of Alagoas. Socio-economic, anthropometric, biochemical and dietary intake data were assessed at baseline and after a follow-up period of 4 years. Energy expenditure (using doubly labelled water) and physical activity (using triaxial accelerometers) were assessed only in a subgroup of women after 4 years. A total of eighty-five women were assessed. Participants showed an altered biochemical profile, increased systolic blood pressure, decreased thyroid hormone levels, and body-weight gain. However, dietary intakes of the participants did not include large quantities of highly processed and high-glycaemic index foods. The energy intake of the participants did not differ from their total energy expenditure (7990·3 (7173·7–8806·8) v. 8798·1 (8169·0–9432·4) kJ, respectively; P= 0·084). Multivariate analyses showed a significant effect of time spent watching television (β = 0·639 (0·003 to 1·275); P= 0·048) and dietary diversity score (β = − 1·039 ( − 2·010 to − 0·067); P= 0·036) on weight gain. The present study indicates that poor women, who are mothers of malnourished children and have a reasonably balanced dietary intake, exhibit weight gain and are at risk of developing chronic diseases.

The reactivation of dormant alpha-human herpesvirus (αHHV) has been attributed to various causes often referred to as stressors. However, no clinical study investigating the relationship between stressors and reactivation exists in humans at this time. Herpes simplex virus type-1 (HSV-1), an important αHHV, was shown to have its gene expression and replication regulated by thyroid hormone (TH) using molecular biology approaches. Varicella zoster virus (VZV) is categorized in αHHV superfamily and shares similar homology with HSV-1. We hypothesize that a history of TH imbalance may be associated with the incidence of shingles (VZV reactivation). This current pilot study, based on a hospital medical claims database, was conducted as a retrospective case-controlled investigation to determine if a putative link between TH imbalance and incidence of shingles is present. An odds ratio of 2·95 with a χ2 value of 51·74 was calculated for the total population diagnosed with TH disruption and shingles. Further analyses indicated that African American males exhibited a much higher chance of simultaneous diagnoses. These results show that a TH imbalance history may affect VZV reactivation at different incidence rates in different races and age groups.

Individuals with congenital hypothyroidism (CH), even those diagnosed and treated early, experience selective cognitive deficits, the most striking of which involves the visuocognitive domain. However, the range and nature of their visuocognitive disturbances is not fully understood. We assessed a range of higher-order visuocognitive abilities in 19 children and adolescents with CH and 19 age- and sex-matched typically developing peers (TD) using a battery of neuropsychological tests and a novel self-report measure of sense of direction. CH scored lower than TD on direct tests of visuocognitive function (judging line orientation, parts-to-whole localization, copying three-dimensional block towers, discriminating designs, and matching unfamiliar faces in ¾ profile-view) as well as on self-reported problems in spatial ability. Visuocognitive problems were not global as CH and TD did not differ at copying two-dimensional block designs, mentally rotating and matching abstract shapes, or at matching unfamiliar front-view faces, design features, or designs that engaged either figure-ground segregation, visual constancy, or closure. Early and concurrent thyroid stimulating hormone (TSH) levels were associated with visuocognitive ability, although attention and working memory were not. Individuals with CH exhibit selective visuocognitive weaknesses, some of which are related to early and concurrent TSH levels. (JINS, 2013, 19, 1–9)

This study investigated the relationships of thyroid hormones, serum energy metabolites, reproductive parameters, milk yield and body condition score with the different patterns of postpartum luteal activity in the postpartum period. A total of 75 multiparous healthy (free of detectable reproductive disorders) Holstein dairy cows (mean peak milk yield = 56.5 ± 7.0 kg/day) were used in this study. Transrectal ultrasound scanning and blood sample collection were performed twice weekly. Serum concentrations of progesterone (P4) were measured twice weekly and beta-hydroxybutyrate (BHBA), non-esterified fatty acids, thyroxine (T4), 3,30,5-tri-iodothyronine (T3), free thyroxine (fT4) and free 3,30,5-tri-iodothyronine (fT3) were measured every 2 weeks from the 1st to the 8th week postpartum. On the basis of the serum P4 profile of the cows, 25 (33.4%) had normal luteal activity (NLA), whereas 30 (40%), 10 (13.3%), 6 (8%) and 4 (5.3%) had prolonged luteal phase (PLP), delayed first ovulation (DOV), anovulation (AOV) and short luteal phase, respectively. Serum T4 concentrations in PLP cows were higher than that in NLA cows at the 3rd week postpartum and did not change during the period of study, whereas in the NLA cows the concentrations increased (P < 0.05). Further, the least square (LS) mean of serum fT4 concentrations in the DOV and AOV cows were significantly lower than in the NLA cows during the study period (P < 0.05). In addition, the AOV cows had higher LS mean serum BHBA and T4 concentrations than the NLA cows in early weeks postpartum (P < 0.05). In conclusion, the serum thyroid hormones’ profile differs in high-producing dairy cows showing PLP, AOV and DOV in comparison with the postpartum NLA cows.

Congenital hypothyroidism is a pediatric endocrine disorder caused by insufficient endogenous thyroid hormone production. Children with congenital hypothyroidism have difficulties with episodic memory and abnormalities in hippocampal structure, suggesting deficient hippocampal functioning. To assess hippocampal activation in adolescents with congenital hypothyroidism (N = 14; age range, 11.5–14.7 years) compared with controls (N = 15; age range, 11.2–15.5 years), a functional magnetic resonance imaging visuospatial memory task was used. In this task, participants had to decide if object pairings were novel or were previously studied or if object pairs were in the same location as they were at study or had switched locations. Despite no group differences in task performance, adolescents with congenital hypothyroidism showed both increased magnitude of hippocampal activation relative to controls and bilateral hippocampal activation when only the left was observed in controls. Furthermore, the increased activation in the congenital hypothyroidism group was correlated with the severity of the hypothyroidism experienced early in life. These results suggest that perinatal deprivation of thyroid hormone has longstanding effects on hippocampal function and may account for memory problems experienced by adolescents with congenital hypothyroidism. (JINS, 2012, 18, 49–56)

We describe the course of a toddler who ingested a massive amount of levothyroxine and review treatment options for such overdoses. A 2½-year-old boy presented shortly after an ingestion of up to 7.6 mg of levothyroxine (potentially as much as 700 µg/kg). He was initially asymptomatic, treated with oral charcoal 1 g/kg, and discharged home from the emergency department after a few hours. He returned approximately 24 hours later with a temperature of 38.5°C, heart rate of 163 beats per minute, respiratory rate of 30 breaths per minute, and blood pressure of 136/70 mm Hg. He had a slightly decreased appetite and no signs or symptoms of infection. He was admitted to hospital and treated with oral acetaminophen. The initial free thyroxine (T4) was > 100 pmol/L and free triiodothyronine (T3) was 35.3 pmol/L. The patient had desquamation of the palms and soles, hair loss, and irritability during the month following the ingestion. Resolution of the elevated free T4 occurred by 12 days post-ingestion and normalization of the thyroid-stimulating hormone by 7 weeks post-ingestion. There were no longterm sequelae. Levothyroxine overdose can result in significant complications, including seizures and arrhythmias, both of which should be monitored for. However, as our case illustrates, massive ingestion of levothyroxine in children typically follows a benign course.

Developmental plasticity is the property of a given genotype to produce different phenotypes in response to the environmental conditions experienced during development. Chordates have two basic modes of development, direct and indirect. Direct development (mode of humans) was derived evolutionarily from indirect development (mode of many amphibians), the major difference being the presence of a larval stage with indirect development; larvae undergo metamorphosis to the juvenile adult. In amphibians, environmental conditions experienced during the larval stage can lead to extreme plasticity in behaviour, morphology and the timing of metamorphosis and can cause variation in adult phenotypic expression (carry-over effects, or developmental programming). Hormones of the neuroendocrine stress axis play pivotal roles in mediating environmental effects on animal development. Stress hormones, produced in response to a deteriorating larval habitat, accelerate amphibian metamorphosis; in mammals, stress hormones hasten the onset of parturition and play an important role in pre-term birth caused by intra-uterine stress. While stress hormones can promote survival in a deteriorating larval or intra-uterine habitat, costs may be incurred, such as reduced growth and size at metamorphosis or birth. Furthermore, exposure to elevated stress hormones during the tadpole or foetal stage can cause permanent neurological changes, leading to altered physiology and behaviour later in life. The actions of stress hormones in animal development are evolutionarily conserved, and therefore amphibians can serve as important model organisms for research on the mechanisms of developmental plasticity.

The present study was aimed to investigate the mechanism underlying the influence of maternal low-protein (LP) diet on offspring growth in the chicken. One hundred and twenty Chinese inbred Langshan breeder hens were allocated randomly into two groups fed diets containing low (10 %, LP) or normal (15 %) crude protein levels. Low dietary protein did not affect the body weight of hens, but significantly decreased the laying rate and egg weight. The yolk leptin content was significantly lower in eggs laid by LP hens, while no differences were detected for yolk contents of corticosterone, tri-iodothyronine (T3) or thyroxine. Despite significantly lower hatch weight, the LP offspring demonstrated obviously higher serum T3 concentration, which is in accordance with the faster post-hatch growth rate achieving significantly heavier body weight and pectoralis major muscle weight 4 weeks post-hatching. Expression of 20-hydroxysteroid dehydrogenase (20-HSD) mRNA in the yolk-sac membrane was significantly down-regulated at embryonic day 14, whereas that of transthyretin and leptin receptor (LepR) was not altered. Moreover, hypothalamic expression of 20-HSD, glucocorticoid receptors, thyrotropin-releasing hormone and LepR mRNA was significantly up-regulated in the LP group compared with their control counterparts. In the pectoralis major muscle, significantly higher expression of insulin-like growth factor (IGF)-I and IGF-I receptor mRNA was observed in LP embryos. The present study provides evidence that maternal LP diet programmes post-hatch growth of the offspring. The associated alterations in yolk leptin deposition as well as in yolk-sac membrane, fetal hypothalamus and muscle gene expression may be involved in mediating such programming effect in the chicken.

We have investigated the spatial distribution of the α and β isoforms of myosin heavy chain in the force-producing ventricular myocardium, the ventricular conduction system and the atrioventricular junctional region of five neonatal human hearts–three born prior to and two at term. The results can be summarized as follows: 1) the force-producing myocardium: in each heart, the β isoform was found to be the predominating isoform, β-negative cells never being observed. Considerable amounts of the α isoform were observed only in those hearts that were obtained from patients dying within the first two weeks of postnatal life. This transient expression is probably correlated with the postnatal increase in levels of circulating thyroid hormone. 2) the ventricular conduction system: in addition to the expression of the β isoform, a strong expression of the α isoform was detected in all the components of the ventricular conduction system in the two full-term hearts. In the preterm hearts, however, this strong expression was mainly restricted to the atrioventricular node and the penetrating atrioventricular bundle. The level of expression of the α isoform in the conduction system of the neonatal hearts, therefore, might reflect the state of maturity of this system at the time of birth. 3) the atrioventricular junctional region: in each heart examined, structures were detected that resembled immunohistochemically and morphologically the atrioventricular node. Although the expression of the isoforms of myosin heavy chain in the conduction system, and in these comparable structures, cannot, as yet, be interpreted with regard to function, these resemblances, coupled with the same developmental background for these structures (they all develop from the so-called “primary ring”) suggest functional affinities during this stage of cardiac development.

An inadequate supply of iodine during gestation results in damage to the foetal brain that is irreversible by mid-gestation unless timely interventions can correct the accompanying maternal hypothyroxinemia. Even mild to moderate maternal hypothyroxinemia may result in suboptimal neurodevelopment. This review mainly focuses on iodine and thyroid hormone economy up to mid-gestation, a period during which the mother is the only source for the developing brain of the foetus. The cerebral cortex of the foetus depends on maternal thyroxine (T4) for the production of the 3′,3,5-tri-iodothyronine (T3) for nuclear receptor-binding and biological effectiveness.

Maternal hypothyroxinemia early in pregnancy is potentially damaging for foetal brain development. Direct evidence has been obtained from experiments on animals: even a relatively mild and transient hypothyroxinemia during corticogenesis, which takes place mostly before mid-gestation in humans, affects the migration of radial neurons, which settle permanently in heterotopic locations within the cortex and hippocampus. Behavioural defects have also been detected.

The conceptus imposes important early changes on maternal thyroid hormone economy that practically doubles the amount of T4 secreted something that requires a concordant increase in the availability of iodine, from 150 to 250–300 μg I day− 1. Women who are unable to increase their production of T4 early in pregnancy constitute a population at risk for having children with neurological disabilities. As a mild to moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia, the birth of many children with learning disabilities may be prevented by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible, in order to ensure that their requirements for iodine are met.

Objective: Thyroid hormone has important effects on cardiovascular performance. This study was performed to evaluate the changes in levels of triiodothyronine following the first stage of reconstruction for hypoplastic left heart syndrome. Methods: We enrolled 14 newborns with hypoplastic left heart syndrome scheduled for first stage reconstruction. Blood samples were obtained pre-, intra-, and post-operatively. Levels of free and total triiodothyronine were determined by radioimmunoassay. Statistical comparison was performed using Wilcoxon's signed rank test. Results: The levels of free triiodothyronine decreased from a baseline of 355 ± 31 pg/dl to 205 ± 21 pg/dl upon the institution of bypass, and declined to a level of 135 ± 9 pg/dl at 24 hours postoperatively. Similarly, levels of total triiodothyronine decreased from 101 ± 15 ng/dl to 65 ± 4 ng/dl upon the institution of bypass, and continued to decline during the first 24 hours postoperatively. Levels of free and total triiodothyronine had returned to baseline by the fifth postoperative day. Conclusions: The data demonstrate significant decreases in levels of free and total triiodothyronine during the early postoperative period. These changes in levels of thyroid hormone may have adverse effects on cardiac function during this phase of recovery.

The abundance and spatial distribution of retinal cone photoreceptors change during thyroid hormone (TH)-induced and natural development of rainbow trout (Oncorhynchus mykiss). These changes are thought to allow the fish to adapt to different photic environments throughout its life history. To date, the ontogeny of rainbow trout cone photoreceptors has been examined using physiological and morphological approaches. In this study, we extended these observations by measuring opsin gene expression in retinal quadrants during natural and TH-induced development. Gene expression during natural development was investigated in retinae from fish at both parr and smolt stages. The role of TH in modulating opsin gene expression was determined in TH-treated parr and control fish sampled after two, nine, and 22 days of treatment. Total RNA was isolated from each retinal quadrant and steady-state opsin mRNA levels were measured using reverse transcriptase real-time quantitative polymerase chain reaction (QPCR) analysis. Expression of ultraviolet-sensitive opsin (SWS1), rod opsin (RH1), middle wavelength-sensitive opsin (RH2), and long wavelength-sensitive opsin (LWS) transcripts vary spatially in the parr retina. Smolts, compared to parr, had downregulated SWS1 expression in all quadrants, lower LWS expression dorsally, higher RH1 expression nasally, and higher RH2 expression dorsally. In TH-treated parr, SWS1 opsin expression was downregulated in the nasal quadrants by two days. SWS1 displayed the greatest degree of downregulation in all quadrants after nine days of treatment, with an increase in short wavelength-sensitive (SWS2) and RH2 opsin mRNA expression in the temporal quadrants. This study reveals that opsin genes display spatially significant differences within rainbow trout retina in their level of mRNA expression, and that regulation of opsin expression is a dynamic process that is influenced by TH. This is particularly evident for SWS1 gene expression in parr following TH-induced and natural development.

Recent studies suggest that children with different etiologies of attention disorder also differ as to the types of errors they make on attention tasks. Because these errors are reflective of the core deficits underlying their attention problems, we sought to compare error patterns in children with different attention disorders. Studied were 144 children aged 7–12 years, 43 with attention deficit hyperactivity disorder (ADHD), 35 with congenital hypothyroidism (CH), and 68 controls. Two variations of the continuous performance task (CPT) that differed in demands on inhibitory control and memory were used. One variation, the CPT:A-not-X task, required subjects to observe a continuous stream of letters shown at different rates on the computer screen and respond to all stimuli except “X”. The other variation, the CPT:AX task, required them to respond whenever a specified combination of letter such as “A” followed by “X” appeared on the screen. On the CPT:A-not-X task, children with ADHD differed from controls in commission errors, signifying difficulty with inhibitory control, whereas children with CH differed in perceptual sensitivity or signal detection. Although the CH and ADHD groups both performed more poorly than controls on the CPT:AX task, children with CH made more errors to the first stimulus item, suggesting a problem holding information in memory, whereas children with ADHD made more errors to the second item, suggesting impulsivity. These results therefore signify the utility of these tasks in identifying the different mechanisms underlying the specific attention deficits of different groups of children.

Even though early treatment of congenital hypothyroidism (CH) with newborn screening prevents the mental retardation previously seen in cretinism, affected children still exhibit subtle persisting neurocognitive deficits. One of their commonest problems is poor attention, which reflects both early disease severity and later (high) circulating thyroid hormone levels. While attention is currently regarded as multicomponential in nature, with different processing components supported by different brain regions, the specific components of attention affected by CH have not been identified. In light of animal evidence showing that neonatal thyroid hormone deficiencies impede the neurodevelopment of structures important for selective aspects of attention, we proposed a multicomponential approach to study attention in children with CH. This was accomplished via retrospective analysis of existing data on adolescents with CH whose attention was previously evaluated using multiple tests. Results showed significantly poorer overall attention in CH than controls with differences occurring mainly on focus and inhibit indices. However, performance on various indices was associated with different disease parameters. Poor encode and focus were correlated with more severe hypothyroidism and a longer period of thyroid hormone insufficiency and poor select and shift with higher thyroid hormone levels at testing. These results signify that thyroid hormone is important for the development and later regulation of brain structures supporting distinct aspects of attention. (JINS, 2001, 7, 734–744.)