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There are a number of developmental disorders that are caused by thyroid dysfunction. Listed below are a number of scientific papers with quotes, indicating the range of effects that can occur.
Interactions of Persistent Environmental Organohalogens With The Thyroid Hormone System: Mechanisms And Possible Consequences For Animal And Human Health. Brouwer A., Morse D. C., Lans M. C., Schur A. G., Murk A. J., Klasson_Wehler E., Bergman A., Visser T. J. Toxicology and Industrial Health 14 (1/2) 1998, 59-84. Abstract Several classes of environmental contaminants have been claimed or suggested to possess endocrine-disrupting potency, which may result in reproductive problems and developmental disorders. In this paper the focus is on the multiple and interactive mechanisms of interference of persistent polyhalogenated aromatic hydrocarbons (PHAHs) and their metabolites with the thyroid hormone system. Evidence suggests that pure congeners or mixtures of PHAHs directly interfere with the thyroid gland; with thyroid hormone metabolising enzymes, such as uridine-diphosphate-glucuronyl transferases (UGTs), iodothyronine deiodinases (IDs), and sulfotransferases (SULTs) in liver and brain; and with the plasma transport system of thyroid hormones and experimental animals and their offspring. Changes in thyroid hormone levels in conjunction with high PHAH exposure was also observed in captive as well as free ranging wildlife species and in humans. Maternal exposure to PHAHs during pregnancy resulted in considerable fetal transfer of hydroxylated PHAHs, which are known to compete with thyroxine (T4) for plasma transthyretin (TTR) binding sites, and thus may be transported to the fetus with those carrier proteins that normally mediate the delivery of T4 to the fetus. Concomitant changes in thyroid hormone concentrations in plasma and in brain tissue were observed in fetal and neonatal stages of development, when sufficient thyroid hormone levels are esential for normal brain development. Alterations in structural and functional neurochemical parameters, such as glial fibrillary acidic protein (GFAP), synaptophysin, calcineurin, and serotonergic neurotransmitters, were observed in the same offspring up to postnatal day 90. In addition, some changes in locomotor and cognitive indices of behaviour were observed in rat offspring, following i utero and lactational exposure to PHAHs. Alterations in thyroid hormone levels and subtle changes in neurobehavioural performance were also observed in human infants exposed in utero and through lactation to relatively high levels of PHAHs. Overall these studies indicate that persistent PHAHs can disrupt the thyroid hormone system at a multitude of interation sites, which may have a profound impact on normal brain development in experimental animals, wildlife species, and human infants. Quotes Many classes of chemicals, both natural and of anthropogenic origin, have been claimed to possess endocrine-disrupting potential, in particular on the sex steroid systems. In addition, these classes of "endocrine disruptors" have been linked with abnormalities in sexual development, gonadal functions, and reproduction in wildlife and in humans. ...there also exists a wide body of evidence for interations of similar classes of chemicals with the thyroid hormone system. Thyroid hormones, as well as sex steroids, are very important in normal structural and functional development of sexual organs and the brain. ...Therefore it is important to include potential disruptions of the thyroid system in the evaluations of the possible impact of chemicals in our food and environment on health and normal development. Hypothyroidism and Brain Development Thyroid hormones are known to be very important for normal development. Disruption of the thyroid hormone system during pregnancy may have serious consequences for structural and functional aspects of normal development of the brain and sexual organs, among other things. Hypothyroidism is known to lead to disorders of neuronal process growth in the developing brain Another aspect of hypothyroidism may be an interference or disruption of neurotransmitter systems. Thyroid hormones are shown to be modulators of nonadrenergic, serotonergic, and dopaminergic receptor function. ...hypothyroidism is associated with emotional instability, which may actually be a consequence of changes in the serotonergic neurotransmitter system. Other behavioural and functional consequences of developmental hypothyroidism involve retarded development of cognitive and neuromotor funtions.
Resistance To Thyroid Hormone: Implications For Neurodevelopmental Research On The Effects Of Thyroid Hormone Disruptors. Hauser P., McMillin J. M., Bhatara V. S. Toxicology and Industrial Health 14 (1/2) 1998, 85-101. Abstract Thyroid hormones are essential for normal behavioural, intellectual, and neurological development. Congenital hypothyroidism, if not treated, can result in irreversible mental retardation, whereas thyroid diseases with more moderate impairment of thyroid function, such as resistance to thyroid hormone, cause less severe intellectual and behavioural abnormalities, including attention deficit hyperactivity disorder. There is increasing evidence the exposure to certain synthetic compounds, including dioxins and polychlorinated biphenyls (PCBs), during the perinatal period can also impair learning, memory, and attentional processes in offspring. Animal and human studies suggest that exposure to these environmental toxicants impair normal thyroid function. Although the precise mechanisms of action of the adverse effects these toxicants have on neurodevelopment have not yet been elucidated, it is possible that they are partially or predominantly mediated by the alterations in hormone binding to the thyroid hormone receptor. The convergence of studies that examine neurodevelopmental consequences of moderate impairment of thyroid function, such as is found in resistance to thyroid hormone, with those studies that demonstrate the adverse behavioural and cognitive effects.
The Importance Of Thyroid Hormone For Auditory Development In The Fetus And Neonate. Sohmer H., Freeman S. Audiology and Neuro-Otology 1 1996, 137-147. Abstract It seems that many auditory maturational events are regulated by thyroid hormone since elevation in thyroid hormone level always precedes the onset of hearing in the fetus-neonate; low thyroid activity in the developing human fetus or rat neonate leads to hearing loss; earlier, elevated thyroid levels in rat neonate lead to earlier onset of hearing. The hormone, bound to its receptors in the nucleus, acts as a transcription factor activating genes which lead to the synthesis of several proteins and enzymes involved in the structural and functional development of many tissues (e.g. brain, heart, kidney, skeletal muscle) including the ear. Several types of congenital hearing loss of unexplained etiology may be due to abnormalities in one or more stages of this gene cascade since several types of congenital hearing loss have been shown to involve defects in genes related to these events. Quotes There is accumulating evidence that an important factor in the programmed development of auditory function in the fetus in utero is the presence and level of thyroid hormone. A hearing loss may also be associated with a defect in the production of thyroid hormone. ...it has been suggested that this hormone functions as a biological timing mechanism for the normal sequence of brain maturation. It has also been shown that the rate of transcription ofthe myelin basic protein gene in rat brain is regulated by thyroid hormone. It is likely that thyroid hormone is also involved in the regulation of the structural development of the brain and the ear. Hearing Loss Related To Disorders In The Thyroid Hormone Cascade. The overall findings presented here show that just as thyroid hormone regulates and is responsible for several aspects of the structural and functional development of several tissues and organs including skeletal muscle, heart, kidney and brain, it is likely that the hormone is also a key factor in the regulation of development of the ear. |