In this fifth and final article in our series of articles on natural treatment of psychological disorders we discuss the underlying mechanisms of developmental disorders, which include autism spectrum disorders (ASD), dyslexia, memory disorders, and othersThe information contained in this article is backed by research which is available upon request.  If you or a family member suffers from a developmental disorder, the issues within this article may begin to unfold the underlying causes, our primary focus at A Path to Wellness.  This article has been filtered for some complex terminology, but unavoidably gets a little deep at times, so please be patient and keep google handy!

            The specific mechanisms by which developmental disorders evolve pre- and post-natally range from high-level metabolic processes to low-level cellular processes.  These processes may affectcerebellar, vestibular, auditory, or optical processing.  Several studies have pursued the underlying causes of disorders of cerebellar function and related sensory learning deficits.  Studies explore the effects of hypo- and hyperthyroidism, endocrine disruptor effects on brain development, and the similarity of endocrine disruptor effects to the effects of thyroid hormone. 

            Thyroid hormone, particularly triiodothyronine (T3), may be under-appreciated in the medical community for its role in brain development.  Generally the realm of endocrinologists rather than neurologists or developmental specialists, thyroid hormone actually appears to be involved in many roles beyond standard metabolic functions.  Over 180 studies have pointed to deficiency of thyroid hormone pre- or post-natally as leading to dysfunctions, cellular changes, and molecular variations via regulation of gene transcription.  These actions are accomplished via binding of thyroid hormone, particularly T3, with thyroid hormone receptors that subsequently bind with thyroid hormone response element DNA sequences.  Thyroid hormone may also induce neurotrophin gene expression, thereby indirectly activating genes. 

            Thus, there are many aspects to the involvement of thyroid hormone on brain development, including several influences on the cerebellum.  Abnormal cerebellar development commonly may be induced by perinatal hypothyroidism (low thyroid function during pregnancy).  These abnormalities may be avoided or reversed to some extent if thyroid hormone is replaced in offspring quickly enough after birth.  One attempt to understand the molecular mechanisms involved in regulation of the development of the cerebellum used pregnant rats treated with propylthiouracil (PTU) to reduce thyroid function.  A significant functional decrease (expressed in protein levels) was observed at day 10, and full function was restored with treatment using thyroid hormone. 

            Since iodine is a major component of thyroid hormone, it is reasonable to consider the role of iodine deficiency in thyroid dysfunction.  This consideration then leads to the important relationship between thyroid dysfunction and developmental issues or the relationship between iodine deficiency and brain damage.  It is important to note that developmental issues, such as memory and learning disorders, may extend beyond clinical hypothyroidism to subclinical hypothyroidism, measured by the same parameters but at low normal functional levels rather than clinically low levels. 

            Additionally, thyroid dysfunction and endocrine disruptors may affect production of the important sex hormones progesterone and estrogen.  Abnormal development of the cerebellum may result from inappropriate sex hormone levels due to thyroid dysfunction.  Rapid action of these hormones may be induced by receptor activity at cell membranes, possibly modulating the activity of neurotransmitters.  In fact, mutations of receptors may occur due to the actions of prescription drugs or environmental toxins, including endocrine disruptors, as well as the actions of hypothalamic hormones thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH).  CRH and TRH are precursors to hormones adrenocorticotropic hormone (ACTH) and TSH that are released from the anterior pituitary to stimulate thyroid and adrenal activity in a concerted effort to balance our metabolisms.  This suggests that TSH and ACTH should beused to assess metabolic activity and the status of hormones pre- and post-natally.

            A rather interesting and widely-debated contributor that may affect thyroid-related developmental pathways is thimerosal (a preservative found in some vaccinations).  A study that examined the effect of ethylmercury (Et-Hg) from thimerosal on the developing brain examinedauditory, motor, thyroid, and cerebellar dysfunction.  The study hypothesized that perinatal exposure to thimerosal impaired development of the cerebellum, and central nervous system (CNS) as a whole, via oxidation.  Dysfunctions such as a delayed startle response and significant cerebellar oxidative stress were found.  A significant reduction in an enzyme involved in the conversion of T4 to T3 was an apparent mechanism, likely related to T3 deficiency in the cerebellum.  Thus, we have further confirmation of the effects of low T3 on the cerebellum, as well as the potential contribution of thimerosal (in vaccines) to developmental disorders.