Article and Reference Links:
“Sernova Announces Collaboration to Advance Therapeutic Cell Pouch Technologies for the Treatment of Hypothyroidism” Sernova Corp. https://mailchi.mp/2d7718709ef6/sernova-press release?fbclid=IwAR3L577HlDX0KJCCIH2naQRdG8497tTFy3kDEL0Gs5wq9uG16_Io4aQ_Xpw. Published 30 Apr. 2019.
Davies, T., (2013). “Is Thyroid Transplantation on the Distant Horizon?” US National Library of Medicine. National Institutes of Health. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3570830/
“PAX8 gene- paired box 8” US National Library of Medicine. Genetics Home Reference. https://ghr.nlm.nih.gov/gene/NKX2-1. Published 30 Apr. 2019.
“NKX2-1 gene-NK2 homeobox 1” US National Library of Medicine. Genetics Home Reference. https://ghr.nlm.nih.gov/gene/NKX2-1. Published 30 Apr. 2019.
Hypothyroidism is a medical condition associated with the endocrine system in which results in the underproduction of thyroid hormone. Thyroid hormone is essential to regulate a person’s metabolism (i.e. a person’s metabolism helps to regulate energy and stamina, weight, heart rate, immune health, bone health, and cognitive and neural functioning), and to also keep someone alive. People generally develop hypothyroidism from several causes such as autoimmune disease (i.e. Hashimoto’s thyroiditis, an autoimmune condition in which the antibodies affect thyroid tissue which results in too little thyroid hormone), or a response to treatment associated with Graves’ disease (an autoimmune condition in which the antibodies affect thyroid tissue and it results in too much thyroid hormone), or hyperthyroidism, such as Radioactive Iodine Therapy (RAI) which helps to shrink and destroy the thyroid gland from producing too much thyroid hormone which eventually results in someone developing hypothyroidism. Individuals who have had their thyroids surgically removed (generally a total thyroidectomy) due to Graves’ disease, hyperthyroidism, or thyroid cancer, will no longer be able to naturally produce thyroid hormone which also results in the development of hypothyroidism. Symptoms that people generally experience associated with hypothyroidism are, but not limited to fatigue; weight gain; cold intolerance; constipation; dry skin; hyperlipidemia (elevated lipids which translates to elevated blood cholesterol); bradycardia (decreased heart rate); depression; and memory problems. Treatment for hypothyroidism is essential as untreated hypothyroidism can result in cardiovascular issues (heart problems); mental health issues; damage to nerves associated with brain and spinal cord (aka peripheral neuropathy); and, if not treated long term, it can result in myxedema coma which can be life-threatening.
Generally, the recommended treatment for hypothyroidism is Levothyroxine which is an oral medication that is used to regulate normal thyroid functioning, and to alleviate, or even, eliminate the symptoms associated with hypothyroidism. People who take Levothyroxine daily will need lifelong and, “intermittent blood testing and adjustment of medication dosing” (Sernova, 2019). Although people that take Levothyroxine to treat hypothyroidism can produce effective results, “patients often suffer from side effects including weight gain, depression, headaches, and cardiovascular disease, with resultant negative impact on quality of life, and costs to the healthcare system” (Sernova, 2019). Hypothyroidism cannot be cured, hence, as a result of this, some people with hypothyroidism can experience challenges associated with independent living such as employment where someone may not be able to work, or work at most, part-time given the nature and severity that hypothyroidism can bring to individuals, and as a result, individuals try to collect disability while trying to pay health expenses for ongoing labs and follow-ups with primary care providers and endocrinologists. However, Sernova Corp, a regenerative medicine company stated that they, “announced today a collaboration with the University of British Columbia’s, Dr. Sam Wiseman for development of a Cell-Therapy based program for the treatment of hypothyroidism” (Sernova, 2019). The question I pose for this cell-therapy based program is the following: What implications could cell based therapy have in attempting to treat individuals with hypothyroidism?
Reviewing and analyzing an article from the National Institutes of Health, a clinical trial was conducted in which, “thyroid cells thrived when cultured in a gelatinous protein mixture secreted by Engelbreth-Holm-Swarm (EHS) mouse sarcoma cells” (Davies). In other words, thyroid cells were able to regulate from the cancer cells in soft tissue associated with the mouse. Davies’ theory was to remove the cancer cells from the soft tissue of the mouse, and then excrete the cancer cells into separate thyroid cells. What this combination would create is reproductive cells that promote proteins to produce thyroid hormone. However, according to the study, “mature thyroid cells have limited growth capacity, and such structures were unable to expand into a useful organ” (Davies). As a result, this affected thyroid stimulating hormone (TSH) levels which resulted in uncertainty regarding the production and regulation of thyroid hormone, and determining the adequate amount needed in order to balance one’s metabolism. In another study, however, stated that, “In 2005, Altmann et al. (14) showed that a liver cell had the potential to be turned into a thyroid cell by transfecting Pax8 and NKX2-1 into Morris rat hepatoma cells as evidenced by thyroglobulin and thyroid peroxidase promoter/enhancer activation in their culture system” (Davies). Altmann is stating that by taking a gene that transcribes into a protein after birth to activate the development of the thyroid gland (the Pax8 gene, also known as the paired box 8 gene), and by taking another gene that also transcribes into a protein to activate thyroid gland development (the NKX2-1 gene, also known as the NK2 homeobox 1 gene), you take the genetic material associated with these genes and proteins, and then transfer the genetic material into the clotted blood cells of a Morris rat which can help to activate and produce thyroid hormone. Altmann’s theory is that the proteins associated with the Pax8 and NkKX2-1 genes, which are then transferred into the clotted blood cells of a Morris rat, the proteins associated with the clotted blood cells of a Morris rat can be introduced into the liver cell which can help alter the transformation of a liver cell into a thyroid cell.
After thorough analysis of the scientific data to address the question about the possibility of cell based therapy as an alternate solution to the treatment of hypothyroidism, more research and data will need to be gathered to gain a further understanding into the anatomy and physiology; biology; and chemistry of gene regulation and its relationship with the thyroid hormone activation and regulation in connection with the thyroid gland. Although cellular therapy may be a possibility for those with congenital hypothyroidism or with thyroid cancer according to the study, unfortunately, “in patients with Hashimoto’s thyroiditis or patients with Graves’ disease after radioactive iodine or thyroidectomy, the immune system will no doubt also attack such transplanted cells unless the immune response has waned” (Davies). People with Graves’ disease or Hashimoto’s thyroiditis, even after with treatment with radioactive iodine therapy or thyroid surgery, would probably not be the best candidates for thyroid cell therapy unless there was a way to stop antibodies from affecting thyroid tissue in order to prevent a negative immunological response to the individual with Graves’ or Hashimoto’s. Thyroid cell therapy may benefit some people with hypothyroidism, but in my opinion, thyroid cell therapy, given the current scientific data, which in the future can change, would not likely help to treat everyone with hypothyroidism (especially those who have had a history of Graves’ disease or Hashimoto’s thyroiditis).
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