Hashimoto’s thyroiditis is one form of hypothyroidism. It occurs when one’s immune system assaults the thyroid gland. The autoimmune destruction of the thyroid gland results in the failure to produce adequate thyroxine (also known as T4 or thyroid hormone).
The body responds by increasing thyroid-stimulating hormone (which does exactly what its name suggests). But escalating thyroid-stimulating hormone is unable to normalize thyroid in patients with Hashimoto’s thyroiditis because the thyroid gland is itself damaged.
Autoimmunity and Neuroinflammation
Automimmune diseases have been a hot topic in psychiatry and neurology in the last decade.
It was recently discovered that narcolepsy (the irresistible propensity to sleep at inappropriate times) is actually an autoimmune disease. An overzealous immune system attacks orexinergic neurons in the brain. These neurons are important for the maintenance of wakefulness, and so their destruction increases sleep pressure.
Neuroinflammation refers to inflammation of nervous tissue. For a long time, the brain was thought to be immunologically privileged, like the eyes. This is mostly true because peripheral immune cells are blocked by the blood-brain barrier. But a compromised blood-brain barrier can let peripheral immune cells into the brain, unhindered.
Neuroinflammation is increasingly linked to schizophrenia, depression, and dementia. Even obesity may have a neuroinflammatory component. Excess consumption of sugar and fat promotes an inflammatory milieu, particularly in adipose tissue but also possibly the brain. Obesity-related neuroinflammation may then impair hormones that regulate appetite like leptin and ghrelin, leading to a vicious cycle.
The textbook example of a neuroinflammatory disease is multiple sclerosis, where the myelin sheath surrounding axons is damaged by inappropriate immune activation in the brain.
Hashimoto’s Thyroiditis and Autoimmunity
It’s well known that hypothyroidism negatively impacts mood, cognitive function, and general well-being. Hashimoto’s thyroiditis is no different, and produces this same pattern of symptoms.
But Hashimoto’s thyroiditis is indicative of a deeper underlying pathology: automimmunity and immunological hyperactivity.
The immune system is programmatically calibrated because of the inherent trade offs. If the the immune system is too weak, an individual will be susceptible to infection. But an overzealous immune system can damage tissues and contribute to autoimmune diseases like Hashimoto’s thyroiditis.
The biochemical markers of the disease are thyroid peroxidase, in addition to thyroglobulin antibodies. Twin concordance studies have revealed that Hashimoto’s has a strong genetic component. Genes encoding leukocyte antigen, cytotoxic T lymphocyte antigen-4, thyroglobulin and the vitamin D receptor are specifically implicated.
The most important risk factors for the development of Hashimoto’s are female gender and pregnancy with postpartum depression. Excess iodine intake, infections, exposure to chemicals and certain drugs are all significant risk factors.
Autoimmune thyroiditis encephalopathy is an example of a consequence of how autoimmunity can unfold to harm the brain. It should be better recognized that patients with Hashimoto’s are at-risk for the development of other diseases with an immunological aspect.
Zaletel K, Gaberšček S. Hashimoto’s Thyroiditis: From Genes to the Disease. Curr Genomics. 2011;12(8):576-88.
Li Y, Nishihara E, Kakudo K. Hashimoto’s thyroiditis: old concepts and new insights. Curr Opin Rheumatol. 2011;23(1):102-7.
Available at: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025658/. Accessed January 17, 2016.