Melatonin: Hashimoto’s friend or foe?
Melatonin, or the “darkness hormone”, plays a major role in our well being. It helps us to achieve balanced sleep/wake cycles and has been marketed as a medicine that can fix many additional problems, such as severe headaches. People have even claimed it helps resolve some, if not many, modern diseases, such as autoimmune conditions.
But a lot of things remain unclear about melatonin’s connection to and impact on Hashimoto’s. Scientific research on Hashimoto’s has been limited. However, melatonin has a direct impact on thyroid function, as well as on several autoimmune diseases. This effects as reported in scientific literature might have a conflicting impact on the overall well being of Hashimoto’s patients. Melatonin can also be taken as a medication. People diagnosed with hypothyroid disorder are in general advised to check their thyroid levels if they start regularly using melatonin.
Melatonin helps the body to maintain its circadian rhythm, an internal 24-hour “clock”. It is produced by the pineal gland, a tiny gland located near the center of the brain.
Melatonin is normally produced at night, if we live under normal light/dark conditions. The main function of melatonin is to transfer information about day and night cycles to the body’s cells and organs. This helps with timing functions of the cells, such as regulating our core body temperature, blood sugar regulation, hormone production and sleep/wake cycles. Our immune system depends on the melatonin’s signals, too.
What is the difference in function between one’s own and medical melatonin? Research has not conducted enough studies, and has focused only on some aspects of it (dose, but not the duration).
Disruptions in melatonin production can be a sign of high stress or an illness, and the other way around: an illness can disturb melatonin production. All of this can lead to a more severe symptoms, or impair success of the treatment or disease management [1-3].
Impact of melatonin on the thyroid gland
Science has focused mostly on one specific function of melatonin in regard to the thyroid gland function; melatonin is, like vitamin C, an antioxidant. Antioxidants remove potentially damaging reactive oxygen species (ROS) from our cells and organs.
ROS are very important for everyday cell functioning; they trigger so called oxidative reactions in our cells, and they occur in all tissues and organs. When in excess, ROS causes oxidative damage to molecules in our cells, making them dysfunctional.
Some research showed that specialized cells, called C-cells, that are found in thyroid gland are capable of production of melatonin, and that this is under thyroid stimulating hormone (TSH) control. It seems that melatonin and TSH balance themselves out.
Melatonin blocks thyroid cell proliferation and thyroid hormone synthesis and if used as a medicine for prolonged periods of time one should check thyroid hormone levels [4-6].
Impact of melatonin on the immune system and its role in autoimmunity
Melatonin plays a very important role in the immune system function. It interacts with many, if not all, the cells of the immune system, and can activate some and suppress other functions.
Melatonin suppresses molecules that promote inflammation. Importantly, melatonin modulates the immune system in a dose-dependant way. The differences in it’s function come from the dose when it is taken as a medication, which can be 10 or 100 times higher than the levels produced by healthy body.
Melatonin regulates the immune system in our gut and protects against inflammation, and possibly reduces the immune reaction in the body. This was so far shown in ulcerative colitis (UC), a chronic inflammatory disease of the colon .
Melatonin production is deregulated in multiple sclerosis (MS), and treatment with melatonin blocks onset of the flare-ups. The role of melatonin in systemic lupus erythematosus (SLE) is more complicated and it seems to be gender dependant. Melatonin has a disease-promoting effect in rheumatoid arthritis (RA), and is also gender dependant. Melatonin can be beneficial in type 1 diabetes, as it stimulates insulin production. Lastly, melatonin helps in irritable bowel syndrome (IBS), reducing the flare-ups in intensity and duration .
Melatonin therapy in autoimmune diseases has been studied in many animal models and in a few human clinical trials. For all the conditions except rheumatoid arthritis (RA), melatonin has been shown to have the potential to reduce the severity of symptoms.
These findings indicate that melatonin treatment could be an important strategy for the Hashimoto’s condition, too. However, the research on this topic is lacking, especially in light of melatonin’s potential dual role in thyroid function and in immune response.
In the case of opposing effects, research should dig deeper and understand what is more beneficial: blocking the autoimmune part of Hashimoto’s while tampering with the thyroid hormone production, or the other way around? And how can the optimal effect be acchieved with the proper dosing of melatonin.
More research is needed to better understand the delicate balance between melatonin and the thyroid gland function. Hopefully in the future there will be more research geared towards understanding this connection.
Claustrat B, et al Melatonin: Physiological effects in humans. Neurochirurgie, 2015
Skene DJ, et al. Human circadian rhythms: physiological and therapeutic relevance of light and melatonin. Ann Clin Biochem, 2006
NIH. Circadian Rhythms Fact Sheet, 2010
D’Angelo G, et al. Atopy and autoimmune thyroid diseases: melatonin can be useful, 2016
Garcia-Marin R, et al. Melatonin in the thyroid gland: regulation by thyroid-stimulating hormone and role in thyroglobulin gene expression, 2015
Karbownik M, et al. The role of oxidative stress in physiological and pathological processes in the thyroid gland; possible involvement in pineal-thyroid interactions, 2003
Chojnacki C, et al. Evaluation of melatonin effectiveness in the adjuvant treatment of ulcerative colitis, 2011
Lin GJ, et al. Modulation by melatonin of the pathogenesis of inflammatory autoimmune diseases, 2013