Lithium is an essential nutrient and important in brain health. It has been shown to decrease stress reactivity, improve GABA function, and help with bipolar disorder and other forms of depression.
Unfortunately, pharmacological doses (300mg+) of lithium carbonate have been shown, in some people, to interfere with the production of another essential factor in mood and brain health: thyroid hormone. Lithium use is frequently associated with goiter and hypothyroidism. Nevertheless, in severe cases of bipolar disorder, the adverse effects on thyroid function have been seen as acceptable (with reservations) by mainstream medicine in light of the beneficial effects of lithium on mood and functioning. Thankfully, lithium does not appear to contribute to thyroid autoimmunity.
Goiter and hypothyroidism are exacerbated by iodine insufficiency or deficiency and, unfortunately, iodine levels in the general population here in the US have been declining over the last few decades due to inadequate intake of iodine-rich foods (like seaweed) and iodine-supplemented table salt.
To my knowledge, nutritional doses (5mg-30mg) of lithium orotate have not been studied in the literature for their effects on thyroid function. I suspect that the dramatically lower doses of lithium usually administered for nutritional supplementation (as compared to pharmacological dosing) are insufficient to cause appreciable decline in thyroid function, but this has yet to be studied specifically.
One major biochemical mechanism of benefit from lithium is the moderation of dopamine and other catecholamine “spikes” associated with mania and psychological stress. Lithium seems to help moderate catecholamine spikes in part through inhibition of tyrosine utilization to form dopamine, although the mechanism is not completely understood.
Tyrosine is not only used for catecholamine production, but is the primary precursor for thyroid hormones T3 and T4. The thyroid gland uses tyrosine to create thyroid hormone, and lithium has been shown to decrease circulating levels of tyrosine as well as inhibit thyroid tissue’s ability to utilize tyrosine. The connection between lithium administration and decreased thyroid hormone production (hypothyroidism) is quite possibly due to decreased availability of tyrosine for the synthesis of T3 and T4.
This begs the questions:
- Do nutritional doses of lithium suppress thyroid function?
- Would co-administration of tyrosine (and/or iodine) ameliorate the decrease in thyroid function caused by lithium administration?
I would love to see some studies done on this question. If you know of any studies or have other comments, please comment below.
Inhibitory effect of lithium on uptake and incorporation of tyrosine into protein in three thyroid preparations in vitro. – PubMed – NCBI.
Laakso, M. L., & Oja, S. S. (1979). Transport of tryptophan and tyrosine in rat brain slices in the presence of lithium. Neurochemical Research, 4(3), 411–423.
Marcus, S. R., Nadiger, H. A., Chandrakala, M. V., Rao, T. I., & Sadasivudu, B. (1986). Acute and short-term effects of lithium on glutamate metabolism in rat brain. Biochemical Pharmacology, 35(3), 365–369.
McFarlane, H. G., Steele, J., Vinion, K., Bongiovanni, R., Double, M., & Jaskiw, G. E. (2011). Acute lithium administration selectively lowers tyrosine levels in serum and brain. Brain Research, 1420, 29–36. http://doi.org/10.1016/j.brainres.2011.08.054
Kupka, R. W., Nolen, W. A., Post, R. M., McElroy, S. L., Altshuler, L. L., Denicoff, K. D., et al. (2002). High rate of autoimmune thyroiditis in bipolar disorder: lack of association with lithium exposure. Biological Psychiatry, 51(4), 305–311.