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Magnesium deficiency and hypothyroidism

Trace elements, such as iodine and selenium, are closely related to autoimmune thyroiditis and thyroid function. Low serum magnesium is associated with several chronic diseases; however, its associations with autoimmune thyroiditis and thyroid function are unclear. The research investigated the relationships between low serum magnesium, autoimmune thyroiditis, and thyroid function in 1,257 Chinese participants.

Role of Magnesium

Magnesium is the fourth most abundant essential mineral in the human body after sodium, potassium, and calcium, and is a cofactor for more than 300 enzymes that regulate a variety of biochemical processes, such as DNA/RNA synthesis, protein synthesis, oxidative phosphorylation, and glycolysis. Magnesium is mainly absorbed through the diet, and high-magnesium foods include nuts, seeds, whole grains, and leafy greens.

Insufficient magnesium intake and low serum magnesium are associated with a variety of chronic diseases, including insulin resistance and type 2 diabetes mellitus, metabolic syndrome, hypertension, cardiovascular disease, stroke, migraine, attention deficit disorder, Alzheimer’s disease, and asthma.

Magnesium is closely related to the immune system; in vitro experiments have showed that intracellular free magnesium ions are an important second messenger in the immune activation of T lymphocytes and B lymphocytes, and magnesium channels and transport proteins play an important role in normal immune function. Moreover, magnesium is also associated with cellular oxidative stress and inflammatory reactions. The homeostasis of magnesium ions in mitochondria is important for cellular energy metabolism and for the ability to respond to oxidative stress. Magnesium citrate supplementation can downregulate genes related to metabolic and inflammatory pathways.

Autoimmune thyroiditis is a common endocrine disorder that is caused by a variety of environmental factors and is based on genetic susceptibility. A range of trace elements are related to the pathogenesis of autoimmune thyroiditis, among which the most important is iodine, followed by iron, selenium, and others. There are few studies on the relationship between magnesium and thyroid disease. For example, a study on patients with Graves’ disease found that they exhibited a lower serum magnesium concentration than normal control participants, and that the serum magnesium concentration was negatively correlated with lymphocyte activation. An Austrian study found that low serum magnesium was associated with abnormal thyroid function, which was improved after supplemental magnesium therapy. To further clarify the relationship between serum magnesium levels and autoimmune thyroiditis, as well as thyroid function, we performed a cross-sectional study among the permanent residents of Tianjin.

Magnesium in the human body is mostly located in the cells and bone tissues; only 1% of total body magnesium is located in extracellular fluids, and only 0.3% of total body magnesium is present in serum1. However, the detection of intracellular magnesium ions is difficult, while the detection of serum magnesium ions is simple and convenient. Therefore, serum magnesium is still used to assess individuals’ magnesium nutritional statuses. Hypermagnesaemia and magnesium poisoning are rare in clinical practice, and only occur in patients with severe renal failure. The main clinical manifestation of magnesium nutrition imbalance is low serum magnesium, the definition of which varies among different populations and methods of detection.

The study found that serum magnesium levels ≤0.55 mmol/L were related to the risk of TGAb positivity and prevalence of HT. There are at least two explanations for this: first, severely low serum magnesium can increase TGAb via the abnormal activation of immune cells and induction of an autoimmune response. A study on patients with Graves’ disease found that their serum magnesium concentrations were lower than in normal individuals, and that the serum magnesium concentration was inversely related to the activation levels of CD3+, CD4+, CD8+T, and CD19+B cells. It was speculated that low serum magnesium might lead to decreased immune tolerance and abnormal activation of immune cells. Second, given its function as a coenzyme, magnesium is involved in a variety of antioxidant metabolism pathways, such as glutathione synthesis; low serum magnesium could therefore reduce the antioxidant response capacity in cells and allow the accumulation of free radicals, resulting in oxidative stress and tissue damage. Epidemiological studies have shown that insufficient magnesium intake is associated with a variety of chronic inflammatory diseases and elevated serum C-reactive protein levels.

The different effects of severely low serum magnesium on the two autoantibodies examined in the study indicated that its effect on the thyroid autoantibody might primarily be caused by inflammation and oxidative stress, rather than by activating autoimmune responses. In other words, severely low serum magnesium is not the initiating factor of autoimmune thyroiditis, but might be an aggravating factor via inflammation.

This study found that non-severely low serum magnesium (0.551–0.85 mmol/L) is not associated with thyroid autoantibody levels or thyroid function. Another study on the relationship between low serum magnesium and metabolic syndrome with low-grade inflammation also found that inflammatory factors were elevated only when magnesium levels were severely low (<0.5 mmol/L). Animal studies found that the inflammatory response caused by mild-to-moderate magnesium deficiency could be compensated for, or aggravated, by other factors. Hegsted et al. found that reducing the magnesium intake in rats to 50% of their required levels did not inhibit their growth; however, placing these rats in a cold environment (13 degrees) reduced their growth rate significantly compared with control rats with normal magnesium intake. This indicated that the effects of mild versus moderate magnesium deficiency in different individuals might be more complex; therefore, studies of different populations may well produce different results. Additionally, results can differ based on different definitions of low serum magnesium levels and varying cut-off points.


Severely low serum magnesium is associated with increased risks of positive anti-thyroglobulin antibody and hypothyroidism: A cross-sectional study, by Kunling Wang, Hongyan Wei, Wanqi Zhang, Zhen Li, Li Ding, Tong Yu, Long Tan, Yaxin Liu, Tong Liu, Hao Wang, Yuxin Fan, Peng Zhang, Zhongyan Shan, and Mei Zhu, Sci Rep. 2018; 8: 9904. Published online 2018 Jul 2. doi: 10.1038/s41598-018-28362-5

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