Sciatica and thyroid disease?

After working with patients that have both thyroid disease and degenerative spinal disease and/or sciatica, I suspected that these conditions were related somehow. It became clear that there are many connections.

Generalized joint laxity is thought to be a risk factor for the development of degenerative spondylolisthesis^1,2, and hypothyroidism is a cause of joint laxity^3,4. In children, hypothyroidism can cause abnormal development of the spine, leading to wedge-shaped lumbar vertebrae which are predisposed to spondylolisthesis⁵. Hypothyroidism may also be related to ossification of the posterior longitudinal ligament, which is a cause of spinal stenosis⁶. In addition, degenerative disc disease is common in patients with autoimmune thyroid disease⁷.

It was recently discovered that the hormone triiodothyronine (T3) is important in the synthesis and cross-linking of collagen type I⁸. Analysis of disc material of patients with spondylolisthesis shows a deficiency of collagen type I⁹. Is it possible that lack of normal thyroid hormone leads to a deficiency in collagen, creating joint laxity and degenerative spinal disease?

Another interesting angle to look at is the use of iodine baths to treat lumbosacral radiculopathy^10,11. It is astonishing to find that instances of iodine in treatment of sciatica dates back to the mid 1800’s, even though the full connections between iodine and the thyroid, thyroid hormones and collagen, and collagen and ligament laxity, and ligament laxity and degenerative spinal disease were not known until recently.

Historical use of iodine in treatment of back pain and sciatica.

Iodine, aside from supporting normal thyroid hormone, and in turn, collagen production, has separate anti-inflammatory and antioxidant effects that could explain its historical usage for back pain. Iodine can lower C-reactive protein, and Interleukin-6¹², which are inflammatory cytokines involved in the pathogenesis of sciatica and radiculopathy^13,14. Iodine also acts as an antioxidant and protects against reactive oxygen species¹⁵, which contribute to neuropathic pain¹⁶, and increases plasma glutathione peroxidase¹⁵.

Hypothetical model for involvement of iodine in degenerative spinal disease and sciatica: Iodine is required for the production of triiodothyronine, which promotes production and cross-linking of collagen type I and prevents ligament laxity (shown here as a spondylolisthesis). Iodine also protects against inflammation in the spine by lowering C-reactive protein (CRP) and interleukin 6 (Il-6). Lack of iodine could allow for spondylolisthesis, inflammation, and sciatica.

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2.       Bird, H., Eastmond, C., Hudson, A. & Wright, V. Is generalized joint laxity a factor in spondylolisthesis? Scand. J. Rheumatol. 9, 203–205 (1980).
3.       Dorwart, B. B. & Schumacher, H. R. Joint effusions, chondrocalcinosis and other rheumatic manifestations in hypothyroidism: a clinicopathologic study. Am. J. Med. 59, 780–790 (1975).
4.       Golding, D. N. The musculo-skeletal features of hypothyroidism. Postgrad. Med. J. 47, 611 (1971).
5.       Hefti, F. et al. Pediatric Orthopedics in Practice. (Springer, 2007).
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9.       Roberts, S., Beard, H. & O’Brien, J. Biochemical changes of intervertebral discs in patients with spondylolisthesis or with tears of the posterior annulus fibrosus. Ann. Rheum. Dis. 41, 78 (1982).
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11.     Lysenko, V. V. [Treatment of patients with lumbosacral radiculitis by Krasnodar’ iodine-bromine baths]. Vopr. Kurortol. Fizioter. Lech. Fiz. Kult. 36, 460 (1971).
12.     Soriguer, F. et al. Iodine intakes of 100–300 μg/d do not modify thyroid function and have modest anti-inflammatory effects. Br. J. Nutr. 105, 1783–1790 (2011).
13.     Kang, J. D. et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 21, 271–277 (1996).
14.     Sturmer, T. Pain and high sensitivity C reactive protein in patients with chronic low back pain and acute sciatic pain. Ann. Rheum. Dis. 64, 921–925 (2005).
15.     Winkler, R., Griebenow, S. & Wonisch, W. Effect of iodide on total antioxidant status of human serum. Cell Biochem. Funct. 18, 143–146 (2000).
16.     Yowtak, J. et al. Reactive oxygen species contribute to neuropathic pain by reducing spinal GABA release. PAIN 152, 844–852 (2011).