Are Your Bones a Hormonal Organ?
It is common for adolescent girls with idiopathic scoliosis to have delayed menarche (beginning of their menstrual cycle). Why is this?
One theory promotes the idea that as estrogen is increased during menarche, bone growth is stimulated, but spinal cord growth (and flexibility) may not be. If spinal-cord tension already exists as the main mechanism driving a girl’s scoliosis, bones that suddenly grow at a more rapid rate could significantly increase her curve. This adds more strain on tight spinal nerves. Could withholding the release of estrogen by delaying the onset of menses be one way the body attempts to stop adding increased spinal cord tension to the spine?
A 2017 study in the journal, Mechanisms in Endocrinology, found bone formation was decreased in the presence of diabetes; considering it as a process of slower bone growth. This may be due to altered levels of bone hormones (fibroblast growth factor 23 and osteocalcin), as the bone has been recognized by some researchers to be an endocrine (hormone) organ.
These bone-derived hormones may very well affect glucose balance according to recent studies. These hormones can inhibit vitamin D production via the kidneys. Animal genetics studies have shown that osteocalcin causes the pancreas to increase glucose (blood sugar) utilization.
We find it quite interesting that most adolescent females we see with scoliosis tend to have just this: Low vitamin D levels and lower fasting blood sugar or hypoglycemia! So, when menses begins, bone can grow faster. Faster bone growth can trigger the kidneys to alter vitamin D levels.
Rapid bone growth may also lower blood sugar. These are only a few, but very powerful vectors that may affect a girl’s spinal cord flexibility, nerve-growth, and scoliosis curve progression. A better understanding of bone growth in scoliosis may be a key to developing more effective scoliosis treatment that helps reduce the rate of scoliosis surgery.
D. Lepp, DC
Brunetti, Giacomina; D’Amelio, Patrizia; Wasniewska, Malgorzata; Mori, Giorgio; Faienza, Maria Felicia (2017): Editorial: Bone: Endocrine Target and Organ. In Frontiers in endocrinology 8, p. 354. DOI: 10.3389/fendo.2017.00354.
Fukumoto, Seiji; Martin, T. John (2009): Bone as an endocrine organ. In Trends in endocrinology and metabolism: TEM 20 (5), pp. 230–236. DOI: 10.1016/j.tem.2009.02.001.
Kulis, Aleksandra; Goździalska, Anna; Drąg, Jagoda; Jaśkiewicz, Jerzy; Knapik-Czajka, Małgorzata; Lipik, Ewa; Zarzycki, Daniel (2015): Participation of sex hormones in multifactorial pathogenesis of adolescent idiopathic scoliosis. In International orthopaedics 39 (6), pp. 1227–1236. DOI: 10.1007/s00264-015-2742-6.
Skogland, L. B.; Miller, J. A. (1980): Growth related hormones in idiopathic scoliosis. An endocrine basis for accelerated growth. In Acta orthopaedica Scandinavica 51 (5), pp. 779–780.
(Kulis et al. 2015; Skogland and Miller 1980; Brunetti et al. 2017; Fukumoto and Martin 2009)