Melatonin Signaling Dysfunction
PNUTTRO
Melatonin Signaling Dysfunction doesn't mean that kids don't produce Melatonin.
One of Melatonin's jobs is to shut down the molecule cAMP. For whatever reason children with Scoliosis produce Melatonin but it doesn't do it's job and flush out the cAMP in bones.
I am guessing that this buildup of cAMP produces inflammation which elevates OPN. Melatonin doesn't do it's job and flush out cAMP but perhaps since it has anti-inflammatory properties this helps keep OPN levels down.
I dunno, I guess we'll find out soon enough.
Osteopontin and inflammation
Osteopontin is a huge, red flag for inflammation.
Osteopontin: A Multifunctional Molecule Regulating Chronic Inflammation and Vascular Disease
Quote:
Osteopontin (OPN) is a multifunctional molecule highly expressed in chronic inflammatory and autoimmune diseases, and it is specifically localized in and around inflammatory cells. OPN is a secreted adhesive molecule, and it is thought to aid in the recruitment of monocytes-macrophages and to regulate cytokine production in macrophages, dendritic cells, and T-cells. OPN has been classified as T-helper 1 cytokine and thus believed to exacerbate inflammation in several chronic inflammatory diseases, including atherosclerosis. Besides proinflammatory functions, physiologically OPN is a potent inhibitor of mineralization, it prevents ectopic calcium deposits and is a potent inducible inhibitor of vascular calcification. Clinically, OPN plasma levels have been found associated with various inflammatory diseases, including cardiovascular burden. It is thus imperative to dissect the OPN proinflammatory and anticalcific functions.
Fish oil is an effective, well documented anti-inflammatory. A few months after my son was diagnosed with Scoliosis I started giving him pharmeceutical grade fish oil supplements on the off chance that inflammation played a role. I'll never know for sure but I think that one might have paid off big time.
Hooray fish oil! :)
One thing really stood out
Quote:
[0065] Mean plasma OPN concentration in patients with AIS were significantly higher (p-value <0.001) in patients with AIS having a Cobb's angle >45° (965 ± 414 nanograms per milliliter) than that in healthy controls (570 ± 156 nanograms per milliliter) and than that in AIS patients with a Cobb's angle <45° (799 ± 284 nanograms per milliliter). Diagnostic sensitivity and specificity of OPN for AIS was 84.4 percent and 90.6 percent respectively (cut-off value > 800 nanograms per milliliter). Subgroup analysis showed that 47.9 percent of children at risk had OPN values higher than 800 nanograms per milliliter as opposed to only 8.6 percent for the controls indicating that elevated plasma OPN levels precede scoliosis formation. There were no significant differences in mean plasma sCD44 levels and HA levels between all groups.
The "at risk" group consisted of children without Scoliosis who had 1 parent with Scoliosis. Approximately 50% of these children had dangerously high levels of OPN. If OPN was only implicated in Scoliosis it wouldn't be as stunning. It seems implausible to me that half of the offspring produced by parents with Scoliosis would be saddled by heredity with a potentially fatal health time-bomb. I think this discovery might provide evidence as to what the environmental half of Scoliosis is.
This story comes to mind.
LA Times: Rats' virus holds clues to diabetes
Quote:
The BioBreeding, or BB, rat naturally develops diabetes at about 2 months of age, and researchers have attributed the disease to genetics. The new findings suggest that there is indeed a genetic susceptibility but that the precipitating event is a viral infection.
it's going to be interesting
Pooka1
It certainly could work that way. I'm really curious to see how this all turns out over the next few years.
I hope someone interviews Dr. Moreau and he offers an explanation for the high OPN levels in kids with and without Scoliosis. This is where a twin study would really be useful.