There's a Battle Being Fought Between the ScoliScore Folks and the ICONS Folks

[Dingo]

PNUTTRO

increased melatonin, increases osteopontin, and suppresses cAMP.

EEEEeeeee... that makes things a bit more complicated. Melatonin suppresses cAMP which in theory should be a good thing. Once again page 5 on this chart shows that children with Scoliosis don't inhibit cAMP properly in response to Melatonin.

I can't get to the study you listed. Does the study suggest that these hormones merely trigger and work together or are they suggesting that something like a Melatonin supplement would cause Osteopontin to shoot up?

For example I can take all the Vitamin B I want and anything over a normal level gets flushed. But if I ate iron supplements like candy my skin would turn orange.

[Pooka1]

EEEEeeeee... that makes things a bit more complicated.

A bit? A BIT???

This stuff is more intrinsically complex than landing a man safely on the moon and returning him safely to earth.

There is a reason why there are long-standing, unsolved medical dilemmas. And it's not for lack of a bunch of lay folks discussing it on a scoliosis forum. (I apologize for the preceding remark and for the fact it is a penetrating glimpse into the obvious.)

Half the battle is just getting to point where you begin to form some nascent sense of just how complex this stuff is (or it would have been solved by now). I don't think most of the players here have arrived at that point. Pnuttro obviously has as this is her field. And that's about it. I commend her restraint.

[Dingo]

PNUTTRO

So, if the melatonin (or osteopontin, or cAMP) is high, maybe curve progression is simply a consequence of a fast rate of bone growth.

Height certainly does appear to be a risk factor for Scoliosis. I thought about it but I don't think it could be the cause. According to the study I just posted a couple of times a few messages back all children with Scoliosis have Melatonin Signaling Dysfunction.

So for whatever reason something has gone wrong and this ultimately leads to an increase in OPN.

[PNUTTRO]

Melatonin secretion is regulated by the activity of allylalkylamine N-acetyl transferase (AA-NAT) which is usually but not always [38], considered the rate-limiting enzyme in the synthetic pathway of melatonin [39, 40]. Recent studies suggest that estrogen suppresses the synthesis of AA-NAT protein [41, 42]. It is therefore assumed that melatonin secretion decreases in response to an increase in estrogen levels in adolescent women, as their markedly increased estrogen suppresses the synthesis of melatonin via AA-NAT activity. Judging from the results of recent studies which show that melatonin is a physiological factor that promotes bone formation [22, 26], there is a possibility that expression of the melatonin receptor in osteoblasts is upregulated to compensate for a decrease in melatonin action caused by the abrupt increase in estrogen levels occurring in adolescent women.

[Ballet Mom]

Height certainly does appear to be a risk factor for Scoliosis.

Probably just because they have a longer time to grow and develop a more severe curve. I have a friend who's daughter is in ballet and has just been officially diagnosed with scoliosis and she's under five feet tall......but she does have hyperextended joints! Luckily, she probably won't grow much more because her mom and dad are both quite short.

[PNUTTRO]

Probably just because they have a longer time to grow and develop a more severe curve. I have a friend who's daughter is in ballet and has just been officially diagnosed with scoliosis and she's under five feet tall......but she does have hyperextended joints! Luckily, she probably won't grow much more because her mom and dad are both quite short.

I'm talking about a rate of growth, not a period of time.

[PNUTTRO]

Fig. 4. (A) Intracellular cAMP production induced by forskolin
was suppressed by melatonin in a dose-dependent manner (**:
p < 0.01). (B) The suppressive effect of melatonin was blocked by
treatment with luzindole or PTX (a: p < 0.01 vs 100 lM melatonin,
b: p < 0.01 vs 200 lM melatonin). Values are mean ± SE
from two independent experiments performed in triplicate.

[Ballet Mom]

I'm talking about a rate of growth, not a period of time.

Sorry, PNUTTRO, I was responding to Dingo's comment. I wasn't even aware you were posting.



Heh, never mind....I realize he was responding to your comment....

[CAmomof2]

Our daughter is involved in this study at Ste. Justine.
The 1st time the parents need to give a saliva sample and our daughter had blood taken. Only she will have blood taken each time she goes for x-rays, every 6 months or so.
This study may or may not benefit her, but it could help children in the future... who knows, maybe even our grandchildren someday!!

[Dingo]

Osteopontin is triggered by and protects the body from bacterial infection.

Osteopontin expression correlates with clinical outcome in patients with mycobacterial infection.

We conclude that osteopontin expression correlates with an effective immune and inflammatory response when humans are challenged by a mycobacterial infection and that osteopontin contributes to human resistance against mycobacteria.

Increased expression of osteopontin in the brain with scrapie infection

Immunohistochemically, OPN was intensely immunostained in neurons of the midbrain at the time of scrapie infection initiation.

Osteopontin Regulates Infection-stimulated Periapical Bone Loss

these results are consistent with a model in which OPN is expressed at the site of infection, and acts to facilitate migration of neutrophils and macrophages out of the circulation into the area of infection. In the absence of OPN, reduced neutrophil or macrophage numbers and/or function may result in reduced bacterial killing. The increased bacterial load ultimately results in an increased inflammatory response and increased bone loss.

Attenuated Host Resistance against Mycobacterium bovis BCG Infection in Mice Lacking Osteopontin

When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria.

[PNUTTRO]

PNUTTRO



Height certainly does appear to be a risk factor for Scoliosis. I thought about it but I don't think it could be the cause. According to the study I just posted a couple of times a few messages back all children with Scoliosis have Melatonin Signaling Dysfunction.

So for whatever reason something has gone wrong and this ultimately leads to an increase in OPN.

So if you have melatonin signaling dysfunction, how will more melatonin in your diet help?

[Dingo]

PNUTTRO

Increased Melatonin cannot repair Melatonin Signaling Dysfunction.

However there is some non-definitive evidence that low Melatonin correlates with curve progression. Melatonin is an antioxidant and has anti-inflammatory properties. If it's helpful this might be why.

Personally I would not give my child Melatonin supplements unless the science was definitive. It's free to sleep in a dark room and that simple behavior probably boosts melatonin production to an optimal, natural level.

[PNUTTRO]

Personally I would not give my child Melatonin supplements unless the science was definitive. It's free to sleep in a dark room and that simple behavior probably boosts melatonin production to an optimal, natural level.

While I agree that its a good idea for good overall health, there is an inherent contradiction when you say that one needs to boost melatonin levels (by diet or dark rooms) when

all children with Scoliosis have Melatonin Signaling Dysfunction.

p

[Dingo]

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.

[Dingo]

Osteopontin is a huge, red flag for inflammation.

Osteopontin: A Multifunctional Molecule Regulating Chronic Inflammation and Vascular Disease

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!