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It is largely agreed that adolescent idiopathic scoliosis is a multi-factorial condition in which environmental influences combine with one's genetic pre-disposition for scoliosis to create the condition.

Here is a wonderfully short list of how the genetics and environmental factors most likely come together to create the spinal curvature known as "idiopathic scoliosis".

This is the concensus opinion provided on the scoliosis causes and progression theories form the SOSORT text book. PP. 33-35

1. The origins of Adolescent Idiopathic Scoliosis (AIS) is most likely linked to a genetic defect of the central control or processing by the central nervous system (Pons and hind brain) that affects the growing spine.

2. It appears that factors that pre-dispose/initiate AIS are separate from the factors that drive curve progression.

3. The consensus is that Relative Anterior Spinal Overgrowth (RASO), results largely from biomechanical spinal growth modulation (Hueter-Volkmann).

4. The Neuro-Osseous Timing Of Maturation (NOTOM) concept was formulated to explain why adolscent girls are more susceptible than boys to curve progression. Based on the timing of adolescent growth spurts (earlier in females) in relation to the timing of postural maturity (similar in boys and girls).

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Could you reduce the risk of passing scoliosis genes onto your children?

Admittedly, I'm a little behind on some of my reading, but the article in the January 18, 2010 issue of Time magazine on "Epigenetics" is really great.

So what in the heck are "epigenetics".....I didn't know either until I read the article, but here is the concept in a nutshell.

1. The human body has trillions of cells, each of which as a nucleus (command center). In each nucleus, DNA is tightly coiled around proteins called "histones" that serve as a support structures for the genes

2. Gene contain the codes for cells to produce various proteins and Darwin tells us that it takes many generations to "rewrite" this basic genetic code.

3. Various chemicals called "epigenetic marks" sit atop genes adn offer basic instructions to them (basically they serve as an on or off switch)

4. All cell types contain the exact same DNA. Epigenetic markers silence certain gene sequences and active others. If the marks don't work properly, cancer or cell death is possible.

5. (This is the really cool part) Stressors like a fatty diet can activate epigenetic markers, modifying histones, or adding methyl groups to DNA strands. These changs can turn genes on and off and/or may affect what get's passed down to your offspring.

6. If you overstimulate gene for a certain condition (Scoliosis for example), you kids can inherit these over-activated sequences. That could mean a lifetime of battling unfavorable gene expression.

This means you don't have to be a victim of your genetics AND environmental factors can ultimately change both factors in this condition (genetic and environmental factors), but that isn't the biggest point to this post......

YOU MAY BE ABLE TO CHANGE THE SCOLIOSIS GENETIC RISK OF YOUR CHILDREN THOUGH ELIMINATING/REDUCING YOUR ENVIRONMENTAL SCOLIOSIS RISK FACTORS NOW!

Here is an example......

When pregnant rats were fed a fatty diet, both their daughters and granddaughters proved to be at greater risk of breast cancer. In fact, even if the daughters of the first generation of rats ate healthily, their offspring—the third generation—were still at greater risk of disease.

According to the New Scientist:

“… a fatty diet may cause “epigenetic” DNA modifications that can be passed on to future generations.”

How epigenetic changes transmit consequences of nutritional exposure from one generation to the next,” published in the journal Genes & Nutrition, highlights the dilemma we’re increasingly faced with:

“Epigenetics is unravelling a continuous cross talk between our genetic profile and the environment.

Indeed, genome is much more “flexible” than previously thought and such flexibility underscores the relevance of “good eating” for maintenance of good health.

Future nutritionists will have to face the challenge of elucidating the mechanism of nutrition-induced epigenetic changes during pre and post-natal life, to optimize nutritional interventions in a “personalized” perspective.”

Likewise, a more recent article in the journal Human Molecular Genetics, states:

“Traditionally, we understand that individual phenotypes result primarily from inherited genetic variants together with environmental exposures. However, many studies showed that a remarkable variety of factors including environmental agents, parental behaviors, maternal physiology, xenobiotics, nutritional supplements and others lead to epigenetic changes that can be transmitted to subsequent generations without continued exposure.

Recent discoveries show transgenerational epistasis and transgenerational genetic effects where genetic factors in one generation affect phenotypes in subsequent generation without inheritance of the genetic variant in the parents.

Together these discoveries implicate a key signaling pathway, chromatin remodeling, methylation, RNA editing and microRNA biology. This exceptional mode of inheritance complicates the search for disease genes and represents perhaps an adaptation to transmit useful gene expression profiles from one generation to the next.” [Emphasis mine.]

a recent article by Georgetown University Medical Center discusses the effects of alcohol consumption on the expression of certain breast cancer genes, stating that:

“Normal variations in genes may inhibit or enhance the effects of alcohol consumption. For example, work by Shields, Marian and colleagues has shown that variations in the genes ADH1B and ADH1C – both of which code for enzymes critical in alcohol metabolism – may increase a postmenopausal woman’s risk for breast cancer up to two-fold if she consumes alcohol.

This is in part because, during its metabolism, alcohol breaks down into a toxic molecule that causes DNA damage. Variations in the ADH1 genes can change this process, increasing the severity of long-term damage to DNA. In this way, alcohol has the potential to disrupt many cellular pathways…”

Based on these facts, I personally believe that the CLEAR protocols can change the genetic markers in scoliosis by NATRURALLY altering the natural course of the condition via neuro-muscular re-training rehab.

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Back Bracing for Scoliosis. 

  Does it work?

Spinal bracing for Adolescent Idiopathic Scoliosis has NO effect on the natural course of Adolescent Idiopathic Scoliosis (I knew it!)

The creators of the Scoliscore genetic test plotted the results of brace treatment against the expected/predicted genetic course of the condition. Guess what? The two graphs match almost perfectly (see the pic by clicking on the link below), which means spinal bracing doesn't alter the condition in any way, shape, or form. It basically proves that brace treatment is pretty much worthless and does not reduce or eliminate ANY of the environmental factors (forward head posture, loss of normal curve in the neck, hip rotation, ect) that cause AIS when combined with pre-disposing genetic factors. This is EXACTLY why the CLEAR Institute treatment program doesn't recommend invasive, expensive, and ineffective spinal bracing in its treatment programs.

http://www.scoliosisjournal.com/content/4/S2/O59

It should be recognized that this study only used data from North American braces and did not include data from the Spine Cor brace, but I seriously doubt they would perform any differently since the same basic bracing concepts still hold true in those types of braces as well.

Over-correction bracing may produce a "guided growth" type effect via the Hueter-Volkmann principle, but is only achieved through manipulation of secondary adaptations to the condition and cannot be considered working towards a cure. Approximately 1% of genetically pre-disposed AIS patients can and will potentially benefit from this type of approach, but the cost/risk/benefit must be weighted against other guided growth type treatments like vertebral body stapling (VBS). However, VBS seems to be most effective when applied to a skeletally immature spine with a cobb angle of 35 degrees or less. A skeletally immature patient (who is part of the 1% genetically high risk) with a cobb angle greater than 35 degrees probably should be the only patients for which guided growth type bracing should be considered.

Bottom line: For 99% of the non-high risk AIS patients bracing does not change any of the environmental (or genetic) factors that create AIS and therefore has no bearing on the condition's natural course. The entire premise of spinal bracing is fundamentally flawed and any attempts to develop a build off those flawed fundamentals will be flawed by default.

At what point are we going to get our heads out of the sand (or out of other places) and realize that we are doing a major disservice to 99% of scoliosis patients for whom spinal bracing is recommended. It all starts with a major PUSH for earlier & more effective screening, a mass movement towards genetic testing as many AIS kids as possible and genetic risk appropriate early stage scoliosis intervention ASAP.