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  1. #1
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    More on the Genetics of Scoliosis

    http://www.alphagalileo.org/ViewItem...CultureCode=en

    Untwist scoliosis by clipping wings of an overactive ladybird
    13 April 2016 Hiroshima University

    People with scoliosis, a twisting of the spine that can occur as a birth defect or more commonly starts during the teen years, are now closer to a genetic explanation for their condition. An overactive gene, called ladybird homeobox 1 (LBX1), is the start of a genetic chain reaction that causes the spine to grow abnormally. The report from collaborations at Hiroshima University, Kyoto University, RIKEN, and Kanazawa University is the first to demonstrate the functional association of scoliosis with LBX1.

    “A genetic test called the ScoliScore AIS Prognostic Test already exists for adolescents recently diagnosed with scoliosis to predict if the curve of the spine will get worse, which can guide treatment decisions. Studies like ours that identify genes important in causing scoliosis can help further develop this current prognostic test into a clinically predictive genetic test to identify scoliosis before symptoms occur,” said Chisa Shukunami, DDS, PhD, Professor in the Department of Molecular Biology and Biochemistry at Hiroshima University.

    The Problem

    Scoliosis is a polygenetic disease – mutations in multiple genes are responsible and environmental factors may also be relevant. The scientific community already knows one set of molecules, called the Wnt/PCP signaling pathway, is partially responsible for twisting the spine in scoliosis. These new results reveal how the Wnt/PCP pathway becomes problematic and provide insights for restoring normalcy.

    Too little activity of the LBX1 gene has no effect on development. However, the research team suspected that too much LBX1 activity might be problematic. The scientists performed genetic experiments using zebrafish, a small freshwater fish common in research labs, to model scoliosis.

    Researchers genetically manipulated zebrafish so they had too much LBX1 and then observed how their spines grew. The timing of when too much LBX1 started was important for how the fish’s bodies developed.

    Congenital Scoliosis

    During embryonic development, groups of cells form a pattern of mirror images on either side of the body and eventually become many different parts of the spine. In embryos injected with extra LBX1, the cells responsible for becoming the backbone and back muscles were wider than in healthy fish. Fish that survived long enough developed misshapen bones in their backs, which caused their scoliosis. Scoliosis in humans is not fatal, but researchers believe this model represents the birth defect version of scoliosis in humans because the bones are obviously misshapen.

    Adolescent Idiopathic Scoliosis

    Another group of zebrafish were genetically modified to express extra LBX1 throughout their entire lives, but only in some cells, making them what researchers call genetic mosaics. Some of these fish developed bones with the correct shape, but their spines still grew curved as they entered adulthood. This model is typical of the majority of human scoliosis cases, where there are no signs of problems until growth spurts just before or during adolescence. Adolescent idiopathic scoliosis affects 2-4% of all children aged 10 to 16.

    Adolescent-onset scoliosis in humans is more common in girls. Interestingly, researchers noticed more of their female fish developed scoliosis than their male fish. The reasons for why females are more susceptible remains a mystery, but it does further support the strength of the using this zebrafish model to study the genetic causes of scoliosis.

    Route to Disease

    A piece of DNA that regulates LBX1 is mutated, so LBX1 is hyperactive. Excess LBX1 prevents the activity of the wnt5b promoter. An inactive promoter means the gene wnt5b is less active. Insufficient wnt5b means the gene RhoA is not active. This cascade or signaling pathway is the link between LBX1 and scoliosis.

    The Wnt/PCP cell signaling pathway is well mapped and already implicated in causing scoliosis, but no one had yet connected LBX1 to Wnt/PCP. The team of researchers designed additional experiments to see how the genes might interact.

    The wnt5b gene helps control multiple aspects of cell growth, including regulating how cells become bones and muscles early in development. The spine is an interconnected complex of bones, nerves, and muscles whose formation and growth depends on a series of elaborate genetic regulations. Improper control of wnt5b could partially explain the skeletal irregularities that cause scoliosis.

    Detour for Prevention

    Researchers decided to test if artificially replacing wnt5b or RhoA could prevent scoliosis and death in fish modeling the congenital version of scoliosis. When the wnt5b or RhoA was added very early in embryonic development, the fish had significantly less severe scoliosis, but the other associated deformities were still fatal. It is unlikely that this method will prevent or correct adolescent scoliosis because of how early the wnt5b or RhoA needed to be provided to have an effect on straightening the spine.

    “Greater understanding of the genetic mechanisms that lead to adolescent-onset scoliosis is necessary before any genetic interventions for clinical treatments can be designed,” said Prof. Shukunami.
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    “A genetic test called the ScoliScore AIS Prognostic Test already exists for adolescents recently diagnosed with scoliosis to predict if the curve of the spine will get worse, which can guide treatment decisions. Studies like ours that identify genes important in causing scoliosis can help further develop this current prognostic test into a clinically predictive genetic test to identify scoliosis before symptoms occur,” said Chisa Shukunami, DDS, PhD, Professor in the Department of Molecular Biology and Biochemistry at Hiroshima University."
    Evidently these people didn't get the memo. Scoliscore Failed It's Second, Independent Analysis. Every gene in the Scoliscore test was found to be a false positive by two separate, independent labs. Every. Single. One. False. If you spent money on this test maybe try to get your money back before the share price of the company that owns it, Transgenomic falls to 0. It currently sits at 67 cents.

    Don't ask me why I posted this after months of MIA happiness and bliss. After working out with Scott tonight some instinct deep inside told me that I needed to check in.

    Multiple very recent studies have connected Scoliosis not to heredity (which makes zero sense if you believe in natural selection) but to problems with Vitamin-D. Check Pubmed for the latest and ask your child's doctor about a Vitamin-D lamp if he/she doesn't spend a significant amount of time outdoors.
    Last edited by Dingo; 04-23-2016 at 12:58 AM.

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    Interesting article. They need to do mammalian studies to see if the same holds true.
    I'm not so sure about Scoliscore. I am still a strong believer in the genetics of scoliosis because of my family. However, in our case, we've "discovered" that we have an apparent autosomal dominant degenerative neuromuscular disease. My sister is affected and my dad was affected, but neither have/had scoliosis. Whether my grandmother was "affected" or not will remain a mystery as she died at the ripe age of 82 from breast cancer. She had so-called "fibromyalgia" because she was in constant pain (a side effect of this disease) and scoliosis. However, IF she was affected, the progression was VERY slow and didn't shorten her life-span. My dad's life was cut short, but he still made it to 79, the last four years as a quadriplegic. He eventually succumbed to drowning by not having the muscles to cough, typical of MD and ALS patients. We thought it was ALS and the scoliosis was idiopathic. However, when I started having trouble walking and needed a walker at the ripe old age of 45, I knew something else was up and the scoliosis was probably related to the MD (D=disease not dystrophy, the MDA even made the change in terminology) that I have since five out of the seven likely affected have or had, in my son's case, scoliosis (but he does have the vertebral malformation Spina bifida occulta in two vertebrae). Just an FYI, some muscle diseases tend to show up earlier with each generation.

    So, whether Scoliscore failed or not, I AM interested in what this researcher found and whether it plays a role in all scoliosis or just IIS, JIS and AIS. It seems that it could apply to ANY spinal deformity, such as different Spina bifidas including occulta, wedged or misshapen vertebrae, or even extra ribs (my daughter has a cervical rib). Mammalian studies would make it easier to make that determination as the vertebrae would be larger to view. I've never seen a Spina bifida in a fish, but have had fish with scoliosis - they seem to die younger. I suppose other fish would eat them before they could be discovered or they would die upon hatching due to paralysis and then get eaten. I raised mice for snake food and found kyphosis in some of them. They also died younger. I took very good care of them so it wasn't due to neglect.

    Dingo, not to invalidate your point, vitamin deficiencies most certainly can monkey with biomolecular pathways. It is a well known fact that many people that live far north or south of the equator suffer from vitamin D deficiency. It's also a likely scenario even where you live. I lived in Phx and my dad lived there for decades. I also lived in the Mohave Desert where our thermometer peaked out at 131os one very HOT summer and it was in the shade! People in these hotter climates spend a LOT of time indoors, although with access to water, they can also get their fair share of overexposure to the sun. But it also depends on how the body has the ability to convert sunlight into vitamin D.

    There could be numerous vitamin or mineral deficiencies that we have. You may argue that scoliosis goes back millennia and be right. But you have to consider that even those people may not have had a "well balanced" diet as they were limited to what regional food could be found.

    Food for thought. It could be passed down genetically from a hereditary standpoint OR it could be a damaged pathway and have a biomolecular cause. It could also be a random mutation that frequently occurs that causes the pathways to be disrupted.

    Any way you put it, that was a very interesting paper. Of course, it will have to be studied much further, but at least it seems to a valid starting point.
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    Quote Originally Posted by rohrer01 View Post
    vitamin deficiencies most certainly can monkey with biomolecular pathways. It is a well known fact that many people that live far north or south of the equator suffer from vitamin D deficiency. It's also a likely scenario even where you live. I lived in Phx and my dad lived there for decades. I also lived in the Mohave Desert where our thermometer peaked out at 131os one very HOT summer and it was in the shade! People in these hotter climates spend a LOT of time indoors, although with access to water, they can also get their fair share of overexposure to the sun. But it also depends on how the body has the ability to convert sunlight into vitamin D.
    I believe 5 studies have connected Scoliosis with low levels of Vitamin D. However they haven't determined whether it is a cause or consequence of Scoliosis.

    Vitamin-D measurement in patients with adolescent idiopathic scoliosis. 2016 Apr 15

    Association of Calcium and Phosphate Balance, Vitamin D, PTH, and Calcitonin in Patients With Adolescent Idiopathic Scoliosis. 2016 Apr

    Vitamin D is a subject of growing interest because different groups of scientists in different parts of the world are finding the same thing. Not true for the gene hunters. Every gene in the Scoliscore test was UNfound when independently tested. Twice.
    Last edited by Dingo; 04-23-2016 at 11:55 AM.

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    Genetics of Scoliosis is a very hot topic.

    Nobody with a scientific understanding of scoliosis research can doubt genetics is an important field of study. For example, at the IMAST conference coming up for July 2016, a genetics paper won the 2015 John H. Moe Award for the Best Basic Science E-Poster at the Annual Meeting & Course.

    This year the award was presented to E-Poster #219: Functional Analysis of the Newly Identified Gene Clarified the Pathomechanism of Adolescent Idiopathic Scoliosis by Yoji Ogura, MD; Ikuyo Kou, PhD; Yohei Takahashi, MD, PhD; Katsuki Kono, MD; Noriaki Kawakami, MD; Koki Uno; Manabu Ito, MD; Shohei Minami, MD, PhD; Ikuho Yonezawa, MD; Haruhisa Yanagida, MD; Hiroshi Taneichi, MD, PhD; Kota Watanabe, MD; Taichi Tsuji, MD; Teppei Suzuki, MD; Hideki Sudo, MD, PhD; Toshiaki Kotani, MD, PhD; Naobumi Hosogane, MD, PhD; Eijiro Okada; Kazuhiro Chiba, MD, PhD; Yoshiaki Toyama, MD, PhD; Morio Matsumoto, MD; Shiro Ikegawa, MD, PhD
    If you see someone ignorantly claiming genetics is not a hot area of scoliosis research, you know they don't understand the science literature. The ScoliScore situation is not the same as this and other genetic research. You can't just assume it is all the same and lump it together. To a lay person it must all look the same. So whether or not Scoliscore pans out has ZERO to do with this work. But try convincing a lay person that. Good luck.

    Lay people don't like genetics because they don't understand it but that has ZERO bearing on what scientists are working on as we can see from the award winners named above.
    Last edited by Pooka1; 04-23-2016 at 05:23 PM.
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    Quote Originally Posted by Dingo View Post
    I believe 5 studies have connected Scoliosis with low levels of Vitamin D. However they haven't determined whether it is a cause or consequence of Scoliosis.

    Vitamin-D measurement in patients with adolescent idiopathic scoliosis. 2016 Apr 15

    Association of Calcium and Phosphate Balance, Vitamin D, PTH, and Calcitonin in Patients With Adolescent Idiopathic Scoliosis. 2016 Apr

    Vitamin D is a subject of growing interest because different groups of scientists in different parts of the world are finding the same thing. Not true for the gene hunters. Every gene in the Scoliscore test was UNfound when independently tested. Twice.
    Are you are sure about this conclusion as you were about your other conclusion in re the work in Canada on melatonin and inflammation markers?
    Sharon, mother of identical twin girls with scoliosis

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    The evidence is IN

    GENETIC EVIDENCE IN IS

    Is IS genetic?

    The recognition of genetic influences in IS is well-documented [19-25]. Familial forms of IS were described as early as 1922 [26]. Since then, reports of multiple twin sets and twin series have consistently shown higher concordance in monozygotic (MZ) compared to dizygotic (DZ) twins (reviewed in [27]). A meta-analysis of these clinical twin studies revealed 73% MZ compared to 36% DZ concordances [28]. Interestingly, in this series there was a significant correlation with curve severity in monozygous twins (P<.0002), but not dizygous twins. No correlation with curve pattern was found, suggesting the importance of genetic factors in controlling susceptibility and disease course, but not necessarily disease pattern. More recently, Andersen et al. [29] reported their findings using the Danish Twin Registry. They found 25% proband-wise concordance in monozygotic twins (6 of 44 concordant) compared to 0% concordance (0 of 91) in dizygotic twins, with an overall prevalence of approximately 1%. The lower concordances in both groups as compared with prior results may be explained by differences in study design, specifically, ascertainment in clinics versus by registry, and screening by examination versus questionnaire. Nevertheless the overall trend obtained for all studies suggests strong genetic effects in IS. Interestingly, measured concordances in monozygotic twins were below 100%, reflecting the complexity of disease and suggesting the involvement of as yet unknown environmental or stochastic factors in disease susceptibility.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674301/
    Sharon, mother of identical twin girls with scoliosis

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    Quote Originally Posted by Dingo View Post
    I believe 5 studies have connected Scoliosis with low levels of Vitamin D. However they haven't determined whether it is a cause or consequence of Scoliosis.

    Vitamin-D measurement in patients with adolescent idiopathic scoliosis. 2016 Apr 15

    Association of Calcium and Phosphate Balance, Vitamin D, PTH, and Calcitonin in Patients With Adolescent Idiopathic Scoliosis. 2016 Apr

    Vitamin D is a subject of growing interest because different groups of scientists in different parts of the world are finding the same thing. Not true for the gene hunters. Every gene in the Scoliscore test was UNfound when independently tested. Twice.
    I'm only going to respond to what you've said to me. I haven't read the rest, yet. There most certainly could be a common mutation that causes people to have low vitamin D levels. My daughter and I both have/had very low levels, 11 and 12 respectively. However, my other sister was also found to have very low levels does not have scoliosis. So there is more to it than vitamin D deficiency, not saying it doesn't exacerbate it in those with scoliosis. It is also well known to be linked to depression and Seasonal Affective Disorder. Anyone who has prolonged vit D, calcium, or phosphorous deficiencies will be prone to osteopenia and eventually osteoporosis.

    I still think that it's genetic in some cases. Some cases could be caused by malnutrition and a host of other things. The fish and the mice that I mentioned previously ALL died after developing kyphosis, although I have seen plenty of scoliotic fish in other fish tanks that seem to do fine. So maybe there is a difference there. Who knows? I'm not going to argue this post. I looked at your other thread. It belongs on THIS thread. You don't need to start a new thread for the same topic. Just my opinion. I guess you want people to see the new paper? There are productive arguments and there are arguments that people start because they are bored and have nothing more exciting to do. Please don't fall into the latter category because it appears that you are according to the way you introduce the article in the thread you started. I'm not even going to comment on it.

    Rohrer01
    Last edited by rohrer01; 04-25-2016 at 01:07 AM.
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    Quote Originally Posted by rohrer01 View Post
    I'm only going to respond to what you've said to me. I haven't read the rest, yet. There most certainly could be a common mutation that causes people to have low vitamin D levels. My daughter and I both have/had very low levels, 11 and 12 respectively. However, my other sister was also found to have very low levels does not have scoliosis. So there is more to it than vitamin D deficiency, not saying it doesn't exacerbate it in those with scoliosis. It is also well known to be linked to depression and Seasonal Affective Disorder. Anyone who has prolonged vit D, calcium, or phosphorous deficiencies will be prone to osteopenia and eventually osteoporosis.
    I had such a low Vit D level that I was put on 50,000 units daily for 4 months. I am outside a lot and don't use sunscreen (I know... bad) because I know I have low Vit. D. I don't have scoliosis.

    Next.
    Sharon, mother of identical twin girls with scoliosis

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    Quote Originally Posted by Dingo View Post
    Don't ask me why I posted this after months of MIA happiness and bliss. After working out with Scott tonight some instinct deep inside told me that I needed to check in.
    Too bad you didn't resist the urge. The forum has had months of bliss as well.
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    Quote Originally Posted by Dingo View Post
    Evidently these people didn't get the memo. Scoliscore Failed It's Second, Independent Analysis. Every gene in the Scoliscore test was found to be a false positive by two separate, independent labs. Every. Single. One. False.
    How did these labs check these "genes" or DNA segments? Did they check each one individually or grouped together. I would like to know more. I have lost some faith in Scoliscore, but am not convinced entirely either way. I was included in that study and my scoliosis was believed to be idiopathic and it turns out to be neuromuscular. With that in mind, if there are many more like me in the study, it could invalidate the results UNLESS idiopathic scoliosis is related to having muscle diseases, which is quite possible. Not all muscle diseases are fatal. More than two studies are needed for the number of loci found when Scoliscore was developed.

    Muscular Dystrophy, as most laymen know it as there are many forms, is a disease that you would "think" would disappear because of the nature of the disease. It causes extra DNA repeats that when transcribed in the cell make floppy, less functional proteins. With each generation it appears earlier because the offspring for some unknown reason have more repeats on their DNA than their affected parent. This makes the protein more floppy and even less functional. Eventually the chains become so long that the offspring don't live long enough to reproduce, thus ending the disease. YET the same mutation spontaneously appears randomly in other people and they don't know they have it until they are pretty old and have already had children. Thus the cycle starts all over again. I know a family where the dad was still going in his sixties. He didn't KNOW he had MD until LONG after he had FOUR children. Three of his four children developed MD very young and had symptoms before he did. He was tested and found to have it. I knew the youngest three very well. The two oldest were married. The oldest was affected. The two younger girls were much younger than their sisters (yes, all girls and irrelevant). The youngest ones when I knew them were nine and 11. They were already so far gone that they probably didn't make it to adulthood, at least the 9 year old. She had symptoms as young as less than two years old. The "unaffected" one didn't want to be tested so wasn't sure AND she was about to have a baby when I moved and lost track of them. She was pretty paranoid about any muscle twitch she had. I can't understand that logic of not testing, but it was her choice. She could be more like her dad and develop symptoms later on.

    Where does natural selection fit into diseases like this where the same mutation just pops up at random in unrelated families? I'm not saying that natural selection doesn't exist. I AM saying it doesn't exist to the extent that you put faith in, otherwise this just wouldn't happen. The disease would just die out in that family line and be gone forever. "Something" is causing the same mutation to keep appearing. Perhaps something goes commonly wrong during meiosis? It would HAVE to be at that stage. That is the germ cell and from that point on it is heritable. What makes you think it can't happen with scoliosis and have several "brands" for a better word? Just as there are different types of MD, as in my family, there can also be different types of scoliosis.

    Did you know that there is no test for ALS even though there is a familial form? They haven't found the gene. It's usually random in a single person and isn't heritable. But there's the one type that is. If they could find the gene, they could test and see which form. They haven't found it. Does it mean it doesn't exist? No!

    Your whole idea of heredity DOESN'T mean that any of these biomolecular pathways in the cells can't involve disruption in vitamin, mineral, or hormonal (melatonin hypothesis) function in the cells, either. You can't fix it by taking megadoses of the mentioned items if the cells can't process them properly. All you will end up with is normal levels of "whatever" in the blood (normal blood panels) and still have disease. So all these papers you post may point to pathways and give us clues. But they certainly do NOT prove that any form of scoliosis isn't heritable. Does that mean that they aren't valuable? NO! They are. They just don't prove that there is no heredity involved. Could there be forms of idiopathic scoliosis that aren't heritable? Certainly! Look at the example of ALS that I gave. There are, as far as we know, two types; non-heritable and heritable or familial as they call it. So in families where there is no history of scoliosis, you could be right. However, the vast majority of idiopathic cases that I've seen first hand, there are other affected family members making it a genetic disorder. In fact, the random cases could be heritable. You won't know with your son until he has children and grandchildren (recessive forms tend to skip generations unless the mate is a carrier) and none show up. He could be the product of a germ cell malfunction and pass it on. YOU DON'T KNOW and neither do we.

    Food for thought.
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    Quote Originally Posted by rohrer01 View Post
    How did these labs check these "genes" or DNA segments? Did they check each one individually or grouped together. I would like to know more.
    Dingo has no clue how labs check things or do things at all or why the Scoliscore work is not the same as the other molecular work. He can't explain why the SRS still mentions Scoliscore and clearly is misusing terms and isn't making any sense. Some of what he writes isn't even wrong because there is no content to the sentence. It's like he is saying invisible purple unicorns are hollow. He uses terms he clearly does not understand.

    Where does natural selection fit into diseases like this where the same mutation just pops up at random in unrelated families? I'm not saying that natural selection doesn't exist. I AM saying it doesn't exist to the extent that you put faith in, otherwise this just wouldn't happen. The disease would just die out in that family line and be gone forever. "Something" is causing the same mutation to keep appearing. Perhaps something goes commonly wrong during meiosis? It would HAVE to be at that stage. That is the germ cell and from that point on it is heritable. What makes you think it can't happen with scoliosis and have several "brands" for a better word? Just as there are different types of MD, as in my family, there can also be different types of scoliosis.
    Dingo has proven over and over that he doesn't understand natural selection or anything scientific he pretends to understand. This is the latest example.

    Your whole idea of heredity DOESN'T mean that any of these biomolecular pathways in the cells can't involve disruption in vitamin, mineral, or hormonal (melatonin hypothesis) function in the cells, either. You can't fix it by taking megadoses of the mentioned items if the cells can't process them properly. All you will end up with is normal levels of "whatever" in the blood (normal blood panels) and still have disease. So all these papers you post may point to pathways and give us clues. But they certainly do NOT prove that any form of scoliosis isn't heritable.
    Dingo does not understand how any of this works and it shows in every post he makes.
    Last edited by Pooka1; 04-25-2016 at 08:11 AM.
    Sharon, mother of identical twin girls with scoliosis

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