I believe that all three forms of gluten intolerance could cause scoliosis and this could affect an individual at any age throughout their lifespan. Theoretically, scoliosis could be caused by celiac disease (CD), dermatitis herpetiformis (DH), and non-celiac gluten intolerance. With all three forms, antibodies against transglutaminases involved in bone health, antibodies against bone cells, and possibly the presence of arthritis might contribute to scoliosis. An additional factor, malabsorption may be a contributing influence with CD and DH as well.
Scoliosis At BirthWith cogenital scoliosis (birth defects to the spine), it reasonable to suspect that autoimmune factors and poor nutritional status in the mother, due to malabsorption issues (associated with undiagnosed CD and DH), could possibly lead to spinal abnormalities during fetal development. A mother with undiagnosed CD may have low levels of calcium, vitamin D, magnesium, phosphorus, and other nutrients necessary for healthy bone development due to malabsorption issues. Many mothers with CD have very little or no symptoms (silent CD), but still experience nutrient deficiencies. Therefore, this could be a hidden cause.
Autoimmune reactions against transglutaminases involved in bone health or against bone cells could also contribute. The antibodies circulating in the mother’s blood may make their way through to the fetus and affect the health of it’s bones.
Scoliosis In Infants And ToddlersIn infantile idiopathic scoliosis, the abnormal spine curvature is diagnosed at age 0-3 years. Apparently, if the curve is below 30 degrees (on the first doctor’s visit), these children have a good chance of it resolving. Why does the curve resolve in some minor cases of scoliosis? Perhaps, this group has less skeletal symptoms, just as some with gluten intolerance have very little symptoms, and the symptoms can come and go. As well, these patients are likely using nutrient supplements once diagnosed. This may help to compensate for malabsorption issues and resolve the minor form of scoliosis. If there was only minor intestinal villi damage with a silent form of CD, then the supplements might be able to compensate for the current malabsorption and mask the underlying problem (damaged villi).
For others, autoimmune activity and malabsorption associated with a gluten intolerance may affect bone integrity and lead to a more severe form of scoliosis. The gluten intolerance symptoms could be vague or atypical and may not be recognized by medical staff. Even when the symptoms are obvious (I had obvious symptoms for 5 years), the underlying gluten intolerance may not be recognized or diagnosed.
Scoliosis In ChildrenWith juvenile scoliosis, the onset of symptoms is between ages 3-10. The symptoms and damage associated with a gluten intolerance can occur at any age so it is reasonable to suspect that the bone changes could occur later in life. The skeletal effects from malabsorption or autoimmune reactions may not occur until childhood.
Scoliosis In AdolescenceAdolescent scoliosis occurs between ages 10-18 years. Flexibility is at it’s peak in the teen years so this may increase the risk for scoliosis in this age group. Bone changes associated with a gluten intolerance combined with increased flexibility could significantly increase the risk for scoliosis. A nutrient poor diet (common to eat more processed foods in teenage years) along with malabsorption issues (if CD and DH is involved) may be why the scoliosis symptoms are more prevalent in this age group. The negative effects on bone associated with malabsorption issues might be more prevalent in the adolescent years due to the demand for increased bone growth and nutrients. A poor diet may potentiate the effect.
In this age group, scoliosis tends to be more common in girls. As well, generalized low bone mass, and osteopenia has been found in girls with adolescent idiopathic scoliosis (this is a common finding with CD). There are many hormonal changes occurring at this age and this may be the reason why females have a higher prevalence of scoliosis. Perhaps the difference in hormonal shifts between adolescent boys and girls (i.e. estrogens) helps to account for the gender difference. Estrogens have been suspected of playing a role in the development of scoliosis since estrogen can affect bone remodelling and growth. Theoretically, a gluten intolerance could lead to autoimmune activity and this along with nutrient deficiencies could contribute to hormonal changes, bone changes and scoliosis. This seems likely since many reproductive symptoms have been linked to gluten intolerance and reproductive functions are dependent on nutrients and balanced hormonal levels. A gluten intolerance could affect both of these factors. Females also have a loss of minerals in menses so this could contribute to a higher prevalence as well. A vitamin K deficiency can also occur in CD and may add to the blood loss.
Scoliosis In AdulthoodWith a latent or silent gluten intolerance, the symptoms may not be noticeable until adulthood. As well, the symptoms may be atypical and not recognized. This is likely since even the obvious typical symptoms are often missed by physicians and nurses.
SummaryYou can see how an underlying gluten intolerance could cause scoliosis and how the symptoms may surface at any age. Gluten intolerance can be quite elusive and this combined with lack of awareness could lead to the bone changes evident with various forms of scoliosis. Since scoliosis can be debilitating, I think it is important to be aware of this possible underlying cause.
Next In The 5 part SeriesPart 4 Of 5 Part Series: How Could A Lectin Intolerance Contribute To Scoliosis.
Part 5 Of 5 Part Series: My Thoughts About An Association Between Gluten And Scoliosis
References1. Scoliosis Research Society http://www.srs.org/
2. Scoliosis Association Inc. http://www.scoliosis-assoc.org/
3. N.A Sims, S Dupont, A Krust, P Clement-Lacroix, D Minet, M Resche-Rigon, M Gaillard-Kelly, R Baron. Deletion of estrogen receptors reveals a regulatory role for estrogen receptors-? in bone remodeling in females but not in males. Bone, Volume 30, Issue 1, Pages 18-25 (January 2002)