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Scoliosis Research: Hormones and Scoliosis

NEW Study Seeks Connection Between Adolescent Idiopathic Scoliosis (AIS) and Puberty

what causes scoliosis

cause of scoliosisScoliosis in teenagers is one of the most frequent forms of postural distortion and it occurs predominately in pubescent girls. The authors theorize that because of this, one of the many factors that may contribute to the expression of AIS must involve a significant deficiency of estrogens (the hormones that become active and trigger the onset of puberty).

Researchers tested concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) , estrogens, progesterone, osteocalcin, RANKL and the activity of alkaline phosphatase (AP) in prepubescent and post pubescent scoliotic girls and compared them to samples taken from non-scoliotic pre and post pubescent girls. Before we discuss the outcome, here is breakdown of what was tested and how each functions within the body.

 What was tested ?

Follicle-Stimulating Hormone Regulates the development, growth, pubertal maturation and reproductive processes of the body. FSH and LH act synergistically in reproduction.
Luteinizing Hormone Produced by gonadotroph cells in the anterior pituitary gland. In females, an acute rise of LH triggers ovulation. LH and FSH levels rise and fall together during the monthly menstrual cycle.
Estradiol  One of several natural estrogens. Predominant during reproductive years. Regulates menstrual cycles.
Estrone Least abundant of the three estrogens, Estrone converts to estrone sulfate, a long-lived derivative. Estrone sulfate acts as a reservoir that can be converted as needed to the more active estradiol. It is the predominant estrogen in postmenopausal women.
Estriol   One of several natural estrogens. Abundant primarily during pregnancy.
Progesterone Involved in the menstrual cycle, pregnancy, and embryogenesis. Progesterone levels are relatively low during the preovulatory phase of the menstrual cycle, rise after ovulation, and are elevated during the luteal phase. Progesterone levels are relatively low in children and postmenopausal women.
Alkaline Phosphatase A byproduct of osteoblast activity. ALP increases if there is active bone formation. Levels are significantly higher in children and pregnant women.
Osteocalcin Secreted solely by osteoblasts and thought to play a role in the body’s metabolic regulation and is pro-osteoblastic (bone-building).
RANKL  Receptor activator of nuclear factor kappa-B ligand. Through the binding of RANKL, osteoclasts and osteoblasts play a vital role in normal bone remodeling. Overproduction of RANKL is associated with a number of degenerative bone diseases (e.g. rheumatoid arthritis and psoriatic arthritis)

What were their findings?

In premenarcheal scoliotic girls, the levels of FSH, LH and estradiol were lower; the levels of progesterone, estrone and estriol were higher; and the concentrations of estrone and estriol were similar compared to girls without scoliosis. Higher levels of RANKL, osteocalcin and AP were observed in premenarcheal adolescents with AIS compared with non-scoliosis.

In postmenarcheal Scoliotic girls, the levels of FSH, LH, estradiol, and progesterone were lower, estrone were slightly lower and estriol did not differ compared with postmenarcheal girls without scoliosis. Significantly higher levels of RANKL, osteocalcin and AP were observed in postmenarcheal scoliotic adolescents compared with non-scoliosis.

Their research revealed that the levels of FSH, LH, and estradiol in premenarcheal girls with AIS were markedly lower than in girls without scoliosis. The levels of FSH, LH, estradiol, and estrone in postmenarcheal girls with AIS were also lower compared to girls without scoliosis. They suggest that such findings can be explained by delayed puberty. The average age of girls with scoliosis was higher in both the pre- and postmenarcheal groups compared to the groups without scoliosis.

Levels Compared to Groups of Girls without Scoliosis

FSH LH Estrone Estriol  Estradiol Progesterone AP Osteocalcin RANKL

Premenarcheal Scoliotic Girls

lower lower similar to control similar to control lower higher higher higher higher
Postmenarcheal Scoliotic Girls lower lower slightly lower same lower lower higher higher


As the authors state, there is already plenty of research that supports a multifactorial cause of scoliosis and (as we’ve discussed in previous articles about nutrition and scoliosis) the involvement of genetic and epigenetic predispositions and the influence of hormonal factors are also widely accepted. Scoliosis is assumed to be associated with a sex-linked predominant gene with incomplete penetrance (meaning that symptoms are not always present in individuals who have the genetic mutation) and variable expression (meaning variations in type and severity of a genetic disorder can exist between individuals with the same genetic mutation, even within the same family).

“There is an interdependence between the concentration of estradiol and development of scoliosis. Determination of estradiol may have diagnostic value in the screening of spinal pathologies associated with AIS.”

There are twice as many girls with Cobb angles greater than 10° and eight times as many with Cobb angles greater than 30°. Are hormones the only reason AIS occurs more frequently in girls than boys? The article references another study from 2012 that explains how Adolescent idiopathic scoliosis occurs between 2-10 times more frequently in females than in males with the Carter effect. In this situation males would need to inherit a greater number of susceptibility genes (compared to females) in order to develop AIS. They would also be more likely to pass scoliosis to their children and to have siblings with AIS. In the families they tested, AIS was lowest in sons of affected mothers (36%) and highest in daughters of affected fathers (85%). Fathers with scoliosis transmitted AIS to 80% of the children in the test, whereas mothers transmitted it to 56%. There was also significantly higher prevalence of AIS (55%) in siblings of males with scoliosis compared with siblings of females  with scoliosis (45%). They suggest that this presentation of the Carter effect supports the “multifactorial threshold model of inheritance in AIS”.

What role might estrogen play in Scoliosis formation?

It is believed that AIS develops in two stages: initial functional impairment of osteoblasts and osteoclasts (which control the amount of bone tissue: osteoblasts form bone, osteoclasts repair/remodel bone), and the stage of actual spinal deformation. However, the reason, like so much of scoliosis, is still unknown.

Estrogens influence bone growth and remodeling, and control changes in the structure of cancellous bones (spongy bone). The authors are not suggesting that estrogens cause AIS, but that due to their function, they may affect progression. Estrogen deficiency is associated with increased bone turnover, increased osteoclast and osteoblast activity. Estrogens also control the activity of the melatonin receptor and inhibit the synthesis of melatonin. They interact with other hormones and biochemical factors, such as calcium-binding protein calmodulin, as well as with other proteins controlling muscle contractility.

“…understanding the role of estrogens seems vital for explaining the evolution of AIS associated with skeletal growth…”

Read the full article HERE.