Serotonin and Idiopathic Scoliosis: A Review of Related Etiology and Treatment Considerations

Abstract

Recent research has suggested a potential association between serotonin and idiopathic scoliosis, a complex spinal deformity of unknown origin. Studies have explored genetic associations, altered serotonin levels, and the effects of serotonin-related medications in the context of idiopathic scoliosis. Genetic studies have identified significant associations between idiopathic scoliosis and serotonin-related genes, indicating a potential genetic predisposition to the condition. Furthermore, altered serotonin levels have been observed in patients with idiopathic scoliosis, with lower serum serotonin levels reported compared to healthy controls. This chapter reviews some of the published genomic variants associated with idiopathic scoliosis. The effects of serotonin-related medications have also been investigated, highlighting potential therapeutic benefits. However, the exact mechanisms underlying the association between serotonin and idiopathic scoliosis remain unclear, warranting further research. While theoretical and animal models have shown connections between serotonin metabolism and idiopathic scoliosis, there are uncertainties when translating this information into clinical practice for primary care and other musculoskeletal specialty providers. This chapter outlines the serotonergic pathways of musculoskeletal function, serotonin clinical laboratory testing methods, as well as clinical management strategies including pharmacological, nutrient, dietary, and lifestyle-based options.

1. Introduction

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a neurotransmitter that plays a crucial role in the central nervous system (CNS). It is derived from the amino acid tryptophan and is involved in numerous physiological functions, including mood regulation, sleep, appetite, and cognition. Structurally, serotonin is a monoamine neurotransmitter with a chemical formula of C₁₀H₁₂N₂O. It contains an indole ring and an amine group, making it a member of the indoleamine class of neurotransmitters. Serotonin exerts its effects by binding to specific receptors, mainly the 5-HT receptors, which are widely distributed throughout the brain and other tissues. While serotonin’s involvement in mental health disorders like depression and anxiety is well-established, recent research has also highlighted its potential role in the pathogenesis of idiopathic scoliosis, a complex spinal deformity of unknown origin.

Several studies have investigated the potential link between serotonin and idiopathic scoliosis [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11], shedding light on the role of serotonin signaling abnormalities in the pathogenesis of this complex spinal deformity. These studies have explored various aspects, including genetic associations, altered serotonin levels, and the effects of serotonin-related medications. While the exact mechanisms underlying the association between serotonin and idiopathic scoliosis are not fully understood, the findings suggest a potential involvement of serotonin in the development and progression of the condition.

One study conducted by Nelson et al. [5] examined the genetic association between idiopathic scoliosis and serotonin-related genes. The researchers analyzed a large cohort of patients with idiopathic scoliosis and identified several single nucleotide polymorphisms (SNPs) in genes related to serotonin signaling that were significantly associated with the condition. The study provided evidence for a potential genetic predisposition to idiopathic scoliosis linked to abnormalities in serotonin-related genes. Another study by Yang et al. [6] identified the MTNR1B genomic SNP in adolescent idiopathic scoliosis.

Serotonin has also been a target in animal studies of idiopathic scoliosis. In a study by Machida et al. [2], they observed the development of idiopathic scoliosis in pinealectomized chickens, as compared to a matched group that were subsequently given intraperitoneal injections of 5 hydroxytryptophan (5-HTP). They concluded that serotonin may be a therapeutic target in the treatment of idiopathic scoliosis.

In addition to genetic associations and altered serotonin levels, recent observations have been published showing the increased incidence of anxiety, mood changes, and introversion in children with idiopathic scoliosis [12]. Early interpretations of this connection were thought to be due to the psychological impacts of scoliosis treatment, such as wearing a rigid scoliosis brace [13]. However, the newer studies were conducted in children who had not participated in any treatment. Interestingly, many of these symptoms have serotonergic connections, like the serotonergic projections into the spinal and torso musculature.

While these studies provide valuable insights into the potential link between serotonin and idiopathic scoliosis, it is important to note that the underlying mechanisms are complex and multifactorial. Further research is needed to unravel the precise role of serotonin in the pathogenesis of idiopathic scoliosis and to explore potential diagnostic and therapeutic interventions targeting serotonin signaling. Nonetheless, these studies contribute to our understanding of the condition and pave the way for future investigations in this field.

2. Serotonin and the peripheral nervous system

The human body consists of a complex network of nerves that relay messages between the brain and various parts of the body. Serotonin, a neurotransmitter primarily associated with mood regulation and cognition, also plays a role in peripheral nerve pathways that terminate in the torso musculature. Understanding these serotonergic pathways is crucial for comprehending their impact on muscle function and potential therapeutic applications.

The serotonergic peripheral nerve pathways originate from the raphe nuclei, which are clusters of neurons located in the brainstem. The raphe nuclei produce serotonin and send projections that extend throughout the central nervous system (CNS) and peripheral nervous system (PNS). In the context of torso musculature, these pathways involve serotonergic fibers that innervate muscles, including the diaphragm, abdominal muscles, and back muscles.

The diaphragm, the primary muscle responsible for respiration, receives serotonergic innervation. Serotonin acts on receptors located on the diaphragmatic motor neurons, influencing their excitability and activity. Studies have shown that serotonin can modulate the motor output of the diaphragm, affecting its contraction strength and coordination [14]. Dysregulation of serotonergic pathways to the diaphragm may contribute to respiratory disorders such as sleep apnea and respiratory distress syndrome.

The abdominal muscles, including the rectus abdominis and external obliques, are involved in trunk stability and movement. Serotonergic fibers innervate these muscles, and serotonin plays a role in regulating their tone and motor control. Abnormalities in serotonergic pathways to the abdominal muscles have been implicated in conditions such as abdominal muscle weakness and spasticity.

The back muscles, encompassing the erector spinae and latissimus dorsi, are critical for posture, spinal stability, and movement. Serotonergic innervation of these muscles influences their contraction and relaxation, contributing to overall back muscle tone and coordination. Research has suggested that alterations in serotonergic signaling within the back muscles may contribute to conditions such as back pain and muscle imbalances [15].

In addition to their role in muscle function, serotonergic peripheral nerve pathways also interact with other systems in the torso. For instance, serotonin influences the gastrointestinal system, where it plays a role in regulating gastrointestinal motility and secretion. This interaction highlights the multifaceted nature of serotonergic pathways and their impact on various physiological processes.

Understanding the serotonergic peripheral nerve pathways that terminate in the human torso musculature has implications for therapeutic interventions. Modulating serotonin signaling in these pathways holds potential for managing muscle-related disorders and improving functional outcomes. Medications that target serotonin receptors, such as selective serotonin reuptake inhibitors (SSRIs), are commonly prescribed for conditions like depression and anxiety. Their effects on serotonergic pathways may extend to the modulation of torso musculature, offering therapeutic benefits for muscle-related conditions.

3. Serotonin and the central nervous system

The serotonergic central nervous pathways play a vital role in governing the body schema within the central nervous system (CNS). These pathways integrate sensory information from various sources, including cerebellar afferent input and cortical premotor inputs, to modulate motor control, body awareness, and coordination.

One crucial aspect of serotonergic pathways is their influence on the body schema, which refers to the brain’s representation of the body and its position in space. Serotonin receptors are widely distributed throughout the CNS, including the cortex, basal ganglia, and cerebellum, indicating the significance of serotonin in shaping the body schema. Serotonin’s effects are mediated through interactions with specific receptor subtypes, such as 5-HT1A and 5-HT2A receptors, which are abundantly expressed in key regions involved in body awareness and motor planning.

The cerebellum, a structure located at the back of the brain, receives afferent input from various sources, including proprioceptive signals from muscles and joints, as well as sensory information from the vestibular system. Serotonergic projections from the raphe nuclei provide modulatory input to the cerebellum, influencing its function and integration of sensory feedback. This integration enables the cerebellum to contribute to body schema by continuously updating motor commands based on sensory inputs.

Furthermore, the serotonergic pathways interact with cortical premotor inputs, which are responsible for motor planning and execution. These pathways involve the communication between the primary motor cortex, supplementary motor area (SMA), and the basal ganglia. Serotonin modulates the excitability of these areas, facilitating or inhibiting motor outputs based on the context and behavioral demands. By integrating cerebellar afferent input with cortical premotor inputs, serotonergic pathways contribute to the fine-tuning of motor control and coordination.

Studies have shown that dysregulation of serotonergic signaling within these pathways can lead to motor deficits and impairments in body schema. For example, disruptions in serotonin transmission have been implicated in movement disorders such as Parkinson’s disease and essential tremor [16]. Serotonergic dysfunction may contribute to the motor symptoms observed in these conditions, affecting both the body schema and motor control processes.

Additionally, serotonergic pathways have implications beyond motor control. Serotonin is involved in regulating mood and emotions, with serotonin imbalances linked to psychiatric disorders such as depression and anxiety. These disorders can impact body perception and awareness, further highlighting the role of serotonergic pathways in shaping the body schema and body image.

4. Serotonin dysregulation

One potential avenue of investigation is the role of serotonin deficiency in the pathogenesis of idiopathic scoliosis. Several studies have proposed that alterations in serotonin signaling could be a contributing factor to the development of idiopathic scoliosis.

Furthermore, serotonin levels have been found to be altered in patients with idiopathic scoliosis. Winderlich and Shchekolova [17] investigated serum serotonin levels in adolescent idiopathic scoliosis (AIS) patients and found significantly higher levels compared to healthy controls. This may be due to a reduced conversion of serotonin into melatonin. The study suggested that serum serotonin may predict progressive scoliosis.

While these findings suggest a potential association between serotonin deficiency and idiopathic scoliosis, it is important to note that the relationship is complex and likely involves multiple factors. The precise mechanisms by which serotonin deficiency contributes to scoliosis development remain unclear.

Nevertheless, understanding the potential role of serotonin deficiency in idiopathic scoliosis opens up new avenues for diagnostic and therapeutic approaches. For instance, early detection of serotonin abnormalities in individuals with scoliosis may help identify those at higher risk for progression and guide treatment strategies. Moreover, medications that target serotonin signaling, such as selective serotonin reuptake inhibitors (SSRIs), which are commonly used in the treatment of depression, may hold promise for managing idiopathic scoliosis. Further research is needed to explore the efficacy and safety of such treatments.

5. Serotonin signaling dysfunction

Serotonin signaling is known to be involved in the regulation of bone growth and remodeling. Studies have shown that serotonin receptors, particularly the 5-HT2A receptor, are expressed in osteoblasts, cells responsible for bone formation. Serotonin signaling has been implicated in the balance between bone formation and resorption, and dysregulation of this signaling pathway can lead to skeletal abnormalities. In the context of idiopathic scoliosis, disruptions in serotonin signaling may contribute to an imbalance in bone growth, leading to spinal deformities.

Genetic studies have also provided evidence for the involvement of serotonin signaling dysfunction in idiopathic scoliosis. Chu et al. [11] explored the genetic factors associated with idiopathic scoliosis and found several genes involved in serotonin signaling that were significantly associated with the condition. These findings suggest that genetic variations affecting serotonin signaling pathways may contribute to the development of idiopathic scoliosis.

Furthermore, alterations in serotonin levels have been observed in patients changes in bone resorption. Maïmoun et al. [18] conducted a study that compared serum serotonin levels between individuals with adolescent idiopathic scoliosis (AIS) and healthy controls. The study found lower levels of serum serotonin were related to higher levels of bone resorption markers, suggesting a potential serotonin deficiency in these individuals. This serotonin deficiency may disrupt normal bone growth and remodeling processes, leading to the development of spinal deformities.

Animal studies have also provided insights into the role of serotonin signaling dysfunction and conversion in idiopathic scoliosis. For example, Oyama et al. [19] investigated the effects of melatonin and serotonin conversion suppression in scoliosis development in a bipedal mice model. The researchers found that forcing mice into bipedalism in the absence of melatonin (as converted from serotonin) levels resulted in abnormal spinal growth and curvature, resembling the characteristics of idiopathic scoliosis. These findings suggest that serotonin signaling dysfunction can directly impact spinal development and contribute to the pathogenesis of idiopathic scoliosis.

6. Serotonin-melatonin connection in scoliosis

Serotonin and melatonin are two closely related molecules that play important roles in various physiological processes, including sleep regulation and mood. Understanding the metabolic pathways between serotonin and melatonin sheds light on their interplay and the potential consequences of serotonin deficiency or signaling dysfunction on melatonin levels, which may have implications for the development of idiopathic scoliosis.

The synthesis of melatonin begins with the amino acid tryptophan, which is converted into 5-hydroxytryptophan (5-HTP) by the enzyme tryptophan hydroxylase. 5-HTP is then converted into serotonin by the enzyme aromatic amino acid decarboxylase. Serotonin, in turn, serves as the precursor for the synthesis of melatonin in the pineal gland. The conversion of serotonin into melatonin involves several enzymatic steps, including the actions of serotonin N-acetyltransferase (SNAT) and acetylserotonin O-methyltransferase (ASMT).

Serotonin deficiency or signaling dysfunction can lead to melatonin dysfunction through multiple mechanisms. First, reduced levels of serotonin may limit the availability of the precursor molecule for melatonin synthesis, thereby affecting melatonin production. Studies have shown that alterations in serotonin signaling, such as decreased serotonin transporter (SERT) activity, can result in lower levels of serotonin and subsequently impact melatonin synthesis.

Second, serotonin is involved in regulating the activity of enzymes responsible for melatonin synthesis. For example, SNAT, the enzyme responsible for the acetylation of serotonin to form N-acetylserotonin, is regulated by serotonin receptors. Disruptions in serotonin signaling can impair the activity of SNAT and lead to reduced melatonin synthesis. Additionally, ASMT, the enzyme responsible for the final step of melatonin synthesis, is also regulated by serotonin receptors. Altered serotonin signaling can influence ASMT activity and contribute to melatonin dysfunction.

Melatonin dysfunction, resulting from serotonin deficiency or signaling dysfunction, may have implications for the development of idiopathic scoliosis. Melatonin is involved in the regulation of bone metabolism and growth, including the regulation of osteoblast and osteoclast activity. Studies have suggested that melatonin influences the balance between bone formation and resorption, and disruptions in melatonin levels or signaling may affect skeletal development.

In idiopathic scoliosis, alterations in melatonin levels and melatonin receptor expression have been observed. For example, some studies have reported lower melatonin levels in patients with idiopathic scoliosis compared to healthy controls. Melatonin receptors, particularly MT2 receptors, have also been found to be altered in individuals with idiopathic scoliosis. These findings suggest a potential link between melatonin dysfunction and the development of spinal deformities.

The exact mechanisms by which melatonin dysfunction contributes to idiopathic scoliosis are not fully understood. However, melatonin’s role in bone metabolism, its influence on osteoblast and osteoclast activity, and its potential effects on skeletal growth and development provide a plausible connection between melatonin dysfunction and spinal deformities observed in idiopathic scoliosis.

In summary, serotonin deficiency or signaling dysfunction can lead to melatonin dysfunction through various mechanisms, including reduced availability of serotonin as a precursor molecule and alterations in the activity of enzymes involved in melatonin synthesis. Melatonin dysfunction, in turn, may have implications for the development of idiopathic scoliosis due to its involvement in bone metabolism and skeletal development [20]. Further research is needed to elucidate the precise mechanisms underlying the relationship between serotonin, melatonin, and idiopathic scoliosis and explore potential therapeutic interventions targeting these pathways.

7. Diagnostic laboratory testing for serotonin

Serotonin, a neurotransmitter involved in mood regulation and various physiological processes, has garnered significant interest in clinical and research settings. Serotonin lab testing plays a crucial role in diagnosing and monitoring conditions related to serotonin imbalance. This article aims to provide an overview of the different types of serotonin lab tests available, as well as discuss their reliability and validity in assessing serotonin levels.

7.1 Types of serotonin lab tests

Blood Serotonin Level Testing: Blood tests are commonly used to measure serotonin levels. These tests involve drawing a blood sample, typically from a vein in the arm, which is then analyzed to determine the concentration of serotonin. The most commonly used method is high-performance liquid chromatography (HPLC), which separates and quantifies serotonin molecules. Blood serotonin level testing offers a relatively straightforward and accessible option for evaluating serotonin levels.

7.2 Platelet serotonin level testing

Platelets contain significant amounts of serotonin and are used as a surrogate measure of serotonin levels. Platelet serotonin level testing involves collecting a blood sample and isolating the platelets to measure their serotonin content. This testing can provide insight into serotonin uptake and storage mechanisms [20].

7.3 Urine serotonin level testing

Urinary serotonin lab testing is an important diagnostic tool used to assess serotonin levels in various clinical contexts. It involves measuring serotonin or its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in urine samples. This type of testing provides valuable information about serotonin metabolism and can be utilized in both indirect and direct forms [21].

7.4 Indirect urinary serotonin testing

Indirect urinary serotonin testing involves measuring the levels of serotonin metabolites, such as 5-HIAA, in the urine. 5-HIAA is the major metabolite of serotonin and reflects the breakdown and excretion of serotonin in the body. Indirect testing is commonly used to evaluate serotonin production and metabolism in conditions associated with serotonin overproduction, such as carcinoid syndrome and certain types of neuroendocrine tumors [22].

The most common method for indirect urinary serotonin testing is the 24-hour urine collection. During this test, the patient collects all urine produced over a 24-hour period, which provides a cumulative measure of serotonin metabolites. The collected sample is then analyzed to measure the concentration of 5-HIAA. Elevated levels of 5-HIAA may indicate increased serotonin production or impaired metabolism.

7.5 Direct urinary serotonin testing

Direct urinary serotonin testing involves measuring the actual serotonin levels in urine. Unlike indirect testing, direct testing provides information about the actual concentration of serotonin, rather than its metabolites. Direct testing is useful in assessing serotonin excretion and can be employed in research settings or specific clinical situations.

Direct urinary serotonin testing typically involves using high-performance liquid chromatography (HPLC) or similar analytical techniques to separate and quantify serotonin molecules in the urine sample. This method provides a direct measurement of serotonin levels, allowing for a more accurate assessment of serotonin status.

7.6 Interpretation and clinical considerations

Urinary serotonin testing, both indirect and direct, can offer valuable insights into serotonin metabolism and associated disorders. Elevated levels of serotonin or its metabolites, such as 5-HIAA, can indicate conditions such as carcinoid syndrome, which is characterized by excessive serotonin production by neuroendocrine tumors. Monitoring urinary serotonin levels can help assess treatment efficacy and disease progression in these cases.

It is important to consider various factors that may influence urinary serotonin levels, such as dietary intake, medications, stress, and physical activity. Certain foods, such as bananas, pineapples, and walnuts, contain serotonin precursors and may temporarily elevate urinary serotonin levels. Medications, including selective serotonin reuptake inhibitors (SSRIs) and other serotonin-modulating drugs, can also affect serotonin levels.

Furthermore, it is essential to interpret urinary serotonin test results in the context of the individual patient’s clinical presentation and medical history. Diagnostic decisions should be made in conjunction with other diagnostic measures and in consultation with healthcare professionals experienced in serotonin-related disorders.

8. Reliability and validity of serotonin lab testing

Reliability and validity are essential considerations when evaluating the usefulness of serotonin lab testing.

Serotonin lab tests generally demonstrate good reliability, particularly when performed by reputable laboratories using standardized protocols. However, it is important to ensure proper sample collection, handling, and storage to maintain accuracy. Factors such as stress, medications, and diet can also influence serotonin levels, so proper preparation and standardized conditions are crucial for reliable results.

Serotonin lab tests are valid indicators of serotonin levels in the tested samples. However, it is important to note that measuring serotonin levels in peripheral samples (blood, platelets, urine) may not always reflect central serotonin levels in the brain, as serotonin cannot easily cross the blood-brain barrier. Therefore, peripheral serotonin measurements may not directly correlate with neurotransmitter activity in the brain.

Serotonin lab testing provides valuable information for assessing serotonin levels and aiding in the diagnosis and management of various serotonin-related conditions. Blood serotonin level testing, platelet serotonin level testing, and urine serotonin level testing are among the commonly employed options. These tests generally demonstrate good reliability when conducted under standardized conditions. While they are valid measures of peripheral serotonin levels, it is important to interpret results cautiously, as peripheral levels may not always reflect central serotonin activity. Clinical interpretation should consider a comprehensive assessment of symptoms, medical history, and other diagnostic measures. Consulting with healthcare professionals and specialized laboratories can provide guidance on appropriate serotonin lab testing and its application in specific clinical contexts.

9. Serotonin treatment considerations

Serotonin, a neurotransmitter that plays a crucial role in mood regulation and overall well-being, has garnered significant interest in the field of healthcare. Imbalances in serotonin levels have been associated with various mental health conditions. Various treatment options have been reported for serotonin imbalances, including pharmaceutical interventions, dietary supplements, food-based approaches, and lifestyle modifications.

9.1 Pharmaceutical options

Selective Serotonin Reuptake Inhibitors (SSRIs): SSRIs are commonly prescribed medications that work by increasing serotonin levels in the brain. Examples include fluoxetine (Prozac), sertraline (Zoloft), and escitalopram (Lexapro). SSRIs are widely used in the treatment of depression, anxiety disorders, and other mood-related conditions.

Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): SNRIs, such as venlafaxine (Effexor) and duloxetine (Cymbalta), not only increase serotonin but also affect norepinephrine levels. They are prescribed for conditions like major depressive disorder, generalized anxiety disorder, and fibromyalgia.

Tricyclic Antidepressants (TCAs): TCAs, such as amitriptyline and nortriptyline, have been used to treat depression and chronic pain conditions. While they primarily affect norepinephrine and serotonin, they have a broader impact on various neurotransmitters.

9.2 Dietary supplement options

5-Hydroxytryptophan (5-HTP): 5-HTP is an amino acid precursor to serotonin. It is commonly derived from the seeds of Griffonia simplicifolia. Supplementing with 5-HTP may increase serotonin production. However, caution should be exercised, as high doses can have adverse effects and interact with other medications.

St. John’s Wort: St. John’s Wort is an herbal supplement that has been used successfully to alleviate symptoms of depression [23]. Its exact mechanism of action is not fully understood, but it is believed to increase serotonin levels. It may interact with other medications [24], so consultation with a healthcare professional is essential.

9.3 Food-based options

Tryptophan-Rich Foods: Tryptophan is an essential amino acid involved in serotonin synthesis. Consuming foods rich in tryptophan, such as turkey, eggs, nuts, and seeds, may support serotonin production. However, the impact of dietary tryptophan on serotonin levels is influenced by various factors, including the presence of other amino acids in the diet.

Complex Carbohydrates: Consuming complex carbohydrates, such as whole grains, legumes, and fruits, can help regulate serotonin levels. These foods increase insulin levels, which promotes the absorption of amino acids other than tryptophan, allowing tryptophan to enter the brain more readily and support serotonin synthesis.

9.4 Lifestyle options

Lifestyle options are aimed at improving the intrinsic production of serotonin. All of the lifestyle recommendations listed below have been shown to improve serotonin levels in individuals.

Exercise: Regular physical exercise has been shown to increase serotonin levels and improve mood. Engaging in aerobic exercises like jogging, cycling, or swimming can have positive effects on serotonin synthesis and release [25].

Sunlight Exposure: Sunlight exposure stimulates the production of serotonin. Spending time outdoors, particularly in the morning or early afternoon, can enhance serotonin levels. Light therapy using special lamps may also be beneficial for individuals with seasonal affective disorder (SAD) [26].

Stress Management and Relaxation Techniques: Chronic stress can deplete serotonin levels. Implementing stress management techniques like meditation, yoga, deep breathing exercises, and mindfulness practices can help reduce stress and support serotonin balance.

Essential Oils: A study by Schneider [27] showed that 3 to 6 deep and slow inhalations using a specially designed essential oil inhaler increased urinary serotonin output and decreased cortisol output.

Since patients with a history of adolescent idiopathic scoliosis are known to exhibit neurological symptoms [12] consistent with serotonin dysfunction, [28] efforts to recommend lifestyle interventions that are easy to incorporate may promote healthier habits, as well as to improve serotonin utilization.

10. Impact of serotonin treatment on scoliosis outcomes

Although serotonin is thought to play a central role in the onset and progression of idiopathic scoliosis, few studies have attempted to evaluate the impact of serotonin imbalances on the clinical outcomes of scoliosis-specific therapy, such as physiotherapy, bracing, or surgical techniques. One such study by Morningstar et al. [29] evaluated the impact of assessing urinary neurotransmitters, including serotonin, in adolescents who had completed a short course of scoliosis-specific intensive physiotherapy. The entire cohort was divided into 2 groups: Group 1 did not pursue treatment recommendations for improving the neurotransmitter results, and Group2, who did. After 6 months, Group 2 had significantly better clinical outcomes, including Cobb angle measurements, compared to Group 1. This study demonstrates the tangible scoliosis benefits to improving serotonin levels.

11. Conclusions

In conclusion, emerging evidence suggests a potential link between serotonin and idiopathic scoliosis. Genetic associations, altered serotonin levels, and the effects of serotonin-related medications have been investigated, highlighting the involvement of serotonin signaling abnormalities in the development and progression of idiopathic scoliosis. However, further research is necessary to elucidate the underlying mechanisms and to explore the clinical implications of these findings.

Conflict of interest

The author declares no conflict of interest.