Fibrilación cardíaca o palpitaciones

5-HTP is the direct biosynthetic precursor to serotonin, and serotonin signaling dysfunction has been implicated in AIS pathogenesis. Research shows AIS patients tend to have decreased serotonin levels, and serotonin pathway gene polymorphisms (TPH1) are associated with AIS. Animal studies in pinealectomized chickens showed 5-HTP administration prevented scoliosis development, and clinical neurotransmitter research supports 5-HTP as an adjunct in addressing serotonin deficiency in AIS patients.

Alpha-linolenic acid (ALA), a plant-based omega-3 fatty acid, contributes to systemic anti-inflammatory pathways relevant to scoliosis-related spinal inflammation, connective tissue integrity, and neurological function supporting postural control. It is included in scoliosis nutrition protocols alongside EPA and DHA as part of omega-3 supplementation for reducing inflammation around spinal joints and discs.

Boswellic acids (from Boswellia serrata resin) are potent anti-inflammatory compounds that specifically inhibit 5-lipoxygenase and leukotrienes, reducing inflammation in spinal joints and musculoskeletal tissues relevant to scoliosis-related pain and stiffness. They are cited in scoliosis-specific holistic treatment protocols for supporting comfort and joint health in patients with spinal curvature.

Calcium is essential for bone mineralization and density, and low BMD is a recognized prognostic factor for scoliosis curve progression in AIS. Multiple studies show 27–65% of AIS patients have osteopenia or osteoporosis. A randomized interventional trial combining calcium (600 mg/day) with vitamin D and melatonin showed positive effects on curve progression. Calcium deficiency in AIS patients was confirmed by a meta-analysis showing lower serum calcium in AIS vs. controls.

Abnormal collagen composition and distribution in paraspinal muscles has been directly implicated as a contributing factor in idiopathic scoliosis curve initiation and progression. Studies of scoliotic rats demonstrate that TGF-β1–mediated collagen hyperplasia in paraspinal muscles generates asymmetric spinal tension, promoting curvature. Collagen supplementation is used to support spinal connective tissue integrity in scoliosis management.

Curcumin, the active compound in turmeric, is a potent anti-inflammatory agent that reduces joint, disc, and muscular inflammation associated with scoliosis—particularly back pain and stiffness in adult/degenerative scoliosis. It is included in scoliosis management protocols for reducing pro-inflammatory cytokines relevant to disease progression pathways, and is noted in scoliosis-specific clinical nutrition reviews.

Magnesium is an essential cofactor in over 300 enzymatic reactions including ATP-dependent processes in osteoblasts, helps stabilize hydroxyapatite crystals, and controls PTH release. Nutritional deficiency in magnesium is identified in AIS patients alongside calcium and zinc, contributing to reduced bone formation and increased osteoclastic activity. It is consistently cited in scoliosis-focused nutrition literature and multisystem AIS reviews.

Melatonin deficiency has been extensively studied in adolescent idiopathic scoliosis (AIS) pathogenesis, with low melatonin levels correlating with progressive scoliosis. An animal model (pinealectomized chickens) established a scoliosis-inducing effect of melatonin deficiency. A clinical study of 40 AIS patients showed oral melatonin (3 mg) stabilized scoliosis in 12 of 16 patients with low melatonin levels. A randomized Romanian trial combining melatonin (1.5 mg/day) with calcium and vitamin D showed positive effects on curve progression.

Omega-3 fatty acids reduce systemic inflammation affecting connective tissue integrity, joint health, and neurological function related to postural control—all relevant to scoliosis management. They are consistently included in scoliosis-specific nutrition protocols and cited in both practitioner clinical reviews and institutional scoliosis centers as important adjuncts for reducing spinal inflammation and supporting quality of life.

Selenium deficiency has been linked to elevated osteopontin (OPN) levels, which can impair bone health. A study cited in a US patent (US10073101) for scoliosis prevention/treatment, and a Wiley InterScience-referenced study, found many idiopathic scoliosis patients have low selenium and high OPN. Supplementation with 200 mcg/day as L-selenomethionine has been proposed to lower OPN and slow curve progression, though a Chinese cohort study also found high environmental selenium was a risk factor, indicating a complex dose-dependent relationship.

Vitamin C is a required cofactor for collagen synthesis via hydroxylation of proline and lysine residues, directly supporting the structural integrity of spinal connective tissues, ligaments, and intervertebral discs in scoliosis. It also acts as an antioxidant protecting bone cells from oxidative damage. It is consistently cited in scoliosis nutrition protocols for supporting muscles and connective tissue that maintain spinal structure.

Multiple peer-reviewed studies and meta-analyses show that vitamin D deficiency is significantly prevalent in adolescent idiopathic scoliosis (AIS) patients, negatively correlating with bone mineral density and positively correlating with Cobb angle severity. A 2023 meta-analysis (6 studies, 1,428 patients) found vitamin D insufficiency in ~36% and deficiency in ~41% of AIS patients. A Romanian randomized interventional trial (2017–2020) demonstrated that daily supplementation with vitamin D (2,000 IU), calcium, and melatonin positively affected curve progression in children aged 7–16 with idiopathic scoliosis.

Vitamin K is integral to bone metabolism through its role as cofactor for gamma-carboxylation of osteocalcin and matrix GLA protein, both essential for bone mineralization and calcium regulation. In scoliosis, vitamin K2 deficiency is identified as part of a cluster of nutritional deficiencies contributing to low BMD and elevated metabolic risk. It is recommended alongside vitamin D and calcium in AIS management.

Zinc is a structural cofactor for alkaline phosphatase, which deposits hydroxyapatite during bone formation, and is required for osteoblast development and collagen production. Studies link zinc deficiency in AIS patients to delayed bone development and reduced peak bone density. It is also cited in context of abnormal trace element levels in idiopathic scoliosis patients.