20 Years of Growth Hormone May Have Fueled Bone Spurs That Blocked Swallowing

Anterior cervical osteophytes (ACOs) — bony spurs on the front of the vertebral bodies — affect an estimated 20–30% of adults over 60, yet symptomatic dysphagia from esophageal compression remains underdiagnosed. The C3-C6 region is particularly vulnerable because the hypopharynx transitions to the cervical esophagus there, with the esophagus lying in direct apposition to the prevertebral fascia. Most ACO literature focuses on age-related spondylosis or diffuse idiopathic skeletal hyperostosis (DISH); the potential contribution of systemic anabolic factors has rarely been explored.

The patient was a 62-year-old ex-military recreational bodybuilder who presented in January 2025 with cervicalgia and left shoulder pain. His past history included hypertension, lumbar radiculopathy, glenohumeral and acromioclavicular osteoarthritis, rotator cuff tendinitis, and a prior proximal biceps tendon rupture. He reported a cervical hyperextension/hyperflexion injury during Brazilian jiu-jitsu training around 2001–2002. Crucially, he also self-reported approximately 20 years of GH axis stimulation: cyclical somatropin (~2005–2016, 0.4 mg SC up to twice daily), followed by sermorelin plus GHRP-6 (~2016–2019+), and ongoing nightly somatropin at presentation. None of this exposure history was verified through pharmacy records, prescriptions, or laboratory IGF-1 data.

Cervical radiographs showed loss of lordosis, multilevel facet hypertrophy, disc narrowing, and a prominent C3-C4 anterior osteophyte. MRI confirmed esophageal compression at C3-C4, plus moderate-to-severe central canal stenosis at C2-C4 and severe stenosis at C4-C7. On directed questioning, the patient admitted to intermittent dysphagia with large food boluses — a symptom he had not previously volunteered. Symptoms were mild and intermittent without aspiration, weight loss, or dietary restriction. A September 2025 chest x-ray later revealed multiple bony projections along the sternum and diffuse thoracic degenerative changes, raising the possibility of systemic hyperostosis consistent with DISH, though formal Resnick criteria were not applied.

The authors propose a two-hit hypothesis: remote cervical trauma disrupted the anterior longitudinal ligament and periosteum, priming the site for heterotopic bone formation, while decades of GH/IGF-1 axis stimulation — which drives chondrocyte proliferation, endochondral ossification, and periosteal apposition, mirroring the skeletal arthropathy of acromegaly — may have amplified osteophyte growth beyond what aging alone would produce. Conservative management (dietary modification, NSAIDs as needed, home exercise) was initiated; surgical osteophytectomy via an anterior cervical approach was discussed as a future option if symptoms progress. GH cessation and endocrine referral were recommended.

This case is hypothesis-generating rather than confirmatory. Dysphagia was not formally evaluated with barium swallow or videofluoroscopic swallowing study. GH exposure is entirely self-reported. Myelopathy assessment was incomplete despite severe multilevel stenosis. And the skeletal findings could plausibly be explained by age-related spondylosis or DISH alone. Nevertheless, the report makes a clinically important point: patients with cervical spondylosis should be actively screened for dysphagia, and clinicians should routinely inquire about anabolic hormone use as part of the musculoskeletal history.