You’re probably familiar with this clinical picture: shoulder pain that develops gradually, increasing stiffness, worsening nights, and a daily life that’s seriously affected. Adhesive capsulitis—also known as “frozen shoulder”—affects between 2% and 5% of the population. And yet, it remains one of the least understood shoulder conditions.
For a long time, it was treated as a purely mechanical or joint-related issue. Today, science tells us otherwise.
Adhesive capsulitis—commonly known as “frozen shoulder”—is often seen as a simple joint issue. But as highlighted by trusted medical sources like the Mayo Clinic, it is a condition marked by progressive pain, stiffness, and significant limitations in daily life. What’s less commonly discussed, however, is how deeply this condition may be connected to your metabolic and inflammatory health.
What Research Reveals: Much More Than a Stiff Shoulder
A meta-analysis published in 2025 in BMC Musculoskeletal Disorders—a peer-reviewed, indexed journal—analyzed 15 studies involving more than 7,400 people to understand the role of metabolic and inflammatory profiles in adhesive capsulitis (Hamed-Hamed et al., 2025).
The main takeaway is clear: adhesive capsulitis is not just a local shoulder condition. It is a systemic disease, at the intersection of chronic inflammation and metabolic dysfunction.
The biomarkers that stand out
Metabolic side
The most significantly elevated marker in frozen shoulder patients is HbA1c — glycated hemoglobin, which reflects blood sugar levels over 3 months. Not fasting glucose alone, but long-term glycemic control. Why? Because chronic hyperglycemia promotes the accumulation of advanced glycation end products (AGEs), which generate oxidative stress, activate fibroblasts, and lead to excessive collagen deposition in the joint capsule. This is literally the biochemistry of fibrosis. Total cholesterol is also significantly higher in frozen shoulder patients. Dyslipidemia seems to play a role in the inflammatory environment that favors this condition.
Inflammatory side
Two cytokines stand out:
- IL-1β: the most strongly associated with frozen shoulder, playing a central role in fibroblast activation and fibrosis.
- TNF-α: also significantly elevated, sustaining chronic inflammation of the joint capsule.
These mediators are crucial if you work with chronic pain. IL-1β and TNF-α are precisely the pro-inflammatory cytokines involved in central sensitization — the mechanism by which the nervous system amplifies pain signals far beyond the initial injury. It’s no coincidence that frozen shoulder patients often describe disproportionate pain, insomnia, exhaustion, and anxiety: their nervous system is in a state of chronic alert, fueled by systemic inflammation.
The role of leptin: the missing link
The meta-analysis also highlights the role of adipokines, especially leptin. Secreted by adipose tissue, leptin amplifies the production of IL-6, TNF-α, and IL-1β — maintaining a cycle of inflammation and fibrosis. In other words: excess body fat is not neutral in frozen shoulder. It actively fuels the inflammatory fire that “freezes” the shoulder. This is a strong argument for integrating nutrition into management.
What this changes in practice
As a physiotherapist specialized in functional nutrition, this type of data confirms an approach I have long defended: you cannot effectively treat frozen shoulder while ignoring the patient’s metabolic profile. Concretely, this means:
- Assessing glycemic profile (HbA1c, fasting glucose, HOMA-IR if possible) at the initial evaluation.
- Proposing an anti-inflammatory nutritional protocol: reducing fast sugars and pro-inflammatory fats, increasing omega-3s, polyphenols, and antioxidant-rich foods.
- Working on body composition when relevant, especially in cases of associated overweight.
- Educating the patient about the links between diet, metabolism, and pain — because a patient who understands is more engaged in their recovery.
An important — and honest — clarification
This meta-analysis is a serious step forward in understanding frozen shoulder. But as a practitioner, I must be transparent: the authors themselves rate the quality of evidence as “low” according to the GRADE system, due to risk of bias in the included studies (few randomized trials, heterogeneous methodologies). Some biomarkers, such as triglycerides or IL-6, show too much heterogeneity to draw definitive conclusions. This does not discredit the results — but it means we cannot yet establish a direct causal relationship between these biomarkers and frozen shoulder. These are strong associations, not yet proven causality. Prospective studies with standardized methodologies are needed to confirm these findings.
In summary
Frozen shoulder is a systemic, inflammatory, and metabolic condition. HbA1c, cholesterol, IL-1β, and TNF-α are the markers most associated with it. These mechanisms are directly linked to the pathophysiology of chronic pain: low-grade inflammation, central sensitization, and disrupted metabolic environment. Treating the shoulder without addressing the patient’s diet is treating the symptom without addressing the cause.
Reference
Hamed-Hamed D, Rodríguez-Pérez C, Pruimboom L, Navarro-Ledesma S. Influence of the metabolic and inflammatory profile in patients with frozen shoulder – systematic review and meta-analysis. BMC Musculoskelet Disord. 2025;26:475. doi: 10.1186/s12891-025-08706-9
Article written by Sophie Lyon — Physiotherapist DHA, specialized in functional nutrition and chronic pain management — Dubai
If you’re experiencing persistent shoulder pain or stiffness, don’t ignore what your body may be telling you.
Book a consultation today to assess not just your shoulder, but the underlying metabolic and inflammatory factors that may be slowing your recovery.
