Could HBOT Help With Diabetes and Diabetic Wound Healing?

By OxyPlus — Newcastle's Specialist Hyperbaric Oxygen Therapy Clinicoxyplus.co.uk | Updated August 2026 | 8 min read

Diabetes is one of the most prevalent chronic conditions in the UK, affecting over 4.3 million people, with a further 850,000 estimated to be living with undiagnosed type 2 diabetes. For many people with diabetes, the complications that develop over years are as challenging as the condition itself, and among the most serious of those complications is what happens to wounds.

Diabetic foot ulcers affect an estimated 15–25% of diabetic patients at some point in their lives. They are notoriously difficult to heal. They become infected. They deepen. And in the most serious cases, they lead to amputation, diabetes is the leading cause of non-traumatic lower limb amputation in the UK.

Hyperbaric oxygen therapy (HBOT) has been used as an adjunct to standard diabetic wound care for decades. It is one of the longer-standing clinical applications of HBOT, with a research base that includes multiple randomised controlled trials, systematic reviews, and meta-analyses. But the evidence picture is genuinely nuanced - more so than some clinic websites acknowledge - and this post will reflect that honestly.

At OxyPlus, our HBOT clinic in Newcastle, we work with clients managing diabetes and its complications. Here is what the evidence actually shows.

Why Diabetes Makes Wounds So Difficult to Heal

To understand why HBOT is relevant to diabetic wound healing, you need to understand what diabetes does to the body's healing capacity - because it disrupts almost every step of the normal healing process.

Peripheral Neuropathy and Unnoticed Injury

Diabetic peripheral neuropathy (damage to the nerves in the feet and lower limbs) causes loss of protective sensation, causing unnoticed repetitive injuries. A small cut, blister, or pressure sore that a person without diabetes would notice and address can go undetected in someone with neuropathy for days or weeks, by which time infection has often taken hold.

Vascular Insufficiency and Tissue Hypoxia

Both microvascular and macrovascular complications of diabetes reduce tissue perfusion and hinder angiogenesis. The small blood vessels that supply peripheral tissue - particularly in the feet and lower legs - are damaged by chronically elevated blood glucose, reducing the circulation that brings oxygen and immune cells to healing tissue.

The result is wound hypoxia: the tissue surrounding a diabetic wound is already running on a depleted oxygen supply, which means the cells responsible for repair cannot function adequately. Wound hypoxia is well documented in non-healing wounds, representing the strongest risk factor in those patients. Wound healing is oxygen dependent and is limited by its availability at the cellular level.

Impaired Immune Function

Elevated blood glucose impairs the function of white blood cells, particularly neutrophils, that normally clear bacterial infection from wounds. Combined with the vascular insufficiency that limits their delivery to the wound site, diabetic wounds are significantly more vulnerable to infection and significantly less able to clear it once established.

The Non-Healing Cycle

These factors combine into a self-reinforcing cycle: the wound cannot heal because it lacks oxygen; it lacks oxygen because the vasculature is damaged; the damaged vasculature cannot regenerate because angiogenesis requires oxygen; the wound becomes infected because immune cells cannot reach it; infection deepens the tissue damage. Most diabetic foot ulcers do not heal with conventional methods of wound care and progress to become chronic, non-healing ulcers with high morbidity, mortality, and economic stakes.

How HBOT Addresses the Root Problem

The logic for HBOT in diabetic wound healing is direct. If the core problem is tissue hypoxia (an oxygen deficit in healing tissue that disrupts every stage of repair) then dramatically increasing the oxygen available to that tissue is a mechanistically coherent response.

At 2.0–2.5 ATA with 100% oxygen, plasma oxygen levels rise to approximately 15–20 times normal. This oxygen dissolves directly into plasma and tissue fluid, reaching hypoxic wound tissue through diffusion even when the vascular supply is too damaged to carry adequate oxygen via red blood cells.

Patients with chronic ulcers treated with HBOT show several positive physiological changes, including enhanced angiogenesis, improved collagen synthesis, increased white blood cell activity, and reduced swelling. HBOT improves local tissue oxygenation, mitigates hypoxia, and enhances transcutaneous oxygen pressure levels. The antimicrobial properties of HBOT reduce infection risk, expedite healing, and prevent amputation.

The specific mechanisms include:

Angiogenesis - HBOT stimulates vascular endothelial growth factor (VEGF) and other angiogenic signals, driving the formation of new blood vessels into the wound bed. HBOT increases the oxygen gradient between the centre and periphery of the wound, causing significant angiogenic stimulation, which results in increased neovascularisation and fibroblast proliferation. This is not just about the acute session, the new vessels persist after treatment, restoring the structural basis for sustained wound oxygenation.

Collagen synthesis - fibroblasts, the cells responsible for laying down the structural protein that gives healed tissue its integrity, are highly oxygen-dependent. In a hypoxic diabetic wound, fibroblast function is impaired. HBOT restores the oxygen environment they need to proliferate and synthesise collagen effectively. HBOT is essential for promoting neovascularisation, stimulating fibroblast and keratinocyte migration, promoting optimum collagen deposition, and reducing oedema, blood viscosity, and inflammatory reactions.

Antimicrobial effects - oxygen-rich tissue is hostile to anaerobic and facultative bacteria. HBOT's anti-infective action - both by directly inhibiting anaerobic bacterial growth and by restoring leukocyte bactericidal function - addresses one of the most serious threats to diabetic wound healing. HBOT can also inhibit anaerobic bacteria and reduce the use of antibiotics.

Oedema reduction - HBOT causes mild vasoconstriction of healthy blood vessels while maintaining oxygen delivery to damaged tissue, reducing the swelling and oedema that compress tissue and further impair wound oxygenation.

Metabolic effects - beyond the wound itself, there is emerging evidence that HBOT may improve insulin sensitivity and reduce adipose tissue inflammation in the context of metabolic conditions. Preclinical studies have demonstrated that HBOT enhances insulin sensitivity, reduces adipose tissue inflammation, and modulates lipid metabolism. These systemic metabolic effects may support the broader management of diabetes alongside the local wound healing applications.

What the Clinical Evidence Shows

Systematic Reviews and Meta-Analyses

The majority of studies in a 2024 systematic review indicated reduced major amputation rates, improved ulcer healing rates, and decreased ulcer size and depth with HBOT compared to standard care. HBOT treatments typically consisted of 20 to 40 sessions, each lasting 60 to 120 minutes at pressures of 2.0 to 2.5 ATA.

A meta-analysis published in Scientific Reports - drawing on 14 studies including 12 randomised controlled trials and covering 768 participants - found that HBOT was significantly effective in complete healing of diabetic foot ulcers (OR = 0.29; 95% CI 0.14–0.61) and reduction of major amputation (RR = 0.60; 95% CI 0.39–0.92). Many favourable physiological changes, such as augmented angiogenesis, improved collagen deposition, leukocyte activities, and decreased oedema were reported among patients treated with HBOT.

A reduction in major amputation risk of 40% relative to standard care alone, across 12 randomised controlled trials, is a clinically significant finding. For people facing the prospect of limb loss, this evidence is meaningful.

A 2025 network meta-analysis found that HBOT was superior to standard of care for wound area reduction, with greater area reduction in diabetic foot ulcers treated with HBOT when the treatment duration exceeded six weeks.

The Amputation Prevention Evidence

The amputation prevention data is, in some respects, the most compelling aspect of the clinical evidence. Meta-analyses confirmed that HBOT reduced healing time, increased healing rates, and decreased major amputation risks.

The human cost of a major amputation, the loss of function, independence, psychological impact, and mortality risk in the years following, is profound. If HBOT substantially reduces the probability of that outcome in appropriately selected patients, it deserves serious consideration as part of the clinical pathway.

What the Evidence Is Honest About

The evidence for HBOT in diabetic foot ulcers is more established than in many other HBOT applications - but it is not without its complexities, and intellectual honesty requires addressing them.

The evidence is mixed across different wound grades and patient populations. HBOT improved wound healing duration in diabetic foot ulcers of lower severity grades; however, this was statistically significant only for grade 1 ulcers because of the small sample size in the HBOT group. The evidence is strongest for more severe ulcers (Wagner grades 3 and above) where standard care consistently fails.

Some studies show increased adverse events. Some studies noted increased adverse events associated with HBOT, despite overall benefits in wound healing and reduction in major amputation rates. This is why patient selection matters - not every patient with a diabetic foot ulcer is an appropriate HBOT candidate, and a thorough clinical assessment is essential.

Study heterogeneity limits definitive conclusions. Different trials have used different protocols, patient populations, and outcome measures, making direct comparison difficult. Larger, standardised trials are needed. There is no consistent evidence that HBOT is beneficial for healing diabetic foot ulcers, although it has been associated with reduced rates of minor or major amputations and shorter time to wound healing in some studies. The results are promising, and more trials are needed.

HBOT is an adjunct, not a standalone treatment. Every evidence review frames HBOT as an adjunctive therapy - used alongside standard wound care, infection management, vascular assessment, and blood glucose optimisation. It is not a replacement for any of these.

Who Is Most Likely to Benefit?

Based on the clinical evidence and established criteria used by NHS hyperbaric units and international guidelines, HBOT for diabetic wound healing is most likely to benefit:

People with Wagner grade 3 or higher diabetic foot ulcers - deep ulcers with tendon, capsule, or bone involvement, or with significant infection. This is the population in which the evidence for benefit is strongest and where the alternative — amputation — is most serious.

Those with documented tissue hypoxia - transcutaneous oxygen pressure (TcPO2) measurements below 40 mmHg in the periwound tissue are often used as a criterion for HBOT eligibility in specialist centres. This confirms that the tissue oxygen deficit that HBOT addresses is actually present.

Patients where standard care has been insufficient - chronic, non-healing ulcers that have not responded adequately to conventional wound management over weeks or months.

Those with co-existing vascular insufficiency - where revascularisation has already been attempted or where it is not possible, and tissue hypoxia is the limiting factor in healing.

People preparing for or recovering from amputation-related surgery - HBOT can improve tissue oxygenation pre-operatively to optimise wound closure and post-operatively to support healing of the surgical site.

What About Broader Diabetes Management?

Beyond wound healing specifically, HBOT has potential relevance to some of the broader consequences of diabetes:

Mitochondrial dysfunction - diabetes is associated with impaired mitochondrial function in multiple cell types. HBOT's stimulation of mitochondrial biogenesis may support cellular energy production in tissues affected by diabetic metabolic stress. See our post on HBOT and Mitochondrial Function for the detailed mechanisms.

Inflammation - chronic low-grade systemic inflammation is a feature of both type 1 and type 2 diabetes, contributing to vascular damage and complication risk. HBOT's anti-inflammatory effects - reductions in TNF-α, IL-6, and NF-κB pathway activity - are directly relevant. See our post on How HBOT May Reduce Inflammation.

Peripheral neuropathy - HBOT's ability to improve blood flow to peripheral tissue and reduce neuroinflammation may offer some benefit for diabetic neuropathic symptoms, though the evidence base here is less developed than for wound healing specifically.

Post-surgical recovery - diabetic patients undergoing any surgery have significantly higher wound healing risk than the general population. HBOT as a peri-operative adjunct is well-evidenced for improving outcomes in high-risk surgical patients. See our post on HBOT and Surgery Recovery.

HBOT for Diabetes and Wound Healing at OxyPlus Newcastle

At OxyPlus, Newcastle's specialist HBOT clinic, we work with clients managing diabetes and its complications, including wound healing challenges. Here is how we approach it:

Initial Consultation - We discuss your diabetes history, current wound status, existing treatment, and what investigations have been undertaken. For wound healing cases, we liaise with your GP, diabetologist, or vascular surgeon as appropriate, and we are clear about the cases where HBOT is and is not likely to be beneficial.

Personalised Protocol - Clinical evidence supports courses of 20–40 sessions for diabetic foot ulcers, at 60–120 minutes per session at 2.0–2.5 ATA. As oxygen cannot be stored in tissues, frequent HBOT is required to provide an adequate sustained oxygen environment for healing, which is why consecutive daily sessions (or near-daily) produce the best wound outcomes.

Adjunctive Framework - We always work alongside your existing wound care team. HBOT is most effective when integrated with appropriate debridement, infection management, offloading, and glycaemic control — not instead of them.

Monitoring - We track wound progress throughout the course and communicate openly with you and your clinical team about what is happening.

We are based in Newcastle and serve clients from across the North East - including Gateshead, Sunderland, Durham, Northumberland, and Teesside.

Frequently Asked Questions




Next
Next

Why Athletes Are Using Hyperbaric Oxygen Therapy - and What the Science Says