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Recovery

Cancer care and radiation recovery

Hyperbaric oxygen is not a cancer treatment. Where it is used in oncology is for tissue damaged by radiotherapy: the bladder, bowel, jaw and breast. A Cochrane review of 18 trials found it may help late radiation injury, and a Nordic randomised trial showed clear improvement in radiation-induced bladder symptoms. Reviews of the safety question have found no evidence that it encourages tumour growth or recurrence.

Evidence so far
Moderate
Reading timeAbout 12 minutes

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Why this is being studied

Radiotherapy saves lives, but months or years afterwards the irradiated tissue can slowly deteriorate as its small blood vessels are lost, leaving bone, bladder, bowel and skin scarred, short of oxygen and unable to heal. Hyperbaric oxygen is not a cancer treatment; its established role is in repairing this late radiation tissue injury by stimulating new capillary growth and restoring the oxygen that repair requires. Reviews of the laboratory and clinical literature have also found no evidence that HBOT encourages tumour growth or recurrence, which matters for anyone with a cancer history considering it.

Where the evidence stands

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The mechanism

What is going on, and why this might help

What is going on in the body

Radiotherapy damages not only tumour cells but also the small blood vessels and connective tissue in the treatment field. Over months to years, capillaries are lost, the tissue becomes fibrotic and chronically hypoxic, and its ability to heal after minor injury collapses. This is the basis of late radiation injury: osteoradionecrosis of the jaw, radiation cystitis with bleeding, radiation proctitis, chronic non-healing wounds in irradiated skin and soft tissue, and failed dental extractions or surgery in the field. The tissue is hypoxic, hypovascular and hypocellular, a triad described by Marx.

Where oxygen comes in

Hyperbaric oxygen delivers dissolved oxygen into tissue that has lost its capillary bed, and the steep oxygen gradient between healthy and irradiated tissue is the stimulus for new vessel growth through VEGF and HIF-1α-mediated angiogenesis. Marx demonstrated that capillary density in irradiated tissue rises over a course of sessions and that this neovascularisation persists for years. Fibroblast proliferation and collagen synthesis recover as oxygen tension rises, and stem-cell mobilisation (Thom 2006) may contribute cells to the regenerating tissue. Reduced fibrosis and inflammation have been seen in animal models. On the tumour-growth safety question: the concern is theoretical, since angiogenesis could in principle feed residual tumour. Systematic reviews of the clinical and animal literature (Feldmeier et al. 2003; Moen and Stuhr 2012) found no evidence that hyperbaric oxygen promotes tumour growth or recurrence, and in some experimental models it inhibited it. Tumour cells are adapted to hypoxia, and normalising oxygen may in fact reduce hypoxia-driven aggressiveness.

How solid is this

Established. Late radiation tissue injury is one of the best-supported indications in hyperbaric medicine, with randomised trials and a Cochrane review supporting benefit in radiation proctitis, cystitis and osteoradionecrosis prevention. Key references: Marx 1990 (angiogenesis in irradiated tissue); Feldmeier 2003 and Moen and Stuhr 2012 (tumour safety reviews).

Explainer illustration

The studies

Every study is laid out the same way: what the researchers wanted to find out, who took part, what they actually did, what they found, why it might work and where the limits are. No jargon, and a link to the original if you want to read it yourself.

Each study is laid out the same way: what the researchers asked, who took part, what they did, what they found, why it might work, and where the limits are. The clinician layer at the end of each one carries the numbers.

Paper 1

Hyperbaric oxygen therapy for late radiation tissue injury

Lin, Bennett et al. · Cochrane Database of Systematic Reviews · 2023 · systematic review of 18 RCTs, n=1,071

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What they asked

Radiotherapy cures or controls many cancers, but months or years later the irradiated tissue can break down: the jaw bone can die (osteoradionecrosis), the bladder and rectum can bleed and become painful, and the skin and soft tissue can fail to heal after surgery. This Cochrane review, led by Lin and Bennett, asked whether hyperbaric oxygen improves these late radiation injuries and whether it can prevent jaw necrosis when teeth are extracted from irradiated bone. HBOT is not a treatment for cancer; its role here is repairing tissue damaged by cancer treatment.

Who took part

Eighteen randomised trials with 1,071 participants, published between 1985 and 2022, covering osteoradionecrosis of the jaw, head and neck soft-tissue injury and surgical wound breakdown, radiation proctitis and radiation cystitis.

What they did

The reviewers searched to January 2022, assessed risk of bias and rated certainty of evidence using GRADE. Protocols were typical of clinical practice: 100 per cent oxygen at 2.0 to 2.5 ATA (most often 2.4) for 90 minutes, once daily, five days a week, for 30 to 40 sessions. For dental extraction, the Marx protocol gives 20 sessions before and 10 after surgery. Some trials used sham pressurisation; many compared HBOT with standard care alone.

What they found

Pooling five trials, HBOT modestly increased the chance of complete or substantial resolution of the injury. Two trials suggested a large reduction in wound breakdown after head and neck surgery in irradiated tissue. Pain from osteoradionecrosis at twelve months was lower with HBOT. HBOT did not reduce death at one year. Temporary short-sightedness was clearly more common, and ear barotrauma was common in trials without sham pressurisation.

Why it might work

Radiation slowly destroys small blood vessels, leaving tissue scarred, short of oxygen and unable to repair itself. Repeated hyperbaric exposures appear to trigger new capillary growth over several weeks, restore the oxygen needed for collagen formation and infection control, and mobilise repair cells. The effect is gradual, which is why courses are long.

Limits

Most trials were small and certainty was rated low to moderate. Results were not uniformly positive: the UK HOPON trial of 144 people found that HBOT before dental extraction from irradiated jaws did not reduce osteoradionecrosis compared with no HBOT, contrary to the much older Marx trial, and the Danish DAHANCA-21 trial was also null. Which patients benefit, and when, is still unclear. Cost-effectiveness was not addressed.

Paper 2

Radiation-induced cystitis treated with hyperbaric oxygen therapy (RICH-ART): a randomised, controlled, phase 2-3 trial

Oscarsson et al. · The Lancet Oncology · 2019 · multicentre randomised controlled trial, n=79

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What they asked

Radiation cystitis is a late complication of pelvic radiotherapy for prostate, cervical, bladder and rectal cancers: the bladder lining becomes fragile and inflamed, causing urgency, frequency, pain and bleeding that can severely disrupt daily life. Earlier evidence for hyperbaric oxygen came mainly from uncontrolled series. Oscarsson and colleagues ran RICH-ART, the first randomised controlled trial, to test whether HBOT improves urinary symptoms compared with standard care.

Who took part

Adults aged 18 to 80 who had completed pelvic radiotherapy at least six months earlier and had troublesome urinary symptoms, defined as a score below 80 on the urinary domain of the Expanded Prostate Cancer Index Composite (EPIC), a validated 0-to-100 questionnaire. Of 223 screened at five Nordic university hospitals, 87 were randomised (42 HBOT, 45 standard care) and 79 were analysed (41 and 38).

What they did

The HBOT group breathed 100 per cent oxygen at 2.4 to 2.5 ATA for 80 to 90 minutes, once daily, for 30 to 40 sessions. The control group continued standard care with no restrictions on medication or other treatment. There was no sham chamber, so participants knew their allocation. The primary outcome was the change in EPIC urinary score from baseline to six to eight months after randomisation.

What they found

The HBOT group improved by an average of 17.8 points on the EPIC urinary scale, compared with 7.7 points in the standard care group, a difference of about 10 points that was statistically significant and above the threshold usually regarded as meaningful to patients. Around 41 per cent of the HBOT group had mild, temporary side effects, mostly short-sightedness and ear pressure symptoms, which resolved. A later long-term follow-up publication reported that symptom relief persisted.

Why it might work

Radiation gradually destroys the fine blood vessels in the bladder wall, leaving it scarred, oxygen-starved and prone to bleeding and inflammation. Repeated exposure to high-pressure oxygen appears to stimulate new capillary growth in this tissue over weeks, improving oxygen supply and allowing the lining to repair. The improvement builds during and after the course rather than appearing immediately.

Limits

The trial was open-label, so participants and clinicians knew who received HBOT, and the primary outcome was self-reported; expectation may contribute to a symptom difference of this size. Only 79 people were analysed and recruitment stopped short of the planned number, reducing power for secondary outcomes. Objective measures such as cystoscopy findings were not the primary endpoint. Results apply to people with established, symptomatic cystitis in specialist centres. Funding came from Swedish regional research funds and a cancer charity.

Paper 3

Hyperbaric oxygen therapy and cancer: a review

Moen and Stuhr · Targeted Oncology · 2012 · systematic literature review of tumour-growth safety

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What they asked

A long-standing worry has held back hyperbaric oxygen in people with a cancer history: since tumours need blood vessels and oxygen to grow, could flooding the body with oxygen feed a cancer or wake up dormant cells? Moen and Stuhr at the University of Bergen reviewed the research from 2004 to 2012 to answer two questions: does HBOT promote tumour growth or recurrence, and does it have any effect of its own on cancer or on how well radiotherapy and chemotherapy work.

Who took part

This is a literature review of 28 studies identified through PubMed. Most were laboratory experiments in cell cultures or animals, particularly rodent models of breast cancer; a smaller number were clinical studies, mainly of HBOT alongside radiotherapy in cervical, bladder, head and neck and brain tumours.

What they did

The authors grouped findings by tumour type and by the question asked: effect of HBOT alone, HBOT combined with radiotherapy, and HBOT combined with chemotherapy. Experimental protocols varied widely, from single exposures to repeated daily sessions at 1.5 to 2.5 ATA, which limits direct comparison.

What they found

They found no evidence that hyperbaric oxygen stimulates tumour growth or increases recurrence. In several animal breast cancer models HBOT actually slowed growth, increased programmed cell death and reduced blood vessel density, although no human trials of HBOT for breast cancer exist. Prostate cancer models showed no change. Older clinical trials using HBOT during radiotherapy for cervical and bladder cancer showed no improvement in outcome, while a meta-analysis of hypoxia-modifying strategies suggested HBOT was the most effective radiosensitiser studied, with caveats. Some studies showed chemotherapy worked better when given with or just after HBOT.

Why it might work

Tumours are often hypoxic at their core, and hypoxia drives aggressive behaviour and resistance to treatment. Raising oxygen for a short period may push tumour cells towards a less aggressive, more organised state, generate reactive oxygen species that damage cells with weak antioxidant defences, and increase the effectiveness of radiation and some drugs. Crucially, HBOT did not increase new vessel formation in tumours the way it does in injured normal tissue.

Limits

This is a narrative review of mostly animal and cell data; animal results often fail to translate to people. Only 28 studies were included and their designs differ greatly. Certain chemotherapy drugs (doxorubicin, bleomycin, cisplatin among them) may become more toxic with HBOT, so timing matters and concurrent use is avoided. The authors call for properly randomised human studies. Nothing here suggests HBOT should be used as a cancer treatment.