Hyperbaric oxygen can induce angiogenesis and recover erectile function

Hadanny A, Lang E, Copel L, Meir O, Bechor Y, Fishlev G, Bergan J, Friedman M, Zisman A, Efrati S

International Journal of Impotence Research n = 30 2 ATA 40 sessions

Plain English

Hadanny et al. (2018, International Journal of Impotence Research) is the first published trial to demonstrate mechanism-level vascular repair from HBOT in vasculogenic erectile dysfunction — meaning HBOT was shown not just to improve symptoms, but to drive structural change (new blood vessel formation) in penile tissue. What the trial measured. Two primary clinical outcomes: the International Index of Erectile Function (IIEF) questionnaire and a Global Efficacy Question (GEQ). The objective backbone was perfusion MRI of the corpus cavernosum, measured before and after the protocol — designed to detect angiogenic structural change directly rather than infer it from symptom improvement. Who was studied. Thirty men with documented chronic vasculogenic erectile dysfunction (mean age 59.2 ± 1.4 years; mean ED duration 4.2 ± 0.6 years), with reduced penile blood flow confirmed at baseline. The vasculogenic subtype is critical: ED has multiple etiologies (psychogenic, neurogenic, hormonal, vasculogenic), and HBOT mechanism most directly applies to the vascular subtype. Protocol parameters. Forty daily HBOT sessions at 2.0 ATA, 100% oxygen, 90 minutes per session, 5 days per week — totaling approximately 8 weeks. The protocol mirrors the Israeli group's other 40-session trials (Efrati 2013 stroke, Boussi-Gross 2013 TBI), allowing cross-trial mechanism comparison. Results (verbatim from abstract). HBOT significantly improved all IIEF domains by 15–88% (p < 0.01). The erectile function domain itself improved by 88% (p < 0.0001) — a large effect by any clinical standard. 80% of patients reported a positive outcome on the GEQ. Most importantly, perfusion MRI showed a 153.3% ± 43.2% increase in K-trans values in the corpus cavernosum (p < 0.0001) — direct imaging evidence of angiogenesis (new blood vessel formation). This is the structural-change finding that distinguishes the trial from the broader pharmacological ED literature. Limitations. Sample size (n=30) is small. The trial did not have a sham-control arm, limiting blinding. The cohort was specifically vasculogenic ED — the result does not directly extend to ED of other etiologies. Long-term durability was reported at follow-up but the cohort is too small to establish durability with confidence at scale. What it means in practice. The clinical implication is meaningful: HBOT may treat the vascular root cause of ED rather than just the symptom — distinguishing it from PDE5 inhibitors (sildenafil, tadalafil) which produce on-demand vasodilation without repairing the underlying tissue. For men whose ED is part of broader cardiovascular concerns, this represents a fundamentally different therapeutic approach. The 2.0 ATA protocol requires a clinical chamber; 1.5 ATA home chambers cannot replicate it. How it relates to other indexed trials. Hadanny ED 2018 is mechanistically connected to the broader angiogenesis story across the Saturate site — the same biology underlies Hachmo 2021 (dermal angiogenesis +153% K-trans here vs. +significant blood vessel count in skin), Zhang 2022 (wound healing via angiogenesis), and Bennett 2016 (radiation tissue repair). The vascular thread runs through multiple Saturate condition pages. Source: PubMed PMID 29773856.

Key findings

What the trial documented.

HBOT significantly improved all IIEF domains by 15–88% (p < 0.01); the erectile function domain itself improved by 88% (p < 0.0001)
80% of patients reported a positive outcome on the Global Efficacy Question (GEQ)
Perfusion MRI showed a 153.3% ± 43.2% increase in K-trans values in the corpus cavernosum (p < 0.0001) — direct imaging evidence of angiogenesis
First trial to demonstrate mechanism-level vascular repair (new vessel formation) from HBOT in vasculogenic ED

What the trial measured. Two primary clinical outcomes: the International Index of Erectile Function (IIEF) questionnaire and a Global Efficacy Question (GEQ). The objective backbone was perfusion MRI of the corpus cavernosum, measured before and after the protocol — designed to detect angiogenic structural change directly rather than infer it from symptom improvement.

Who was studied. Thirty men with documented chronic vasculogenic erectile dysfunction (mean age 59.2 ± 1.4 years; mean ED duration 4.2 ± 0.6 years), with reduced penile blood flow confirmed at baseline. The vasculogenic subtype is critical: ED has multiple etiologies (psychogenic, neurogenic, hormonal, vasculogenic), and HBOT mechanism most directly applies to the vascular subtype.

Protocol parameters. Forty daily HBOT sessions at 2.0 ATA, 100% oxygen, 90 minutes per session, 5 days per week — totaling approximately 8 weeks. The protocol mirrors the Israeli group’s other 40-session trials (Efrati 2013 stroke, Boussi-Gross 2013 TBI), allowing cross-trial mechanism comparison.

Results (verbatim from abstract). HBOT significantly improved all IIEF domains by 15–88% (p < 0.01). The erectile function domain itself improved by 88% (p < 0.0001) — a large effect by any clinical standard. 80% of patients reported a positive outcome on the GEQ. Most importantly, perfusion MRI showed a 153.3% ± 43.2% increase in K-trans values in the corpus cavernosum (p < 0.0001) — direct imaging evidence of angiogenesis (new blood vessel formation). This is the structural-change finding that distinguishes the trial from the broader pharmacological ED literature.

Limitations. Sample size (n=30) is small. The trial did not have a sham-control arm, limiting blinding. The cohort was specifically vasculogenic ED — the result does not directly extend to ED of other etiologies. Long-term durability was reported at follow-up but the cohort is too small to establish durability with confidence at scale.

What it means in practice. The clinical implication is meaningful: HBOT may treat the vascular root cause of ED rather than just the symptom — distinguishing it from PDE5 inhibitors (sildenafil, tadalafil) which produce on-demand vasodilation without repairing the underlying tissue. For men whose ED is part of broader cardiovascular concerns, this represents a fundamentally different therapeutic approach. The 2.0 ATA protocol requires a clinical chamber; 1.5 ATA home chambers cannot replicate it.

How it relates to other indexed trials. Hadanny ED 2018 is mechanistically connected to the broader angiogenesis story across the Saturate site — the same biology underlies Hachmo 2021 (dermal angiogenesis +153% K-trans here vs. +significant blood vessel count in skin), Zhang 2022 (wound healing via angiogenesis), and Bennett 2016 (radiation tissue repair). The vascular thread runs through multiple Saturate condition pages.

Source: PubMed PMID 29773856.

Protocol used

2.0 ATA, 100% oxygen, 90-minute sessions, 5 days/week for 40 sessions

Full citation

Hadanny A, Lang E, Copel L, Meir O, Bechor Y, Fishlev G, Bergan J, Friedman M, Zisman A, Efrati S. Hyperbaric oxygen can induce angiogenesis and recover erectile function. International Journal of Impotence Research. 2018.

DOI →