HBOT Lengthens Telomeres and Reduces Immune Senescence in Older Adults (Prospective Study)

Key Finding

In a prospective pre–post study with healthy adults aged ≥64 years, a 3-month HBOT program (60 sessions, 2 ATA, 100% O₂, 90 min, 3×5-min air breaks) resulted in >20% longer telomeres in helper T cells, cytotoxic T cells, NK cells, and B cells, along with a marked reduction of senescent T cells (e.g., CD4⁺CD28⁻ −37.3% post HBOT).
Measurement time points: baseline, session 30, session 60, 10–14 days post HBOT. (PubMed / Aging-US)

Study Design & Protocol

• Design: Prospective, single-arm, pre–post study

• Location: Shamir (Assaf-Harofeh) Medical Center / Sagol Center for HBOT, Israel

• Participants: 35 enrolled; 30 completed HBOT; telomere analysis n=25, senescence n=20 (quality/cell count)

• HBOT: 60 sessions (~3 months), 2 ATA, 100% O₂, 90 min, 3×5 min air breaks; multiplace chamber

• Blood sampling: baseline, session 30, session 60, 10–14 days post (Aging-US)

Methods (Summary)

• Telomere length: Flow-FISH (PNA probe), subsets: CD4⁺, CD8⁺, CD56⁺, CD19⁺; relative to reference cell line

• Immune senescence: Proportion of CD28-negative CD4⁺/CD8⁺ T cells (flow cytometry)

• Additional marker: Intracellular HIF-1α to validate adaptive response (Aging-US)

Results (Key Numbers)

Telomeres

• B cells: +25.7% (S30; p=0.007), +29.4% (S60; p=0.0001), +37.6% (post; p=0.007)

• Helper T cells: +21.7% (S30; p=0.042), +23.7% (S60; p=0.012), +29.3% (post; p=0.005)

• Cytotoxic T cells: +24.1% (S60; p=0.0019), +19.6% (post; p=0.023)

• NK cells: +20.6% (S60; p=0.013); +22.2% post (p=0.06)

Immune Senescence

• CD4⁺CD28⁻: −37.3% post (p<0.0001); S30 −19.7% (p=0.09), S60 −11.7% (p=0.20)

• CD8⁺CD28⁻: −12.2% (S30; p<0.0001), −9.8% (S60; p=0.002), −11.0% (post; p=0.0004)

HIF-1α: Increased up to session 60 (10.5 → 19.7; p=0.006), partially normalized 2 weeks post (Aging-US)

Interpretation (Simplified)

HBOT induced strong, measurable anti-aging signals in the immune system: telomere lengthening across multiple lymphocyte subsets and a reduction in senescent T cells. This supports a hormetic adaptation mechanism (the hyperoxic-hypoxic paradox) with potential relevance for healthy aging.
Limitations: single-arm design, reduced sample sizes for some analyses, short follow-up. (PubMed / Aging-US)