Condition Focus: Human In Vivo NO Release — Deep Tissue Effects at 850nm

Much of the NO evidence for PBM comes from cell cultures, animal models, or indirect measurements. This study from Barolet and colleagues is the first to directly measure NO release from human skin in vivo following PBM at the two wavelengths most relevant to the G.O.A.T.: 660 nm (red) and 850 nm (near-infrared).

The key finding: 850 nm NIR induced significant NO release with a profile indicating deep tissue effects — the NO originated from structures below the skin surface rather than from superficial skin stores. This is consistent with 850 nm’s greater tissue penetration depth compared to 660 nm, and it confirms that NIR PBM reaches the vasculature and deeper tissue layers where vasodilation is needed for joint perfusion.

The 660 nm wavelength also released NO, but primarily from photolysis of superficial NO stores in the skin — a rapid but more localised effect. Together, the two wavelengths provide complementary NO release: 660 nm for immediate surface vasodilation and 850 nm for sustained deep tissue perfusion.

For gout, this complementary depth profile is directly relevant. The MTP joint sits beneath skin, subcutaneous tissue, and the joint capsule. Effective vasodilation for joint perfusion requires NO release at depth — not just at the skin surface. This study confirms that 850 nm PBM achieves exactly that in living human tissue.

G.O.A.T. for Gout Alignment:
This study uses the G.O.A.T.’s exact wavelengths — 660 nm and 850 nm — and demonstrates complementary NO release profiles. The 850 nm deep tissue NO release directly supports the G.O.A.T.’s design rationale: NIR reaches the joint, not just the skin. This is the first human in vivo confirmation of the device’s vascular mechanism.

Link to original research here

Editor’s note: The deep tissue NO release confirmed here is the clinical manifestation of the eNOS/Akt pathway mapped in Yokomizo et al 2022. The capillary flow increase that results from this NO release is measured in the RCT by Gavish et al 2020. The hypoxia-enhanced CCO nitrite reductase function that adds to deep tissue NO production is described in Poyton & Ball 2011. The comprehensive NO signalling review is provided by Keszler et al 2023.

Related Articles

• NIR PBM Augments NO via eNOS Phosphorylation – Yokomizo et al 2022
• Microcirculatory Response to PBM: RCT – Gavish et al 2020
• CCO as Nitrite Reductase: Novel PBM Function – Poyton & Ball 2011
• PBM and Nitric Oxide Signaling – Keszler et al 2023
• PBM Stimulates Lymphatic Contractility and Flow – 2020

Key Takeaways

• First direct human in vivo measurement of NO release following PBM at 660 nm and 850 nm
• 850 nm induces deep tissue NO release — reaches vasculature below the skin surface
• 660 nm releases superficial NO stores — rapid but more localised
• Complementary profiles: surface + deep = comprehensive vasodilation for joint perfusion

Study Overview

Full Citation

Barolet D, et al. (2024). In vivo nitric oxide release from human skin following photobiomodulation. Journal of Photochemistry and Photobiology, 19, 100225. View Publication