Spektrum,
seřazené podle důkazů.
Fotobiomodulace – obor, který zkoumá, jak světlo proměňuje biologii – se opírá o více než půl století výzkumu. Publikovanou vědu jsme níže uspořádali tak, jak světlo čte REDelios: vlnovou délku po vlnové délce, od ultrafialové signalizace až po hlubokou energii blízkého infračerveného světla.
Každá vlnová délka
nese vlastní důkazy.
Vyberte vlnovou délku a přečtěte si, jakou hraje biologickou roli, jak hluboko proniká do tkáně a které studie ji zkoumaly.
Vlnová délka povrchového „rozzáření“ – červené světlo pohlcené v horní vrstvě kůže, ležící poblíž červeného píku cytochrom c oxidázy okolo ~620nm a spojované s tónem, jasem a podporou kolagenu.
Deconvolved cytochrome-c-oxidase action spectra place a red absorption maximum near 620nm — the band 630nm sits on.
LabKaru & Kolyakov · Photomedicine and Laser Surgery · 2005
Polychromatic red/NIR raised intradermal collagen density and reduced fine lines in a controlled trial.
RCTWunsch & Matuschka · Photomedicine and Laser Surgery · 2014
Každá studie,
filtrovatelná podle vlnové délky.
150 ohodnocených studií seřazených podle vlnové délky a síly důkazů. Filtrujte podle pásma nebo tématu a knihovnu si zúžíte.
Identifies the human sulfotransferase forming the major sulfated vitamin-D metabolite — sulfation is real biochemistry.
Frequent tanners preferentially choose UV and report relaxation — behavioral reinforcement (β-endorphin not directly measured).
Cholesterol sulfate is the most abundant plasma sterol sulfate — a real membrane/keratinocyte-differentiation molecule.
25(OH)D3-3-sulfate is an abundant real circulating conjugate (~16.7 ng/mL) — the molecule is real (function as transport form unproven).
Chronic UV raises β-endorphin → naloxone-reversible opioid dependence in MICE; human extrapolation unproven.
NO significant rise in circulating β-endorphin after UV in humans (n=6) — a null human result; the human endorphin claim is thin.
"297 nm activates sulfation for bioelectric distribution" — no peer-reviewed mechanism, action spectrum or replication. Fringe.
UVB forms CPDs (and 6-4 photoproducts) → signature mutations in BCC, SCC, melanoma.
UV → cutaneous POMC/HPA → systemic and CNS endocrine signalling — the photohormonal axis.
NO/vasodilation is a UVA (315–400 nm) effect — NOT 297 nm UVB (band caveat).
Calcitriol/VDR regulates a large set of genes; broad genomic footprint of vitamin D.
Comprehensive account of the skin's UV-responsive neuroendocrine regulation of local/global homeostasis.
Solar UV (UVA/UVB/UVC) is Group 1 — carcinogenic to humans.
trans-UCA (stratum-corneum UV chromophore) → cis-UCA mediates UV photoimmunosuppression and photocarcinogenesis.
~2776 VDR binding sites near ~229 genes — the real basis for "vitamin D influences hundreds–1000+ genes" (not literally 2000).
UVB induces CD4+CD25+ Tregs and IL-10 — immunosuppressive and therapeutic, but reduces surveillance.
Authoritative review of vitamin-D physiology, skeletal and extra-skeletal roles.
UV→DNA damage→p53 drives keratinocyte POMC→α-MSH; p53-null mice cannot tan.
Standard vitamin-D action spectrum normalized to ~298 nm (adopted standard, under active revision).
Vitamin D/VDR pathway induces cathelicidin → kills intracellular pathogens — vitamin D as immune signal.
α-MSH→MC1R→cAMP→eumelanin; eumelanin photoprotective against UV damage and tumours.
Skin expresses the full HPA/POMC axis (CRH, POMC→ACTH/α-MSH/β-endorphin, cortisol) — a local neuroendocrine organ.
p53 drives apoptotic clearance of UV-damaged keratinocytes (sunburn cells); p53-mutant cells escape — apoptosis backstop + carcinogenesis.
58% of cutaneous SCCs carry UV-signature p53 mutations (C→T, CC→TT) — sunlight's molecular fingerprint in cancer.
In Boston (42°N) no vitamin D3 was synthesised in skin from November to February; in Edmonton (52°N) none from October to March — winter sun sits too low to make vitamin D.
Optimal previtamin-D3 production at 295–300 nm; ~65% 7-DHC conversion at 295 nm — the vitamin-D action-spectrum peak.
OPN5 mediates UVR-induced melanogenesis in human melanocytes via Ca2+/PKC — OPN5 photoreception in human skin.
Exposed skin contains OPN5-dependent local circadian photoentrainment — light-sensing skin clocks.
Continued UV degrades previtamin/vitamin D3 to inert photoproducts — UVA does NOT synthesize and can degrade vitamin D.
UVA penetrates deep dermis; UV→ROS→MMP-1 (collagenase)→collagen degradation→photoaging.
Ex vivo retina/cornea clocks photoentrain via OPN5, most sensitive to short wavelengths.
Endogenous porphyrins (Soret ~405 nm) and flavins absorb violet/UVA → ROS/singlet oxygen → antimicrobial effect.
Human and mouse OPN5 (neuropsin) absorb maximally at ~380 nm — the first human opsin with peak UV sensitivity, activating Gi.
UVA induces Nrf2 nuclear translocation and HO-1/antioxidant genes — protective antioxidant response.
UVA1 (340–400 nm) is an established phototherapy for morphea/scleroderma, atopic dermatitis, etc.
Placental mammals (incl. humans) lost photolyase — humans repair UV lesions by NER, not photoreactivation.
Optoacoustic penetration measurement: depth rises strongly with wavelength — UVA reaches the dermis, far deeper than UVB.
cis-UCA production peaks in UVB but extends through 305–341 nm — UVA contributes (relevant given sunlight's large UVA fluence).
UVA HO-1 induction is mediated by singlet oxygen via free heme — UVA→¹O2→gene activation (and an oxidizing carcinogen).
Melatonin-suppression action spectrum peaks ~464 nm (melanopsin) — far from 365 nm.
Independent melatonin-suppression peak ~459–464 nm — confirms blue, not UVA, suppresses melatonin.
Repetitive sublethal UVA generates the 4977-bp mtDNA "common deletion" via singlet oxygen — a molecular photoaging lesion.
Low-dose (20 J/cm²) UVA1 cleared >80% of morphea lesions (ultrasound/histology-confirmed).
UVA1 depletes skin T-helper cells by singlet-oxygen-driven FAS/FAS-L apoptosis — the actual mechanism of UVA1 phototherapy.
High-dose (130 J/cm²) UVA1 clears localized scleroderma dose-dependently, via MMP-1 (collagenase) induction.
UVA1 upregulates MMP-1 (collagenase) in morphea fibroblasts — the mechanism of UVA1's anti-fibrotic action.
High-dose UVA1 significantly improves atopic dermatitis vs UVA-UVB — foundational AD/UVA1 trial.
UVA (and H2O2/arsenite) induces HO-1 (HSP32) in skin fibroblasts — a general oxidant-stress defence.
Skin optics: longer wavelengths penetrate progressively deeper; UVA reaches the dermis (melanin/scattering-governed).
Long-wave UVA light prevents lens-defocus myopia in mice, dependent on retinal OPN5 — a direct OPN5/UVA clinical-adjacent mechanism.
Long-wave UVA light (360–400 nm) suppresses myopia progression in chicks and humans (implicates VL-opsin/OPN5/EGR1).
Long-wave UVA (~380 nm) light via hypothalamic preoptic OPN5 neurons suppresses brown-fat thermogenesis — deep-brain OPN5 physiology.
380 nm light via OPN5 drives a retinal dopamine pathway regulating ocular vascular development.
Most skin cell types have autonomous circadian clocks entrainable by central inputs and local cues.
Independently confirms OPN5 λmax ~380 nm; it is a bistable pigment (UV→blue 470 nm photoproduct, reverts) activating Gi.
OPN5 in CSF-contacting deep-brain neurons functions as a photoperiodic/seasonal photoreceptor — deep-brain UV photoreception.
UVA triggers labile-iron release that modulates NF-κB activation — a clean UVA→NF-κB inflammatory link.
Original identification/cloning of mammalian OPN5 (neuropsin) in neural tissue.
SCN-projecting RGCs are intrinsically photosensitive — the non-visual circadian photoreceptor system.
Melanopsin (OPN4, λmax ~480 nm) is the blue-light circadian photopigment — the longer-wavelength counterpoint to OPN5's UV sensing.
UVA → ROS → ERK1/2 phosphorylation → tyrosinase upregulation → melanogenesis (blocked by antioxidant).
Identifies OPN3 (encephalopsin), an extraretinal brain opsin — the broader non-visual opsin family context.
Timed bright light strongly phase-resets the human circadian pacemaker — light timing entrains the master clock.
Self-applied blue LED significantly reduced facial comedones over 8 weeks — a positive clinical signal (single-arm).
14 trials/698 participants: methodological limitations preclude firm conclusions — blue-light acne efficacy modest/uncertain.
OPN3 is the melanocyte sensor for short-wavelength visible light; Ca2+→CAMKII→CREB/MITF→tyrosinase → melanogenesis (persistent hyperpigmentation, esp. darker skin).
ROS mediate 405 nm cytotoxicity, with a differential dose response — bacteria far more sensitive than mammalian cells.
71 RCTs/4211 participants: high-quality evidence is lacking; blue-light acne efficacy is uncertain/modest.
A bactericidal 405 nm dose window exists below the mammalian-cell (osteoblast) damage threshold — selectivity.
Defines the blue-light hazard weighting B(λ), peak photochemical retinal sensitivity ~435–440 nm; 400–450 nm is the most hazardous visible band to the retina.
Continuous 405 nm disinfection reduced surface bacterial contamination 27–75% in occupied burns-unit rooms/clinics.
Ceiling 405 nm light continuously reduced surface staphylococci/MRSA by ~62% beyond standard cleaning — harmless to occupants.
Visible light induces more sustained, darker pigmentation than UVA1 in skin types IV–VI — the melasma/hyperpigmentation risk.
405 nm inactivates Gram-positive and Gram-negative pathogens without exogenous photosensitizer — via endogenous porphyrin excitation → ROS.
Reviews blue-light hazard, lipofuscin/A2E accumulation and its proposed role in age-related maculopathy.
C. acnes endogenous coproporphyrins photoexcited by high-intensity blue light → ROS → bactericidal; mechanistic basis of blue-light acne therapy.
The lipofuscin fluorophore A2E photosensitizes blue-light-induced apoptosis of RPE cells — the retinal-hazard mechanism.
Wearing blue-blocking glasses for 2 h before bed improved sleep onset, duration and quality versus clear lenses in adults with insomnia.
Amber blue-blocking lenses worn for 3 h before sleep improved subjective sleep quality and positive mood versus clear lenses in a randomized crossover trial.
18 RCTs/670 wounds: LLLT (modal 660 nm) significantly improved wound healing and reduced pain vs control.
RCT (136 subjects): polychromatic red/NIR increased intradermal collagen density and reduced fine lines (polychromatic, industry-adjacent).
660 nm LED raised type-I procollagen ~31% and lowered MMP-1 ~18%; clinically reduced wrinkles — direct 660 nm collagen evidence.
CCO-null cells still showed 660 nm proliferation enhancement — challenges the CCO-only mechanism (honest counterpoint).
670 nm reduces nanoscopic interfacial-water viscosity, proposed to ease ATP-synthase rotation — single-lab, speculative.
Penetration increases red→NIR; red (~660 nm) reaches a few mm, less than 810 nm NIR.
Red/NIR dissociates inhibitory NO from CuB of CCO → restored electron transport → ↑ATP/MMP; brief ROS signal.
PBM raises ROS in normal cells but lowers it in oxidatively stressed cells; biphasic; anti-inflammatory via NO/ATP/Ca2+.
660 nm raised ATP ≥24 h and increased COX protein; ATP-synthase inhibition abolished it — wavelength-specific ATP at 660 nm.
Comprehensive mechanism review: NO photodissociation, ATP, ROS/cAMP/Ca2+ signalling, membrane potential.
Consensus on PBM for oral mucositis — a well-evidenced clinical PBM indication with dosimetry/safety guidance.
Red/NIR PBM promotes fibroblast proliferation, collagen synthesis, ATP, NO release, wound healing.
RCT (44 men): 655 nm laser/LED helmet gave ~39% increase in hair count vs sham — androgenetic alopecia.
Red/NIR PBM improves muscle performance, delays fatigue and aids repair after exercise/injury.
Light (810 nm) generates intracellular ROS activating NF-κB and pro-survival genes — the ROS→transcription cascade (NIR study).
Reviews CCO as the red/IR-A photoacceptor and signal transducer (conceptual; exact peak numbers from Karu&Kolyakov 2005).
PBM is biphasic — an optimal dose stimulates, too much inhibits.
LLLT reduced acute and chronic neck pain (up to 22 weeks) vs placebo — the strongest-pedigree PBM analgesia evidence.
Red/NIR activates mitochondria→nucleus retrograde signaling via CCO, with ATP as a signaling molecule.
Deconvolved CCO action spectra: red maxima ~620 & ~680 nm (and NIR ~760 & ~825 nm); 660 nm is on the 680 nm shoulder.
CCO is the primary photoacceptor; lists NO release from CCO among primary mechanisms.
The founding LLLT paper — low-dose red laser accelerated wound/burn regeneration ("biostimulation").
Larger sham-controlled RCT confirming PBM acuity benefit in dry AMD (multiwavelength device).
ATP peaks in the morning; 670 nm raises ATP only when given ~08:00–11:00 — mechanistic basis for the timing effect.
A single 3-min MORNING 670 nm exposure improved colour contrast for ~a week; afternoon exposure did not — timing matters.
Multiwavelength (590/670/850 nm) PBM improved acuity/contrast and reduced drusen vs sham — multi-wavelength, not pure 670 nm.
Small human DME study — preliminary clinical PBM signal.
A single 15-min 670 nm exposure reduced post-OGTT glucose elevation ~28% AUC in healthy subjects — tiny, preliminary.
Longer wavelengths raise ATP/glucose demand while 420 nm suppresses — the spectrum/systemic-glucose mechanism (precursor to the 2024 study).
Brief 670 nm improves colour-contrast and rod thresholds in older humans — small n, surrogate endpoints.
Aged mice on 670 nm for 8 months lost <15% outer segments vs ~30% controls — structural retinal preservation.
670 nm improves aged retinal function, associated with corrected mitochondrial decline.
In-vivo NIRS: 670 nm (not 420 nm) progressively oxidizes CCO in aged retina for up to 2 h — direct in-vivo CCO readout.
670 nm in aged flies raised ATP, improved mobility and extended average lifespan — systemic aging effect.
670 nm restores oxidative-stress-suppressed phagocytosis in human RPE — a cell-level functional mechanism.
670 nm is absorbed by CCO and raises ATP/membrane potential in aged eyes, reducing pathology/inflammation.
670 nm upregulates cytochrome c oxidase and reduces inflammation in an age-related macular degeneration model.
670 nm raises mitochondrial membrane potential and reduces age-related retinal inflammation.
670 nm 3–4 min/day inhibits diabetic-retinopathy pathophysiology in vivo and in vitro.
670 nm pretreatment reduced lipid peroxidation and complement propagation in light-damaged retina — anti-inflammatory.
Foundational: 670 nm LED protects retina against a CCO inhibitor (formic acid) — 670 nm rescues the mitochondrial respiratory chain.
Tested 670/728/770/830/880 nm; 770 nm active; 830 & 670 nm most effective; effects parallel the CCO absorption spectrum.
Reviews transcranial PBM mechanisms and (early, heterogeneous) clinical evidence.
810 nm as a primary transcranial wavelength; reviews penetration and brain applications.
Open-protocol transcranial red/NIR LED improved cognition in mild TBI — small, uncontrolled.
Transcranial 633+870 nm LED improved cognition in chronic TBI — case reports (note: 870 nm, not 810).
810 nm acts via CCO; 980 nm via water-gated temperature/Ca2+ (TRPV1) channels — distinct mechanisms.
808 nm penetrates ~40 mm and has less absorption/scattering than both 660 and 940 nm — the deepest-penetrating tested.
Assigns the ~830–835 nm NIR band primarily to oxidized CuA — the molecular basis of 810 nm absorption.
The largest transcranial-laser trial — terminated early for FUTILITY, no benefit (honest negative).
A representative 940 nm PBM study — real but sparse/lower-impact; no robust replicated 940 nm efficacy base.
Argues bound water, not CCO, is the primary NIR acceptor — a contested minority hypothesis.
A 1267–1268 nm quantum-dot laser increased singlet-oxygen production in tumour cells — direct sensitizer-free ¹O2 generation.
Direct 1270 nm illumination killed cells via singlet oxygen with wavelength-specificity (1270 killed, 1247 nm control did not) — not thermal.
Confirms the direct ³O2→¹O2 absorption bands (765 nm b¹Σ and the ~1270 nm a¹Δ) — the physics of sensitizer-free singlet-oxygen generation.
Pulsed (40/100 Hz) produced distinct cognitive effects vs CW in 56 adults — pulse rate matters, but no clean frequency→effect map.
Pulsed 810 nm at 40 Hz changed resting EEG power in a pilot (small, no comparator frequencies, device-affiliated author).
40 Hz multisensory gamma entrainment is neuroprotective in mice — distinct sensory-network mechanism.
40 Hz light+sound improved pathology/cognition in AD mice — sensory gamma, mouse-dominant; human evidence early/mixed.
Coherence/laser not required — LEDs give equivalent PBM at matched wavelength and power density.
Describes the pronounced biphasic dose response and NO/ROS/ATP secondary cascade.
40 Hz VISUAL FLICKER entrains gamma oscillations and reduces amyloid/modifies microglia in AD mice — sensory, not tissue-PBM, mechanism.
10 Hz pulsed 810 nm was most effective vs CW and 100 Hz in mouse TBI — a specific pulse rate can outperform CW (single rodent study).
Reaffirms biphasic response; documents reciprocity failure — irradiance is an independent determinant, not just total fluence.
Pulsed light is sometimes superior to CW for some conditions; evidence mixed; optimal pulse parameters NOT established (some authors industry-affiliated).
Each absorbed photon activates at most one molecule in the primary photochemical act.
Photochemical effect ∝ intensity × time (total dose) — with biological reciprocity-failure limits.
Only radiation absorbed by a system can produce photochemical change — spectrum must match a chromophore.
Light attenuates exponentially with path length and absorber concentration.
Irradiance from a point source ∝ 1/distance².
— Delta 0.5–4, theta 4–8, alpha 8–12, beta 13–30, gamma 30–100 Hz; 100 Hz is high/fast gamma, not high-beta.
Jména,
ke kterým se literatura stále vrací.
Napříč tisíci pracemi se v citacích opakuje hrstka jmen. Tohle je práce, na které celý obor stojí.
Autor zásadních přehledových prací o tom, jak červené a blízké infračervené světlo působí na mitochondrie a buňku.
Klíčová práce – protizánětlivé mechanismy fotobiomodulace (2017)
Určil cytochrom c oxidázu jako klíčový fotoakceptor červeného a blízkého infračerveného světla v buňkách.
Klíčová práce – primární mechanismy červeného/NIR světla v buňkách (1999)
Výzkum blízkého infračerveného světla, funkce mitochondrií a stárnoucího zraku v pozdějším věku.
Klíčová práce – světlo 670 nm zlepšuje stárnoucí lidský zrak (2020)
Vedl výzkum financovaný NASA, který využíval LED světlo k hojení ran a obnově tkání.
Klíčová práce – LED světlo NASA pro hojení ran (2001)
Zmapoval, jak načasování světla seřizuje cirkadiánní hodiny, které řídí spánek, energii a metabolismus.
Klíčová práce – cirkadiánní načasování světla a metabolismus
Ukázal, že sluneční světlo uvolňuje oxid dusnatý uložený v kůži, a podporuje tak prokrvení i krevní tlak.
Klíčová práce – UVA, oxid dusnatý a krevní tlak (2014)
Klinický výzkum fotobiomodulace a protokolů laserové terapie napříč medicínou a stomatologií.
Klíčová práce – přehledy terapie fotobiomodulací
Klinická fotobiologie a měření (dozimetrie) terapeutického světla v medicíně.
Klíčová práce – klinická fotobiologie a dozimetrie světla
Určil aktivní formu vitaminu D a způsob, jakým ji v lidské kůži vytváří UVB sluneční světlo.
Klíčová práce – vitamin D, sluneční světlo a lidské zdraví (2007)
Výzkum vlastní odpovědi kůže na světlo – melatonin, metabolismus vitaminu D a stresová signalizace.
Klíčová práce – kožní neuroendokrinologie a fotoprotekce
Uvedeni za své publikované přínosy vědě o světle. Afiliace odrážejí významné pozice v jejich práci; jejich uvedení zde neznamená žádnou podporu značky REDLIGHT.DOCTOR ani jejích produktů.
Světlo,
oceněné Nobelovou cenou.
Biologie světla není okrajová – Nobelův výbor ji oceňuje už více než století.
Světlo jako medicína. Oceněn za léčbu nemocí soustředěným světlem – první Nobelova cena za terapeutické světlo (fototerapii).
Světlo proměněné v život. Zmapoval, jak se světelná energie zachytí a uloží do chemie živých organismů (fotosyntéza).
Jak oko čte světlo. Fyziologie a chemie zraku – jak fotoreceptory mění světlo v biologický signál.
Hodiny, které seřizuje světlo. Molekulární mechanismus cirkadiánního rytmu – denní hodiny těla, sladěné světlem.
Výzkum ukázal jediný směr.
My jsme postavili přístroj.
REDelios ONE převádí celé biologické spektrum – UV, viditelné červené i blízké infračervené – do jediného promyšleného systému.