Red Light Therapy for Brain Health, Mental Health & Vision

Transcranial photobiomodulation (tPBM) — the application of red and near-infrared light to the brain through the skull — represents one of the most rapidly expanding frontiers in photobiomodulation research. Over the past decade, studies have demonstrated that near-infrared light can penetrate the skull, reach cortical tissue, and produce measurable neurological effects.

Separately, a body of research on ocular photobiomodulation — applying specific wavelengths of light to the eyes — has produced some of the most striking recent findings in the field, particularly around age-related decline in vision.

This page covers both domains: the brain (depression, anxiety, TBI, neurodegeneration, cognitive function, sleep) and the eyes (macular degeneration, myopia, retinal health). The evidence ranges from strong pre-clinical data with encouraging clinical trials to genuinely preliminary explorations. We distinguish clearly between the two.

Part 1: Transcranial photobiomodulation (tPBM)

How light reaches the brain

A common and reasonable objection: can light really penetrate the skull? The answer is yes — but only specific wavelengths and only to a limited depth.

Tedford et al. (2015, Lasers in Surgery and Medicine) measured light transmission through human cadaver skulls and found that approximately 2-3% of near-infrared light at 810 nm penetrates through the skull to reach the cortical surface. Whilst this percentage seems small, the absolute photon flux at therapeutic power levels (100-500 mW) is sufficient to activate cytochrome c oxidase in cortical neurons.

Key points about transcranial penetration:

• Wavelength matters enormously. Red light (630-660 nm) barely penetrates the skull. Near-infrared light (810-850 nm) penetrates significantly better, with 810 nm showing the best skull transmission in most studies.
• Power matters. Higher power at the surface delivers more photons to the cortex. Clinical tPBM devices typically use 100-500 mW per LED/laser diode.
• Location matters. The frontal cortex (prefrontal cortex) is closest to the skull surface and has the thinnest overlying tissue, making it the most accessible target. Deeper structures (hippocampus, basal ganglia) are harder to reach.
• Scalp and hair absorb light. Darker skin and thicker hair reduce transmission. Parting the hair or applying the device to bare scalp improves delivery.

Mechanisms in the brain

Once NIR photons reach cortical neurons, the downstream effects parallel those seen in other tissues but have particular significance in the brain:

1. Increased neuronal ATP production — the brain is the body’s most metabolically demanding organ, consuming roughly 20% of total energy at 2% of body weight. Even modest improvements in mitochondrial efficiency can have meaningful functional effects.

2. Increased cerebral blood flow — PBM promotes nitric oxide-mediated vasodilation, improving blood flow to treated cortical areas. Salgado et al. (2015, Behavioural Brain Research) demonstrated increased cerebral blood flow in treated regions using functional near-infrared spectroscopy (fNIRS).

3. Reduced neuroinflammation — chronic neuroinflammation is implicated in depression, Alzheimer’s disease, TBI sequelae, and age-related cognitive decline. PBM reduces pro-inflammatory cytokines and microglial activation (Hamblin, 2016, BBA Clinical).

4. Neuroprotection — PBM has been shown to protect neurons from apoptosis (programmed cell death) by upregulating anti-apoptotic proteins (Bcl-2) and reducing pro-apoptotic signals. This is particularly relevant for neurodegenerative diseases and TBI.

5. Neurogenesis and synaptogenesis — animal studies suggest PBM may promote the formation of new neurons (neurogenesis) and synaptic connections, particularly in the hippocampus (Xuan et al., 2015, Neuroscience).

6. Neurotransmitter modulation — emerging evidence suggests PBM influences serotonin, dopamine, and norepinephrine pathways, which has direct implications for mood disorders.

Depression

The evidence for tPBM in depression is the most advanced among neuropsychiatric applications, with several well-designed clinical trials.

Schiffer et al., 2009 — The first clinical trial

Schiffer et al. (2009, Behavioural and Brain Functions) conducted the first clinical trial of tPBM for depression, applying 810 nm LED light to the forehead (bilateral prefrontal cortex) in 10 patients with major depressive disorder and anxiety. A single treatment session produced a significant reduction in Hamilton Depression Rating Scale (HAM-D) scores at 2 and 4 weeks post-treatment.

Whilst the sample size was small and the study open-label, it established proof of concept and set the parameters for subsequent research.

Cassano et al., 2015 — Open-label series

Cassano et al. (2015, Journal of Clinical Psychiatry) treated 4 patients with major depressive disorder using 810 nm LED tPBM applied to bilateral prefrontal cortex, twice weekly for 8 weeks. All four patients showed clinically significant improvement, with HAM-D scores decreasing by 44-100%.

Cassano et al., 2018 — Larger trial

Cassano et al. (2018, Psychological Medicine) expanded to a larger study of 21 participants with MDD receiving 823 nm tPBM to the prefrontal cortex. Significant reductions in depression severity were observed, with response rates (>50% reduction in HAM-D scores) of approximately 50%.

Disner et al., 2016 — Dose-response

Disner et al. (2016, Journal of Psychiatric Research) demonstrated a dose-response relationship: participants receiving higher irradiance tPBM showed greater improvements in depression scores and cognitive function tests than those receiving lower doses.

Mechanism in depression

The prefrontal cortex is hypoactive in major depression — a finding consistently demonstrated by neuroimaging studies. tPBM may work by directly increasing metabolic activity and blood flow in this underperforming region. Additionally, PBM’s effects on serotonin synthesis (potentially by increasing tryptophan hydroxylase activity through enhanced mitochondrial function) provide a plausible neurochemical mechanism.

Evidence strength: Moderate — multiple clinical studies with consistent positive results, but most are small and unblinded. A large, multicentre, double-blind RCT is needed.

Typical protocol: 810 nm, applied to bilateral prefrontal cortex (forehead, F3/F4 sites), 20-30 mW/cm2 at the scalp, 10-20 minutes per session, 2-3 times weekly for 6-8 weeks.

Deep dive: Red light therapy for depression

Anxiety

The anxiety evidence is less developed than for depression but shows promise. Several depression studies (including Schiffer 2009 and Cassano 2015) measured anxiety as a secondary outcome and found significant reductions.

Maiello et al. (2019, Journal of Affective Disorders) conducted a double-blind, sham-controlled trial of tPBM for generalised anxiety disorder (GAD) in 42 participants. The active treatment group showed significantly greater reductions in GAD-7 scores compared to sham.

The mechanism likely overlaps with the depression pathway: improved prefrontal cortex function enhances top-down regulation of the amygdala, reducing excessive anxiety signalling.

Evidence strength: Preliminary to moderate — encouraging results but limited by small sample sizes.

Deep dive: Red light therapy for anxiety

Traumatic brain injury (TBI)

TBI is perhaps the most compelling neurological application of tPBM, with a convergence of strong pre-clinical evidence and encouraging clinical data.

Pre-clinical evidence

Multiple animal studies have demonstrated that tPBM applied after experimental TBI significantly reduces brain lesion size, inflammation, and neuronal death whilst improving functional recovery. Xuan et al. (2013, Annals of Biomedical Engineering) showed that 810 nm laser applied transcranially to mice after controlled cortical impact reduced lesion volume by approximately 30% and improved neurological severity scores.

Oron et al. (2007, Journal of Neurotrauma) demonstrated that a single tPBM treatment administered 4 hours after TBI in mice significantly reduced neurological deficits at 28 days compared to untreated controls.

Clinical evidence

Naeser et al. (2011, Photomedicine and Laser Surgery) reported a case series of 11 patients with chronic TBI (ranging from 10 months to 8 years post-injury) treated with 633 nm and 870 nm LED arrays applied to the scalp. After 6 months of treatment, patients showed significant improvements in attention, executive function, and verbal learning — deficits that had been stable or worsening before treatment.

Henderson and Morries (2015, Neuropsychiatric Disease and Treatment) treated 39 patients with chronic TBI using high-power 810/980 nm NIR laser applied transcranially. Significant improvements were reported in neuropsychological testing, mood, and self-reported quality of life.

Figueiro Longo et al. (2020, JAMA Network Open) conducted a double-blind, sham-controlled pilot trial of tPBM in 68 patients with moderate TBI. Whilst the primary endpoint (Glasgow Outcome Scale) did not reach statistical significance, secondary measures of cognitive function and daily functioning showed promising trends.

Evidence strength: Moderate — strong pre-clinical foundation, multiple positive clinical studies, but large definitive RCTs are still underway.

Deep dive: Red light therapy for TBI

Alzheimer’s disease and neurodegeneration

Pre-clinical evidence

The pre-clinical evidence for PBM in Alzheimer’s disease (AD) is remarkable. Purushothuman et al. (2014, Alzheimer’s Research & Therapy) demonstrated that 670 nm light treatment reduced amyloid-beta plaque burden and tau neurofibrillary tangles in transgenic mouse models of AD. Treated mice also showed improved performance on spatial learning and memory tasks.

De Taboada et al. (2011, Journal of Alzheimer’s Disease) showed that 808 nm tPBM reduced beta-amyloid plaques, reduced brain inflammatory markers, and improved cognitive performance in APP/PS1 transgenic mice.

Clinical evidence

Saltmarche et al. (2017, Photomedicine and Laser Surgery) reported a case series of 5 patients with mild to moderate Alzheimer’s disease treated with intranasal and transcranial 810 nm PBM. After 12 weeks, all five patients showed improvements in Mini-Mental State Examination (MMSE) scores, with family members reporting better sleep, reduced anxiety, and fewer outbursts.

A larger pilot trial by Berman et al. (2017, Journal of Clinical Neurology) treated 11 AD patients with a home-use tPBM device (810 nm) and reported trends toward improved ADAS-cog scores (the standard AD cognitive assessment) after 28 sessions.

These results are encouraging but must be interpreted cautiously. Sample sizes are tiny, blinding is often absent, and the natural variability of AD symptoms makes uncontrolled observations unreliable. However, given the devastating lack of effective AD treatments and the excellent safety profile of PBM, this research area deserves urgent expansion.

Evidence strength: Preliminary — strong animal data, small but encouraging human studies. Far from definitive.

Deep dive: Red light therapy and Alzheimer’s | Brain health

Brain fog and cognitive performance

“Brain fog” is not a medical diagnosis but a common complaint encompassing poor concentration, mental fatigue, slow processing speed, and memory difficulties. tPBM has been studied in both healthy subjects and those with cognitive complaints.

Barrett and Bhatt-Sanders (2013, Lasers in Medical Science) found that a single session of tPBM (1064 nm) to the right prefrontal cortex improved performance on sustained attention and working memory tasks in healthy university students. The effect was significant compared to sham treatment.

Blanco et al. (2017, Neurobiology of Learning and Memory) replicated and extended these findings, demonstrating that tPBM improved response times and accuracy on executive function tasks in healthy adults.

These are acute effects from single sessions rather than sustained cognitive enhancement from chronic treatment. Whether regular tPBM use can produce lasting cognitive improvements in healthy individuals remains unclear.

Evidence strength: Preliminary for cognitive enhancement in healthy individuals; more evidence needed for clinical “brain fog” populations.

Deep dive: Red light therapy for brain fog

Serotonin, dopamine, and neurotransmitter effects

The neurotransmitter effects of PBM are an area of active research. Several lines of evidence suggest that tPBM modulates monoamine neurotransmitter systems:

• Serotonin: Cassano et al. (2016, Photobiomodulation, Photomedicine, and Laser Surgery) hypothesised that PBM enhances serotonin synthesis by improving mitochondrial function in raphe nucleus neurons, where tryptophan hydroxylase (the rate-limiting enzyme for serotonin synthesis) is tightly coupled to mitochondrial energy production.
• Dopamine: Mitrofanis (2017, Reviews in the Neurosciences) reviewed evidence that PBM protects dopaminergic neurons in animal models of Parkinson’s disease, potentially by reducing mitochondrial dysfunction and oxidative stress in the substantia nigra.
• Norepinephrine: PBM may modulate locus coeruleus function, though direct evidence is limited.

Evidence strength: Preliminary — largely pre-clinical and theoretical. Important for understanding mechanisms but not yet clinically actionable.

Deep dive: Red light therapy and neurotransmitters

Sleep and circadian rhythm

The relationship between red light and sleep operates through two distinct mechanisms:

1. Circadian rhythm support

Unlike blue light (which suppresses melatonin and disrupts circadian rhythm when viewed in the evening), red light has minimal effect on melatonin suppression. This is because melanopsin — the photopigment in intrinsically photosensitive retinal ganglion cells (ipRGCs) that signals “daytime” to the suprachiasmatic nucleus — has peak sensitivity around 480 nm (blue) and is minimally responsive to wavelengths above 600 nm.

Using red light in the evening (rather than blue-rich white light) therefore allows normal melatonin production. Some commercial “red light bulbs” marketed for sleep are based on this principle.

2. Direct PBM effects on sleep

Zhao et al. (2012, Journal of Athletic Training) conducted an RCT with 20 female athletes and found that 30 minutes of whole-body 658 nm LED therapy improved sleep quality (measured by Pittsburgh Sleep Quality Index), serum melatonin levels, and endurance performance over 14 days of treatment.

The mechanism may involve PBM’s effects on mitochondrial function in the pineal gland (where melatonin is synthesised) or broader systemic effects on inflammation and stress hormones that influence sleep architecture.

Evidence strength: Preliminary — one well-designed RCT plus theoretical support from circadian biology. More studies needed.

Deep dive: Red light therapy for sleep

Part 2: Vision and eye health

Glen Jeffery’s retinal research

Professor Glen Jeffery of University College London has produced some of the most striking findings in recent photobiomodulation research. His work focuses on the ageing retina and the role of mitochondrial decline in age-related vision loss.

The ATP decline problem

Jeffery’s foundational observation (Jeffery et al., 2015) is that retinal photoreceptors have extraordinarily high metabolic demands — they contain more mitochondria per cell than almost any other cell type. As mitochondria decline with age, photoreceptor function declines accordingly. By age 70, retinal ATP production may be reduced by approximately 70% compared to age 30.

The 670 nm intervention

Begum et al. (2013, Neurobiology of Aging) demonstrated in aged mice that short, daily exposures to 670 nm light (just 3 minutes per day) significantly improved retinal function as measured by electroretinography (ERG). The effect was attributed to enhanced mitochondrial function in photoreceptors.

Human translation

Shinhmar et al. (2020, The Journals of Gerontology: Series A) translated these findings to humans in a landmark study. Twenty-four healthy participants aged 28-72 received 3 minutes of 670 nm light exposure to one eye per day for 2 weeks. In participants over 40:

• Colour contrast sensitivity (cone function) improved by 22% (not a misprint — twenty-two per cent)
• Scotopic sensitivity (rod function) improved by 8%
• No improvement was seen in participants under 40 — consistent with the hypothesis that the benefit derives from reversing age-related mitochondrial decline

This study, published in one of the top gerontology journals, received widespread media coverage and represents a genuine breakthrough in understanding how simple light exposure can improve age-related physiological decline.

Shinhmar et al. (2021, Scientific Reports) followed up by demonstrating that the effect was time-of-day dependent: morning exposure to 670 nm light produced significant improvements in colour contrast sensitivity, whilst afternoon exposure did not. This aligns with the known circadian cycling of mitochondrial membrane potential, which peaks in the morning.

Evidence strength: Moderate to strong — well-designed human studies from a leading university lab, published in high-impact journals. But sample sizes are still small and long-term effects are not yet characterised.

Macular degeneration

Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in the developed world. Given Jeffery’s findings on mitochondrial decline in the ageing retina, PBM has emerged as a potential intervention.

Merry et al. (2017, Retina) conducted a pilot study of PBM for dry AMD using a multiwavelength device (590 nm, 660 nm, 850 nm). After 3 treatments over 2-3 weeks, 95% of treated eyes showed improvement in visual acuity (mean improvement: 5 ETDRS letters), with improvement sustained at 6-month follow-up.

Markowitz et al. (2020, Clinical Ophthalmology) published results from the LIGHTSITE I study — a prospective, double-masked, randomised controlled trial of PBM for dry AMD. Treated eyes showed significant improvements in visual acuity, contrast sensitivity, and microperimetry compared to sham-treated eyes. Drusen volume was also significantly reduced.

The LIGHTSITE II study (Burton et al., 2023, Ophthalmology Science) confirmed these findings in a larger multicentre trial, demonstrating that multiwavelength PBM reduced drusen volume and improved best-corrected visual acuity compared to sham treatment.

Evidence strength: Moderate — randomised, sham-controlled trials with positive results. This is among the most promising clinical applications of PBM for eye health.

Deep dive: Red light therapy for macular degeneration

Myopia — repeated low-level red light (RLRL)

A separate but related application is the use of repeated low-level red light (RLRL) therapy for myopia control in children. This has become a significant area of clinical research, particularly in East Asia where myopia rates are epidemic.

Jiang et al. (2022, Ophthalmology) conducted a multicentre RCT of 264 myopic children treated with 650 nm red light (3 minutes per session, twice daily) versus single-vision spectacles. At 12 months:

• Axial elongation was reduced by 69.4% in the RLRL group compared to controls
• Myopia progression was reduced by 76.6%
• Choroidal thickening was observed, consistent with increased choroidal blood flow

He et al. (2022, Ophthalmology) published a parallel trial with similar results, establishing RLRL as one of the most effective myopia control interventions studied to date.

The mechanism is thought to involve increased choroidal blood flow (via NO-mediated vasodilation) and choroidal thickening, which brings the retinal plane closer to the focal point and reduces the hyperopic defocus signal that drives axial elongation.

Caution: Whilst the efficacy data is striking, long-term safety data for repeated retinal exposure to 650 nm laser light in children is still accumulating. Some reports of reversible retinal changes have been noted (Liu et al., 2023, British Journal of Ophthalmology). This therapy should only be undertaken under ophthalmological supervision.

Evidence strength: Moderate to strong for efficacy; long-term safety data still emerging.

Deep dive: Red light therapy for myopia

Other eye conditions

Glaucoma

Pre-clinical evidence suggests PBM may protect retinal ganglion cells from the oxidative stress that drives glaucoma-related neurodegeneration. Albarracin et al. (2011, Investigative Ophthalmology & Visual Science) demonstrated neuroprotective effects of 670 nm light in animal models. Clinical evidence in humans is limited to case reports.

Evidence strength: Preliminary.

Deep dive: Red light therapy for glaucoma

Floaters

There is no credible evidence that red light therapy eliminates vitreous floaters. Floaters are structural (collagen aggregates in the vitreous humour) and are not amenable to photobiomodulation. Claims to the contrary should be treated with scepticism.

Evidence strength: Insufficient / not supported.

Deep dive: Red light therapy for floaters

Eye safety — critical considerations

Eye safety is the most important practical consideration in this entire article. The approach to eye safety differs fundamentally between:

Intentional ocular PBM (under clinical supervision)

The studies by Jeffery, Merry, Markowitz, and Jiang all involved controlled, measured doses of specific wavelengths delivered to the retina. These protocols use carefully calibrated devices with known irradiance, exposure times, and wavelengths. They should only be replicated under professional supervision.

Incidental eye exposure during tPBM or facial treatment

When using a red light panel for facial skin treatment or a tPBM device for brain health, incidental eye exposure occurs. At typical consumer device irradiances (10-100 mW/cm2) and treatment durations (10-20 minutes), the evidence suggests this is safe for visible red wavelengths (630-670 nm), provided you do not stare directly into the LEDs at close range.

Near-infrared wavelengths (810-850 nm) are invisible and therefore do not trigger the protective blink reflex. Prolonged, direct NIR exposure at high irradiance could potentially damage the retina without warning. Use the eye protection provided with your device, particularly for NIR.

Practical eye safety guidelines

• Red light panels for skin/face: Brief, indirect exposure is safe. Do not stare directly into LEDs at close range for extended periods.
• tPBM devices: Follow manufacturer instructions precisely. Most tPBM devices are applied to the scalp/forehead, not directly to the eyes.
• NIR wavelengths: Always use provided eye protection when using high-power NIR devices near the face.
• Intentional retinal PBM: Only under professional supervision with calibrated devices.
• Children: Extra caution warranted given developing retinas.

Device considerations for brain and vision

For tPBM (brain applications)

• Wavelength: 810 nm is the best-supported wavelength for transcranial delivery
• Power: Higher power improves transcranial penetration. Clinical studies typically use 100-500 mW per diode
• Application site: Bilateral prefrontal cortex (forehead) is the most common and best-studied location
• Form factor: Dedicated tPBM devices (headbands, helmets) ensure consistent placement. General-purpose panels can work if positioned correctly

For vision applications

• Wavelength: 670 nm for Jeffery-type retinal PBM; 590 nm + 660 nm + 850 nm for AMD (LIGHTSITE protocol); 650 nm for myopia RLRL
• These are clinical protocols — do not attempt to replicate AMD or myopia treatments with consumer devices without professional guidance

For device recommendations, see our best red light therapy devices guide.

The bottom line

Brain and vision applications represent some of the most exciting — and most preliminary — areas of photobiomodulation research. The scientific plausibility is high, the pre-clinical data is strong, and the early clinical results are encouraging.

For depression, the evidence is moderate: multiple clinical studies show consistent benefit, but large definitive RCTs are still needed.

For TBI, the convergence of strong animal data and positive clinical studies makes this one of the most promising applications, particularly given the lack of alternative treatments for chronic post-concussive symptoms.

For Alzheimer’s and neurodegeneration, the pre-clinical data is remarkable but human evidence remains limited.

For vision, Glen Jeffery’s work on 670 nm retinal PBM is among the most impressive recent findings in the entire PBM field, and the AMD clinical trials (LIGHTSITE series) show genuine therapeutic potential. Myopia control with RLRL is rapidly generating high-quality evidence.

The common thread: these applications require careful attention to wavelength, dose, and application site. “Shining a red light at your head” is not tPBM; controlled delivery of specific wavelengths at known doses to targeted brain regions is. Similarly, retinal PBM requires clinical-grade precision. As the evidence matures, we expect clearer protocols and potentially dedicated consumer devices for these applications.

References

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