Red light therapy, also known as photobiomodulation (PBM) therapy, low-level laser therapy, or cold laser therapy, is a phototherapy technique that uses red (wavelengths between 600-700 nm) and near-infrared (wavelengths between 700-1440 nm) lights [1] from lasers or light-emitting diodes (LEDs). While lasers are commonly used in animal studies, LEDs are preferred in clinical trials due to their low price and easy assembly [2]. As the wavelength increases, the light penetrates deeper into tissues. Pulsed wave light also penetrates deeper into tissues than continuous wave light at the same wavelength in ex vivo experiments [3-6]. The pulsed wave frequency can be adjusted to trigger specific beneficial biological effects [7].
PBM was first described by Endre Mester in 1968 when he observed an unexpected acceleration of hair regeneration in mice exposed to low-energy lasers with a wavelength of 694 nm [8]. Since then, PBM has demonstrated beneficial effects in managing non-healing wounds, ulcers, scars, musculoskeletal disorders, persistent pain, and immunological regulation [9]. The scientific literature on PBM has grown significantly in recent years [10].
Read on to learn more about how PBM therapy works and its many benefits, but if you're already familiar, then check out this article on the synergistic effects of methylene blue combined with red light!
How does photobiomodulation or low-level laser therapy work?
The interaction of red light (RL) or near-infrared light (NIR) at specific wavelengths with tissues activates endogenous chromophores (groups of atoms that interact with light to create color). PBM triggers biological effects in a non-thermal and non-cytotoxic manner [11,12]. One of its most recognized mechanisms of action involves the mitochondria [13]. RL and NIR photons are absorbed at the cellular level by mitochondria, which contain sensitive photo-acceptors to the length used with PBM, like the cytochrome C oxidase enzyme. When tissues are stressed, mitochondria produce nitric oxide, which competes with oxygen at the cytochrome C oxidase site in the respiratory chain. This process reduces adenosine triphosphate (ATP) synthesis, increases oxidative stress, and triggers inflammation [14]. However, when exposed to RL or NIR photons, cytochrome C oxidase absorbs their energy, dissociating nitric oxide. This release enhances ATP production, reduces oxidative stress [15], and influences various cellular components, including the cytosol, membrane, and nucleus. Through these mechanisms, RL and NIR indirectly impact gene transcription, cell proliferation, migration, viability, and inflammation [16]. Systemic effects can also be observed via light activation of blood and lymph cells [17,18].
Therapeutic applications
The biological effects identified in preclinical and clinical studies include anti-inflammatory and analgesic actions, enhanced blood circulation, promotion of angiogenesis, and stimulation of tissue healing, regeneration, and proliferation [19-21]. This wide range of effects makes PBM suitable for various therapeutic applications, including pain management, neurological disorders, and radiation dermatitis.
PBM and pain management
Experiments in animals showed that, at optimal doses, PBM is as effective as non-steroidal anti-inflammatory drugs to treat pain [22].
Via its effects on the mitochondrial cytochrome C oxidase enzyme, PBM has been shown to increase cell proliferation and migration by fibroblasts, reduce cytokines, growth factors, and inflammatory mediators, while increasing tissue oxygenation, reducing pain, and improving wound healing in humans [23-25]. Clinical trials have confirmed that PBM also enhances wound healing in diabetic patients [26] and reduces the incidence of post-herpetic neuralgia when applied early to herpes zoster eruptions [27].
PBM has shown effectiveness in alleviating acute pain in various conditions, such as oral surgery [28,29], nipple pain from breastfeeding [30], plantar fasciitis [31], and carpal tunnel syndrome [32], with positive results in reducing pain intensity in women with chronic myofascial pain [33]. It has also alleviated pain after coronary artery bypass surgery [34] and improved sensory function in neuropathy [35]. PBM is commonly used to manage dental pain after oral surgery, reducing orthodontic pain for up to a week [36]. However, some studies have shown inconsistent results, such as those for plantar fasciitis [37] or knee osteoarthritis [38].
PBM offers a promising non-invasive option for pain management across a range of conditions.
PBM and neurological diseases
Alzheimer’s disease
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory loss and cognitive decline, primarily associated with the accumulation of amyloid-β (Aβ) peptide and tau protein tangles in the brain. Mitochondrial dysfunction is related to the main pathological feature of AD: neuronal dysfunction [39].
In a rat model of AD, transcranial PBM at 808 nm was found to have suppressed Aβ aggregation, improving long-term spatial and recognition memory [40]. PBM at 808 nm in a transgenic mouse model of Aβ peptide amyloidosis showed an increase in soluble Aβ peptide, mitochondrial function, and ATP with a decrease in inflammatory markers, suggesting an overall improvement in neurological function [41]. Similarly, transcranial PBM at 633 nm reduced Aβ production and plaque formation by shifting amyloid precursor protein (APP) processing toward the nonamyloidogenic pathway in a mouse model of AD, resulting in memory and cognitive improvements [42]. At 633 nm, PBM also inhibited the activity of c-Jun N-terminal kinase 3 (a signal molecule related to neurodegeneration), a possible target of AD treatment [43]. Recent evidence suggests an involvement of the gut-brain axis in AD: gut microbiota produce peripheral inflammation and immune modulation that may contribute to brain amyloidosis, neurodegeneration, and cognitive impairment in AD. Simultaneous pulsed wave PBM to the head and abdomen for 10 min triggered neuroprotective effects via normalization of all modified behavioral and biochemical parameters in a β25-35 peptide-induced toxicity experiment in mice [44].
In clinical trials, transcranial PBM treatment for 28 days at a wavelength between 1060 and 1080 nm improved cognition and memory in AD patients [45]. Other PBM treatments in patients with progressive neurodegenerative diseases improved cognition, mood, and sleep [45-47].
These findings suggest that PBM presents potential in mitigating AD, shedding light on possible new therapies.
Parkinson's disease
Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies in the brain. The exact cause of PD remains unknown, but evidence suggests that mitochondrial dysfunction and oxidative stress contribute to its pathogenesis.
In animal models of PD, transcranial PBM treatment at 670 and 810 nm alleviated PD pathology in rats, mice, and monkeys [48-52]. PBM has also shown neuroprotective effects and prevented cerebrovascular leakage in the substantia nigra pars compacta region [53]. Additionally, in a rat model of PD, PBM significantly reduced serum levels of pro-inflammatory cytokines [49].
In clinical trials, transcranial PBM at 635 and 810 nm safely improved motor symptoms in PD patients [54], and combinations of other wavelengths (e.g., 670, 810, and 850 nm) also showed benefits for both motor and non-motor symptoms [55]. Due to the exponential attenuation of light through the skull and tissue, various strategies — such as applying PBM to the neck, intranasal passages, and the abdomen combined with transcranial PBM — have been developed and demonstrated effectiveness [56-58].
Overall, current research suggests the great potential of PBM in PD treatment.
Traumatic brain injury
A traumatic brain injury (TBI) is a trauma caused to the brain by an external force and can result in either complete recovery, permanent disability, or death. The pathophysiology of TBI is highly complex and involves inflammation, oxidative stress, mitochondrial dysfunction, and excitotoxic damage.
Experiments in mice showed that transcranial PBM mitigates the death of brain neurons by decreasing neuroinflammation, increasing blood flow [59], and improving brain self-repair abilities via stimulation of synapse formation and proliferation of nerve cells [60,61]. Laser treatment 4 h after TBI significantly improved the neurological severity score (a scale evaluating motor, sensory, and reflex functions) in moderate-to-severe TBI mouse models [62,63]. Combined with lactic acid or pyruvate, two energy metabolism regulators, PBM increased ATP levels more effectively and reduced neuroinflammation, preventing neuronal damage in the injured zone of the brain [64,65]. However, too many PBM treatments in TBI mouse models can temporarily inhibit brain repair, highlighting the importance of developing optimal protocols [66].
In clinical trials, PBM treatment significantly enhanced cognitive performance in mild TBI patients at 633 and 870 nm [67,68], while improving sleep duration at 633 and 810 nm [69] in chronic TBI patients commonly suffering from sleep disturbances. Another study combining intranasal and transcranial PBM treatments at 810 nm for eight weeks showed an increased brain volume and improvements in cerebral perfusion, functional connectivity, and neuropsychological test scores in a 23-year-old TBI patient [70].
Transcranial PBM demonstrates high potential for the clinical treatment of TBI.
Depression
Depression is a disease characterized by a lack of energy, depressed mood, and poor concentration. Typically treated with medication, these drugs often have low efficacy and can cause significant side effects. The pathophysiology of depression involves a complex interplay between inflammation, oxidative stress, DNA damage, impaired DNA repair, and mitochondrial dysfunction [71].
Experiments in rat models showed that PBM at 810 nm promoted neuroprotection effects from stress [72], underwater trauma [73], reserpine [74], and early AD-associated depression [75]. PBM treatment at 808 nm was as effective as citalopram in improving depressive-like behaviors in a rat model of chronic mild stress-induced depression [76].
In clinical trials, transcranial PBM at 810 nm significantly improved the Hamilton depression rating scale and anxiety rating scale scores in depressive patients [77], while demonstrating safety and effectiveness in major depressive disorder patients at 823 nm [78].
Although further research is needed, PBM could be a promising approach for the treatment of depression.
Aging
Aging is characterized by a gradual functional decline at the molecular, cellular, and tissue levels, linked to oxidative stress and mitochondrial dysfunction [79], contributing to cognitive impairment [80].
Comparing aged rats to young rats revealed that aging significantly decreases brain cytochrome C oxidase activity, an effect that PBM treatment at 810 nm reversed [81]. PBM (at 660 or 810 nm) also mitigated inflammatory responses and altered intracellular signaling pathways linked to glucose metabolism, vascular function, and cell survival in the aging brain of rats. PBM treatment (at 660 and 810 nm) also significantly alleviated cognitive and memory decline, while improving mitochondrial function and reducing oxidative stress and cell death in a D-galactose-induced aging mouse model [82,83]. In addition, treatment at 660 nm alleviated cognitive impairment and mitochondrial dysfunction in 18-month-old aging mice [84], while PBM at 670 nm showed beneficial effects on astrocytes and microglia proliferation [85].
In clinical trials, PBM (at 633 and 870 nm) improved depressive symptoms and cognitive function in both healthy participants [86], and those with mild cognitive impairment [87], as assessed by the Eriksen flanker category fluency tests and visual memory span test, respectively. PBM treatment at 1064 nm in elderly participants also improved attention and memory as assessed by psychomotor vigilance tasks and delayed match to sample. These improvements came together with an increased prefrontal blood-oxygen-level-dependent-fMRI activity and elevated levels of cytochrome C oxidase enzymes during the light exposure periods [88]. Beneficial effects on working memory were documented and lasted at least three weeks [89].
Overall, PBM is a promising candidate for age-related cognitive improvement.
PBM and radiation dermatitis
One of the best-studied applications of PBM is the treatment of radiation dermatitis, a skin condition secondary to oncology therapies. Multiple controlled trials showed that PBM efficiently reduces radiation dermatitis severity, worsening, and pain [90-92]. However, other studies following breast cancer radiotherapy provide contradictory results [92,93]. Overall, two recent meta-analyses, including five and seven clinical trials, concluded that PBM presents promising properties to prevent radiation dermatitis severity [94,95].
Conclusion
PBM is a non-invasive therapy that uses red or near-infrared light to penetrate human tissues. By targeting the mitochondrial enzyme cytochrome C oxidase, PBM enhances ATP production and reduces oxidative stress, indirectly influencing gene transcription, cell proliferation, migration, viability, and inflammation. Clinical trials have demonstrated its potential benefits in various applications, including pain management, Alzheimer's disease, Parkinson's disease, traumatic brain injury, and radiation dermatitis, among others. PBM is a cost-effective therapy [96] with a favorable safety profile [97], erythema being the most common and self-limiting adverse effect [1]. It can also be used alongside pharmacological treatments.
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