Light Therapy: Does it Really Work?

Siraj Sabihuddin
Siraj Sabihuddin

A scientist and engineering exploring whether light therapy is bullshit or not. It took considerable time to produce this article for free. If you like this article or want me to do some research for you, you can buy me a coffee via the Donate button or contact me.

The internet is full of people and companies who make tall claims about therapies. Those who claim the efficacy of magic pills, magic diets, magic touch, magic magnets and magic light. The abundance of these magical claims makes it difficult for the public to be able to make informed decisions about what actually works and how they invest their money into treatments that they need. Businesses producing the technology for therapies are prone to exaggerate and occasionally outright lie about their efficacy – there is an incentive to do so if it makes the sale. Compounding this, standards and regulatory organizations such as the FDA (in the U.S.) that regulate devices for public health and safety seem unable to keep up with the sheer number of scams out there. There are also some concerns that organizations such as the FDA may have an incentive from companies producing magic pills or drug to green light their technology. For instance, consider this article from the University of Connecticut that discusses some of the nuance behind this: Why is the FDA Funded in Part by the Companies It Regulates? [1]

My goal in this article is to briefly review the scientific literature and do an initial sanity check to see if light therapies are legitimate and then to understand under what conditions they are effective and to what degree and under what basic conditions. From this information, I aim to find or build a device to help heal my ligament injuries and other injuries – if this is something you are interested in, please let me know! (note that cover photo for this article was taken from [5])

Warning

I am in no way trained in medicine and have just a rudimentary understanding of biology. As such, I have largely parroted opinions of researchers in the field. The article is intended to provide a ball park understanding of the lay of the land for further inquiry only. As such there may be some fundamental misunderstandings in this article especially given the small number of sources used to glean the information presented. I strongly suggest that people use a critical eye when reading this article. As time presents, I will produce additional articles on the topic to dig deeper and try to better understand the impact and mechanism behind light therapy techniques. I encourage those with training to comment and correct any errors I have made on the topic.

How it works

Light therapy is exactly what it sounds like. Shining light on to your skin to speed up recovery of damage or to mitigate the impact of other more chronic conditions. Generally the idea is that humans need light from the sun to stay healthy. And the absence of exposure to this light can have some implications – so light therapy aims to remedy this situation. But does it really work? The short answer is Yes. As suggested by [2], such therapies have shown at least some positive effects for acute and chronic musculoskeletal pain across some 4000 laboratory and clinical studies on PubMed. While I have not done enough search to truly verify this. I accept it as true for now.

I’m interested in buying, building or modifying a device that can more effectively administer light therapy treatments – current devices while much cheaper than before are still quite expensive and dosing is not easily administered. So it pays to understand some of how exactly the therapy works. First and foremost, collectively, these light therapies are called Low Level Laser Light Therapies (LLLTs) – they are also sometimes known as photobiomodulation therapies. Light that penetrates tissue results in a photochemical (rather than thermal) effect and is somewhat similar in nature to plant photosynthesis.

When light is applied to the skin, different frequency of light (or wavelengths) have distinct penetration depths. This is shown in the diagram below (Figure 1) taken from [2].

Figure 1: Absorbance of light of varying wavelengths by different tissue materials. Here Hb refers to Deoxy Hemoglobin and HbO2 to Oxy-hemoglobin – essentially your blood. Melanin is the light absorbant material protecting skin from UV. Sourced from [2].

The optical window is the region of light that is ideal for LLLT – these wavelengths have the deepest penetration and lowest absorbance by intermediary materials in your body. Light from LLLT must penetrate sufficiently beyond the surface water, de-oxygenated hemoglobin (Hb), oxygenated hemoglobin (HbO2) and melanin of our body to reach deep tissue.

When penetration depth is enough for the tissue you are trying to treat, light has a chance to interact with mitochondria in the cell. These mitochondria are the power plants of our cells and convert food and oxygen into energy packaged in the form of Adenosine Triphosphate (ATP). Enclosed in the mitochondrial genome is a transmembrane protein called Cytochrome C Oxidase (COX). This protein spans the entire cell membrane of the mitochondria. See Figure 2 below (from [3]) to get a better sense of what this means.

Figure 2: Taken from [3]. Cytochrome C Oxidase (COX) is a transmembrane protein. It acts as a photo-acceptor for near infrared light.

I don’t claim to know anything about what COX really does in the mitochondria. That said, according to some, it is involved in supporting the production of ATP. What is important for us to know is that it acts as a primary photo-acceptor for near infrared (NIR) wavelengths of light [2]. Nitric oxide (NO) produced in mitochondria is an important signalling molecule for things like muscle relaxation and inflammation mechanisms. But NO can limit respiration by attaching itself to the COX [4]. The binding to COX displaces oxygen in injured or hypoxic (oxygen starved) cells. The light from LLLT essentially knocks the NO from the COX to enhance mitochondrial respiration. The result is essentially improved healing of injuries. Or so the prevailing explanation on the surface seems to go.

Low-intensity LLLT stimulates mitochondria and can raise mitochondrial membrane potential. The supposition here is that it is more likely to increase metabolism and transport of action potentials in neurons rather than decrease it. This presumably has an impact on healing speed. But as intensity increases as with a focused laser spot acting on a nerve, the opposite effect can occur of inhibiting mitochondrial metabolism in c-fibers and a-delta fibers and reduce mitochondrial membrane potential and thereby induce a nerve blockade – presumably reducing pain and slowing down healing [4]. The modulation of neurotransmitters is a another potential mechanism of pain relief. For instance, in animal models both serotonin and endorphin levels have shown increases following laser treatment of myofascial pain. Myofascial pain is muscle pain when pressure is applied to certain sensitive spots.

LLLT has an optimal light intensity above or below which the effectiveness of treatments can become reduced. This response is called a biphasic curve. The figure below demonstrates how dosage can reduce effectiveness (taken from [3]) if it is too high or too low.

Figure 4: A general example of response (biphasic response) to LLLT dosing. If dosing is too high or too low it is less effective. Image sourced from [3].

Figure 5 shows some real data on dosage from the same source.The horizontal axis is called the fluence – basically the surface energy J/cm2. The source neglects to mention the vertical access units, but it seems to correlate with healing rates. Namely the higher the number the shorter the healing time.

Figure 5: Measurements from real experiment with mouse healing. Wound healing time v.s. dosage. 635-nm (+/−15-nm) light used with 100 mW/cm2 power. Note that the fluence is the energy concentration over a cross-sectional region.

In the graph above, the small p-value of 5% indicates statistical significance. The lower the p-value the lower the likelihood, noted in experiment, that the impact of LLLT therapies will be the same as if no LLLT therapy was used. The 0.5% p-value, thus, suggests that over exposure to LLLT is highly likely to reducing healing speed. It is thus critical to accurately gauge the dosage.

Types of Conditions LLLT Treats

LLLT in low doses can be used to treat a whole set of problems. Figure 3 (from [3]) elaborates on some of these. For instance, LLLT can help with reduced inflammation and reduced Edema. Edema is inflammation resulting from fluid build up most noticeable in arms, legs, ankles and feet. It can also Induce analgesia – basically pain reduction.

Figure 3: Some components of the human body that benefit from LLLT. Image sourced from [3].

LLLT is also useful in treating acute (sudden onset) orthopedic conditions such as sprains , strains, post-surgical pain, whiplash injury, muscular back pain, cervical or lumbar radiculopathy (nerve pinching) and tendinitis. It can also be used for chronic conditions such such as osteoarthritis, rheumatoid arthritis, frozen shoulder, neck and back pain, epicondylitis (e.g. tennis elbow), carpal tunnel syndrome (wrist injury), tendinopathy (tendon injuries), fibromyalgia (body wide pain), plantar fasciitis (foot arch problems), post tibial (leg) fracture surgery and chronic regional pain syndrome (localized prolonged pain after injury) [2]. Dental conditions producing pain such as orthodontic procedures, dentine hypersensitivity (cold sensitivity), and third molar surgery respond to LLLT. According to the source. LLLT can also reduce impact of neuro-muscular contractions leading to a reduction of muscle spasms [4].

LLLT works to treat these conditions by acting at low doses to enhance cell proliferation of fibroblasts, keratinocytes, endothelial cells and lymphocytes for instance [2]. Increase transport of action potentials to facilitate this proliferation via increased metabolism. Maybe. Honestly, I have no real idea whether this is true. I’m just rattling off what the paper seems to be suggesting.

  • Fibroblasts are special cells found in places such as skin, tendons and ligaments that excrete collagen. As such LLLT can also help with reduction of wrinkles and the like.
  • Keratinocytes are the main cell found on the skin surface or epidermis – essentially LLLT can help with faster recovery to damage.
  • Endothelial cells form barrier between vessels and tissue to control the flow of substances in and out of a tissue. When such cells are damaged, cells, that shouldn’t, can pass through to neighbouring tissue and cause inflammation.
  • Lymphocytes are a type of white blood cell that operates primarily in the lymphatic system to fight of infections via a combination of cell destruction and immune system suppression.

By contrast, extended dosage reduces transport of action potentials and metabolism and acts to nerve block and reduce pain. Inflammatory cells play a role in collagen-induced rheumatoid arthritis and in acute pulmonary inflammation. The expression levels of these pro-inflammatory cytokines (cell signalling proteins) have shown some reductions by LLLT not only in rheumatoid arthritis and acute pulmonary inflammation but also when treating burn wounds, muscle cryo lesions and in delayed type hypersensitivity [4].

Summarizing then, basically LLLT has the following main impacts on the following particular areas of the body:

  1. At the site of injury to promote healing, remodeling and reduce inflammation.
  2. At the lymph nodes to reduce edema and inflammation.
  3. At trigger points to reduce tenderness and relax contracted muscle fibers
  4. At the nerves to induce analgesia (pain reduction).

All this said, I must note that I’m largely parroting existing references on the topic. And I recommend the reader take care to believe what I’ve written. Ultimately, it is important to remember that LLLT isn’t a catch all solution and seems to have moderate impacts. It shouldn’t be used as a primary treatment and won’t correct intrinsic structural problems in the body. It should be used in combination with other therapy interventions.

On Administering Therapy

I mentioned at the beginning of this article that I have noted some problems with some of the cheaper existing commercial products for light therapy. These can relate to properly assessing dosages and routines for light therapy. So in this section I want to briefly make some notes on administering the therapy. And what to consider in a device that you buy (or potentially make or modify).

Laser devices fall in to various designated classes as shown in the list below. Generally all LLLT devices should fall into this range. One thing to note is that LLLT uses diverging laser beams. This distributes the power over a wider area compared to standard lasers (divergent beam is used). The highly collimated (focused) beam of a standard lasers may in-fact cause damage and prove a higher risk to the eyes from accidental exposure as well – of-course, this ocular risk is diminished over distance even with collimated beams.

  • Class 1/1M – CD player
  • Class 2/2M – laser pointer
  • Class 3R/3B – LLLT and CD and DVD writers
  • Class 4 – Surgical laser

As I showed you earlier in Figure 1, the typical optical window for LLLT is between 600 to 1200nm. Hence any LLLT device must fall in this range. According to some for red light therapy a narrow range of red to near infrared light is used with wavelenths of between 660nm–905nm. The specific frequency response has an impact on penetration depth and cellular response and so dosage needs to account for this absorbance.

The application of light for LLLT is usually accomplished by a low power laser or LED typically in the power range of between 10mW–500mW. The applied power density (irradiance) falls at around 5W/cm2 surface density and is applied to an injury or to a painful site for 30–60 seconds per trigger point a few times a week for several weeks. Some sources suggest that wavelengths in the range of 760–850nm are adequate as well. At these wavelengths, a light source may achieve a light density of 5mW/cm2 at 5cm deep into tissues for a beam power of 1W and surface density of 5W/cm2 [4]. As little as one trigger point may be treated in simple cases, but as many as 10 to 15 points may be treated for more complex dysfunctions such as cervical or lumbar radiculopathy (nerve pinching).

The long term effects of LLLT occur within a week or two and can last for months and sometimes years as a result of improved tissue healing. There is also some evidence of suppressed synaptic activity in second order neurons so that cortical areas of the pain matrix are not activated. In the medium term, it appears that this can mean even faster response to therapy related to local edema and a reduction of inflammation to within a span of hours to days [4]. According to this source, LLLT, when applied with sufficient intensity can inhibit action potential transport to cause 30% neural blockades (and presumably a reduction in pain) within 10 to 20 minutes of application. This impact is reversed within about 24 hours, it appears.

With that. To be continued. I hope that this beginning attempt at a technical understanding of LLLT therapies will benefit those of you seeking to get past the simplistic narratives currently present on the web with regards to red light therapies. I myself remain ignorant on many elements from a scientific perspective and so shall continue a conversation to clarify and correct my mistakes. I encourage those in the medical fields to comment and issue corrections to any mistakes in this article.

References:

  1. C. Michael White. 2021. Why is the FDA Funded in Part by the Companies It Regulates? UConn School of Pharmacy. https://today.uconn.edu/2021/05/why-is-the-fda-funded-in-part-by-the-companies-it-regulates-2/
  2. Howard B Cotler, Roberta T Chow, Michael R Hamblin, James Carroll. 2015. The Use of Low Level Laser Therapy (LLLT) For Musculoskeletal Pain. MOJ Orthop Rheumatol. 2015; 2(5): 00068. https://dx.doi.org/10.15406%2Fmojor.2015.02.00068.
  3. Ying-Ying Huang, Aaron C.-H. Chen, James D. Carroll, Michael R. Hamblin. 2009. Biphasic Dose Response in Low Level Light Therapy. Dose Response. 7(4): 358–383. https://dx.doi.org/10.2203%2Fdose-response.09-027.Hamblin
  4. M Brunori, A Giuffrè, P Sarti, G Stubauer, M T Wilson. 1999. Nitric oxide and cellular respiration. https://doi.org/10.1007/s000180050452
  5. https://www.hindawi.com/journals/ijp/2013/575798/fig1/

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