In this episode, I’m speaking with one of the global authorities on light therapy, Dr. Praveen Arany. Dr. Arany began researching photobiomodulation (PBM), aka light therapy, 25 years ago, and since then, he has become a world-renowned expert in the field.
We get into the nitty-gritty science of light therapy—we discuss specific biological mechanisms of how photobiomodulation works, his research on light therapy and stem cells, and even misconceptions about light therapy that are important for you to consider if it’s part of your healing arsenal.
A little warning: I want to let you know that this is not a good “beginner’s guide” to this topic. I’d say it’s more for health geeks (like me) who are really into learning the fine details of how light interacts with human biology. This podcast is very detailed and very geeked out, so don’t say I didn’t warn you! 🙂
It was an honor to speak with Dr. Arany, and I hope you enjoy the episode. Watch for part 2, where Dr. Arany and I go much deeper into dosing and even the specifics of what to look for when purchasing a red light device.
Table of Contents
In this podcast, Dr. Arany and I discuss:
- How Dr. Arany’s skepticism of light therapy led him to become an active researcher and strong believer in this powerful tool
- How photobiomodulation actually helps your body…Dr. Arany and I translate the complex science into practical points
- The distinction between targeted light therapy (PBM) and sunlight—can’t we get the healing effects of light from the sun? And does the sun in some areas of the world offer more healing effects than others?
- Interactions between light therapy and your stem cells…can light make stem cells more functional?
- 3 primary mechanisms that explain photobiomodulation’s benefits
- Does light therapy act as a pro- or anti-oxidant? Which is it?
- The exciting link between light therapy and melatonin that’s not made in the pineal gland
- If light therapy is better delivered by lasers or LED. Dr. Arany shares his research and perspective
- Major misconceptions about photobiomodulation and the best ways to use light therapy to optimize your health
- What is the right dose of light therapy? Should the device be touching your skin or not?
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Transcript
Ari: Hey, this is Ari. Welcome to The Energy Blueprint podcast. With me in today’s episode is Dr. Praveen Arany, who is one of the top experts in the world on the subject of red and near-infrared light therapy and photobiomodulation. This is something, by the way, that hopefully you know, I wrote a book on in 2018, The Ultimate Guide to Red Light Therapy. That book has since become the most popular book in the world on this subject, I’m very proud to say, and feel fortunate and honored to say that. The book is also in need of an update. Hint, hint, might be one coming soon.
In this episode, it is all about Dr. Arany. I wanted to interview him because he’s one of the foremost experts in the world on the mechanisms, understanding the detailed mechanisms of how photobiomodulation, light biology modulation, photobiomodulation, works in the human body. There’s a lot of different ideas around this. A lot of people have their own theories about how it works, and Dr. Arany is one of the top experts in the world, so I wanted to get, be able to dialogue with him and talk through his understanding of the mechanisms, which was incredibly insightful.
A little about him, his CV is way too long to go through in-depth and list off everything that’s there. He’s a dentist by training. He’s done extensive PhD and postdoctoral training in dental medicine, oral pathology, and bioengineering at Harvard University. He’s a professor in the School of Dental Medicine at the University of Buffalo, and he’s got a long list of awards for his research for nearly 20 years, including the 2024 Investigator Award for Excellence in Photobiomodulation Basic Sciences. Again, he’s one of the foremost researchers and experts in the world on this subject.
Dr. Michael Hamblin, a former Harvard professor who I’ve also had on the podcast, who’s widely regarded as the most prolific researcher and top expert in the field of photobiomodulation, connected me with Dr. Arany and recommended that I interview him. This is a wonderful episode, but I must warn you that this is detailed science. We get nitty-gritty into the mechanisms of how photobiomodulation works, dosing, different aspects of LED versus laser, different aspects and nuances to the use of different devices, myths and misconceptions that are out there.
This is not just a simple, easy user guide of here’s the devices to go by and here’s how to use them. Again, this is very detailed, nitty-gritty science. We get into it here. As long as you’re ready for that and looking for that, I think you’ll get a lot of value from this. With no further ado, enjoy this episode with Dr. Praveen Arany. Dr. Arany, welcome to the show. Such a pleasure to have you.
Dr. Praveen Arany: Thank you for having me, Ari. Glad to be here.
Ari: I would love for you to tell listeners a bit about your background as far as how you got into the field of photobiomodulation and a bit about your research that you’ve been involved in in this field.
Dr. Arany: Thank you, Ari. I started in this field as a disbeliever, like many of us, that this sounds too good to be true. Training as a clinician, I’m a dentist by training and got my clinical training in pathology and my PhD in biomedical engineering, my focus has always been trying to improve patient care. When I heard of this treatment, low-level light treatment, as it used to be known, or photobiomodulation, as it’s known now, I could not believe that you could use light in a therapeutic manner. That was what got me started in the field.
My research has focused on trying to understand how light, a physical form of energy, can actually induce all these molecular responses, biological responses, which eventually result in a therapeutic clinical outcome. I guess the thirst for knowledge or the investigative aspect of my research has been focused on if we understand how this thing works, we can do more reliable and reproducible treatment. That’s what drives a lot of our research.
How red and near-infrared light impacts the body
Ari: Beautiful. When one explores the mechanisms on this topic, it’s interesting because I’ve not only read many hundreds of studies at this point, outlining various mechanisms– In the scientific literature, you find lots and lots of different discussion of different aspects of mechanisms, nuances of what’s going on in the mitochondria and nitric oxide, the hormetic aspect of it involving reactive oxygen species, gene expression changes, expressions, and growth factors. Then you can get into the level of specific cellular, molecular, biochemical mechanisms where you get a list that’s, I don’t know, 50 mechanisms long of all these different things that are going on in a cell.
It can be endlessly complex. Then on top of that, I found in talking to a lot of people who are in this field, not necessarily scientific literature, but, let’s say, owners of companies that sell these devices, many of them have their own theories of how they think it works. They are pretty detached in many cases from the actual scientific literature and from researchers like yourself.
With all of that said, I’m curious how you would conceptualize the core– without getting into overwhelming detail that the listeners are going to blackout on because they’re so overwhelmed with all the different mechanisms that I know you’re capable of getting into, what would you conceptualize as, let’s say, the top two or three core mechanisms of what red and near-infrared light therapy are actually doing to our bodies?
Dr. Arany: As we were just chatting before the call, I think it’s a very convenient explanation in terms of physical energy that light represents being transferred into the energy organelle of the cell, the mitochondria. We know that cytochrome c oxidase, the enzyme responsible for electron transport in the mitochondria is a great first mechanism that was actually ever described. This was seminal work by Tiina Karu, Margaret Wong-Riley, and Harry Whelan. These investigators, I think, brought a lot of legitimacy to the field because people were doing light treatment for the longest time, but they didn’t understand how it worked.
I think their demonstration that an enzyme in the mitochondria, which is the powerhouse of the cell, is capable of receiving this energy and changing its function, it increased ATP and ROS, was a very, very good explanation and is still one of the performance mechanisms or resilience mechanisms that we code. We know this is a very, very important mechanism. However, if you’re in the field and you’ve seen that photobiomodulation or low-level light treatment or red light therapy, all these different terms, they can do a lot more than just one disease. That’s where I think it becomes a little murky that how can one treatment with one mechanism affect all of these different things.
Ari: Right. That’s where a lot of skepticism comes from, especially in the conventional medical community is, “Oh, this sounds like snake oil. How could it possibly be beneficial for so many different types of things?” Because they’re used to thinking of, oh, for this disorder, I have this specific chemical that targets this specific mechanism unique to this disease. How could one therapy affect so many different diseases in different parts of the body?
Dr. Arany: That is where I think a lot of my personal research actually started. I said, how is it possible that light can do everything? It doesn’t make any sense. When I started my research back in ’99, even the cytochrome c mechanism was not discovered. At that point, I was chasing one demonstration of PBM benefit, which is improved wound healing. We know from the very first studies that Dr. Endre Mester did that the wound healing can be improved.
My research actually started there. I was like, “How can you use light and improve wound healing?” The wound is a very dynamic environment with lots of cells and changes that actually are very attractive for many reasons. I found that to be my playground, if you will, for beginning to understand how light is working. In that process, we actually discovered one of the other mechanisms, which turns out to be a growth factor called TGF beta 1. This growth factor is extremely important for many different processes, but specifically for wound healing.
Now, this growth factor turns out to be present normally in the body, in all of our tissues in an inactive, latent form. That is where I think we saw the opportunity. Now, this growth factor is present but is not activated. That’s where we found, after lots of very careful investigation, that a single amino acid, a single methionine on that growth factor is actually responsible for sensing light. We make that analogy of rhodopsin in your eye. We don’t have electronic sensors in our eyes, how come we are able to see?
If you wanted to build a robot, now the big craze is artificial intelligence, if you wanted it to see, visualize something, you would need an electronic detector to do that. We don’t have electronic detectors in our body, how is it that we are able to see visible light? That’s where, if you look very carefully, you will see that there is actually a molecule called rhodopsin in your eye that is capable of sensing light.
If you can have one molecule that is capable of enabling vision, we thought, why would it not be possible to look for other molecules? That’s where we found this growth factor TGF-beta. After very careful investigations in the lab, in vitro, which is in cell culture and cells, to animal models, which we very carefully investigated, we found that there is a single amino acid in this growth factor that is responsible for the light sensitivity. That is our second mechanism.
The UVB and Vitamin D connection
Ari: Okay. Real quick, a slight digression. The mechanisms whereby UVB light affect vitamin D synthesis and also melanin from UV light, wouldn’t those have to be mediated by a similar light sensing mechanism?
Dr. Arany: Not necessarily, because, vitamin D is a great example, the chemical structure of vitamin D, the pre-vitamin D, turns out to be UV sensitive. The sunlight UV that we are getting on our skin actually completes the biochemical synthesis process of pre-vitamin D to vitamin D. People, and I’m sure your audience would be very well informed, sunlight is more than just making us happy and joyful, it actually has a biological health benefit, because it is converting pre-vitamin D into vitamin D, which non-intuitively you would think, what do we need vitamin D for?
Not only your psychological health, but your bone and your teeth absolutely depend on this vitamin and the active form of this vitamin. Good if you’re going out to the sun, going and getting good sunlight. Working out in the sunlight is not only good for your muscles, but vitamin D for your bones is actually benefiting from this.
Ari: Take me through what the distinction is that you’re making between something that’s like rhodopsin that senses light in this way that you’re describing versus the mechanism of how– Our bodies are responding to light in the case of vitamin D and in the case of melanin synthesis. Something is still sensing light in a way or responding to light, but what’s the distinction that you’re making there?
Dr. Arany: I think we get asked this question all the time. If PBM is just like going out into the sunlight, why can’t we just stay out in the sunlight and get that benefit? People ask this question all the time. Sunlight is great. We know sunlight is great for many things. However, if you think about what red light therapy is or photobiomodulation is, it is usually a single wavelength or at least a combination of wavelengths which are pure, which basically means that they are monochromatic. The wavelength is very, very specific.
What happens when you go out in the sunlight is you have all the colors of light in that, and there is potential for interference or not having enough of each wavelength. Those are the problems of why sunlight potentially is not good for trying to do PBM. It has all of its other benefits, but if you want to do PBM, sunlight is probably not the best source.
Why sunlight is not enough when it comes to RLT
Ari: I know we’re going on a little bit of a digression here, and this was actually something I wanted to bring up later with you, is the distinction between photobiomodulation and sunlight, since we’re here. From an evolutionary perspective, presumably, the reason that human physiology or that animal physiology more broadly evolved to the capacity to utilize red and near-infrared light was from millions of years of exposure to sunlight, correct? Would you agree with that?
Dr. Arany: That is true. You can talk to evolutionary biologists, that is one of the reasons light evolved.
Ari: In a way, the argument that you’re making is essentially, it’s saying, “Well, yes, we evolved to utilize these wavelengths from the sun, but the sun is not optimal.” Clearly, the sun has to be doing some of these same photobiomodulation effects. Would the distinction be better conceptualized as saying, “Hey, but with these specific devices, with isolated wavelengths in this range of red and near-infrared that these specific wavelengths that we know work at a certain irradiance or power density applied to a specific area of the body in this way, we can get a better effect than what you could just laying out in the sun”?
Dr. Arany: Correct. We make that analogy. When we start talking about mechanisms, depending on the interest, we can go down to ROS, the redox that is generated, which can be beneficial. When you think about redox, you normally think of cancers and aging, which is a negative thing. When you’re thinking about light in general, why can’t we use any light source, including sunlight to do PBM, we make the analogy that just like we absolutely need water and air to survive, the same water and air in the wrong place at the wrong time can kill you. It can be very toxic.
Similarly, light is all pervasive. It’s everywhere. Not just sunlight, even your indoor lighting. People are asking these very, very important questions, is it just illuminating a room or can we do more of that? Can we do more and include the specific wavelengths within those lighting systems? Especially if you start thinking about interstellar travel where sunlight is not available, that is becoming a bigger and bigger question that people are thinking about.
To conclude that part of our discussion, hopefully, in terms of giving you a reasonably good answer, I think sunlight is beneficial, no question about it. Using it for PBM will probably not get you all the possible benefits, because it doesn’t have the right amount in the right place at the right time.
Ari: One quick additional, maybe slight digression, and then I want to loop back into mechanisms. Following up on what you were just saying there, this also connects with something else I want to talk about later, would you conceptualize the photobiomodulation that we get from sunlight as being generally more superficial in nature, meaning that we don’t get a lot of light in the red and near-infrared range that penetrates to the deep tissues? Would you say that is accurate?
Dr. Arany: That brings up a very important discussion on where you’re getting the sunlight. We know that the Mediterranean belt and the German-Austrian-Swiss border seems to be the optimal place for sun clinics, right? I don’t know if you have seen that literature. There is a very interesting correlation between those areas where sunlight is the most beneficial. People believe that it’s not only the amount of light that you’re getting, but also the wavelengths of light in terms of which wavelengths are actually penetrating.
Now, the reason you don’t get a lot of infrared in your sunlight is because you have humidity in the atmosphere. We know water absorbs infrared. Even though if it is present, by the time the light actually reaches you on Earth on a given surface, it’s all being filtered out by all the humidity in the atmosphere.
Ari: Got it. As far as depth of penetration into the body, would you conceptualize mostly it’s more superficial rather than a lot of that light penetrating to deep tissues? If I lay out in the sun, am I getting a lot of that light penetrating very deeply into my tissues, or is it mostly pretty superficial?
Dr. Arany: Pretty superficial.
Using Photobiomodulation for stimulating healing
Ari: Okay. Let’s loop back to mechanisms. I think the two that we’ve covered so far are TGF-beta and the cytochrome c oxidase. Basically, light is interacting with mitochondria and stimulating mitochondrial energy production. TGF-beta is involved in stimulating wound healing, essentially. Could you conceptualize that broadly as cellular growth and regeneration?
Dr. Arany: Right. That’s where we have done most of our work. We are focused on if it can improve tissue healing, can it actually complete that healing response and do tissue regeneration? That’s where all our work with endogenous stem cells. We don’t transplant stem cells into the patient, but we are trying to program the stem cells in our body to actually help with the healing and regeneration. TGF-beta turns out to be really important for that. [crosstalk]
Ari: This is a related aspect of cellular growth and regeneration, related to TGF-beta and other growth factors that might be involved. This is also a distinct mechanism of now we’re– What’s the right word for it? Mobilizing stem cells to a particular area?
Dr. Arany: Mobilizing and harnessing their regenerative potential.
Ari: Okay. How does that work? We have stem cells latent that are in a particular area or they’re in the bone marrow and the light is activating them? Can you explain in more detail what’s going on there?
Dr. Arany: Sure. I think most of our studies have been activating and mobilizing local stem cells, whether it’s a burn wound, whether it’s inside your teeth when we’re trying to prevent root canals. We have dental stem cells in the gum, in the gingiva, in the pulp tissue, or you have it on the skin when we’re doing burn wound healing. We’ve been focused on that, but other groups have obviously explored the bone marrow mobilization as well as stem cells in the heart, in the liver, in the brain for different regenerative potential.
The way this works is that if you get any kind of injury or a disease process, the stem cells that are present usually will come to that area or get attracted to try and repair it. When they get there, it’s usually a very messy environment. When you do PBM on an injured site or a diseased site, it helps these stem cells program themselves, heal that tissue, and regenerate that tissue. It’s almost like an instruction that is provided to those cells in that local milieu, and then they can actually do their job.
Ari: There’s also an element of local growth factors that are tissue-specific, that if you shine it on muscle, for example, I’ve seen literature showing that it increases IGF-1, insulin-like growth factor 1. If you shine it on the brain, for example, I’ve seen literature showing increases in brain-derived neurotrophic factor or nerve growth factor. We have lots of other tissue-specific growth factor, presumably maybe specific growth factors in glands. You shine it on your thyroid gland or things like that. Maybe there are some other specific growth factors in other tissues.
I think we’re painting a picture more broadly between TGF-beta and mobilizing stem cells and getting them to come in to repair wounds in a particular area or damaged cells, and these other tissue-specific growth factors. It’s painting this broad picture of it’s activating many mechanisms simultaneously that are involved in cellular growth, regeneration, and healing processes.
Dr. Arany: This is a great point of confusion as well. We do a lot of wound healing research. We are very focused on clinical work as well as basic science. I will give you a great analogy, which we think is actually causing confusion. If a patient presents to you with a chronic wound, whether it’s a pressure wound, a venous ulcer, or arterial issue, or a diabetic wound, very common nowadays, unfortunately, these wounds that present to you, our main line of treatment is to curette and debride. Then we put a medication, we disinfect–
Ari: Just briefly explain to people what that is.
Dr. Arany: Okay. When you have a wound, you have all these dead tissue, which you need to get away. It’s either blackish or brownish. It smells very foul. You have to clean that wound. Normal wound care involves repeated cleaning and waiting over time till the healing takes place. If you take these tissues at any point and look for growth factors and changes in blood vessels and different cells, you will find them changing. It does not mean that your metal scalpel or whichever curette you use actually induced the growth factor.
That is where there’s a lot of confusion. People do PBM and they look for PDGF, VEGF, IGF and see a difference. People have tried to do different kinds of analysis after PBM therapies and found these growth factors changing. It does not mean that PBM is inducing these growth factors. It is just a normal– We call them effector responses because these are the way that the tissue will heal. The muscle will increase in its mass. The heart will heal itself. The cardiac myocytes will actually heal themselves.
The BDNF story is actually much more cleaner because we know that light is capable of increasing BDNF, either directly or as an effector response is not clear. We have measured this in concussion, actually, Dr. Hamblin’s work, where they showed that the BDNF levels increase after PBM treatments. It does not mean that PBM is inducing BDNF, but it means that the healing response that has been initiated is actually involving the regular healing cascades.
Ari: I’m trying to conceptualize the distinction you’re trying to make. Let me start by saying, let’s just say, I know that the experiments are often not this simple, but let’s just say, okay, we’re able to sample muscle tissue or brain tissue and get a baseline measurement of how much VEGF or BDNF or NGF or something is in one of these tissues. Here’s baseline. We shine red or near-infrared light on it. Now we take another measurement, it’s elevated. The conclusion from that is photobiomodulation is elevating these growth factors but you’re saying it’s incidental. Are you trying to say that it’s a downstream effect of other more important mechanisms?
Dr. Arany: The mechanism is what light induces. If you focus on that, there are only three mechanisms we are aware of that have actually directly demonstrated light-modulated change. One is cytochrome c oxidase. The other one is TGF-beta. The third one, there’s a category of light-sensitive receptors and transporters. The most famous of them is a non-visual opsin or a pain receptor that Dr. Hamblin actually showed called TRPV1. Those are the only mechanisms which are directly associated with PBM-induced changes.
Ari: Let me rephrase that. When you say those are the only mechanisms associated with photobiomodulation, you’re saying those are the initial first responding mechanisms. The photons of light are interacting directly with those three things that you just mentioned. Then after that, there is a whole downstream cascade of other effects that happen subsequently.
Dr. Arany: Right. We know that when we activate TGF-beta, eventually, if you need blood vessels, it will induce VEGF or it will induce PDGF to get the fibroblast in. That doesn’t mean that light is activating VEGF or PDGF. It’s actually activating an upstream. We have to start thinking upstream and downstream. That’s when–
Ari: Sorry, go ahead.
Dr. Arany: Yes. That’s when the mechanisms will be clearer on what is a mechanism.
Ari: Okay. On a practical level, is this distinction really meaningful? Other than just making sure that we’re clarifying the distinction between mechanism being defined as the initial things in the body that the photons of light are immediately triggering, the initial switches, the light switches, if you want to conceptualize it like that. On a practical level, what we’re interested in is the whole thing. We’re interested in all of the downstream, the whole cascade of mechanisms all together, what is the actual end effect, not just the initial effects.
Dr. Arany: The problem that has plagued our field of photobiomodulation, red light therapy, and low-level light treatment is the lack of consistency and robustness of response. Besides the fact that it works in so many different diseases, we are not able to guarantee that we will always get a therapeutic response to the same level in each patient. That is where the mechanism is important, because if you don’t know how things work, how can you optimize it?
We know that all of us are going to have different amounts of growth factors, different amounts of hormones, different body makeups, right? Right now the problem with the field is everybody is getting the same dose. It’s a one-size-fit-all for everyone. That is not the way. Even if you don’t know anything about medicine, you know you’re not going to pop the same pill for a headache versus a leg pain versus cancers, right?
Why one-size-fits-all treatments don’t always work in PBM treatment
Ari: This sounds like maybe it’s a whole other digression, but the reason that everybody’s getting the same dose has to do with standardization to make studying things easier so that you don’t have such a wide variation. This research group is using this dose and this research group over here is using this other wildly different dose. Is that what you’re getting out there when you say people are getting the same dose?
Dr. Arany: We don’t think they’re getting the same dose because a clinic in Brazil– We have actually done a very, very careful analysis of the evidence for oral mucositis with photobiomodulation. There are some other studies, but this group that actually studied that very, very carefully actually came to the conclusion that completely different protocols in completely different centers were still beneficial, which didn’t help the field because we know that there is a benefit.
Like you’re saying, we only care about the overall outcome, which is true. If we don’t understand what the mechanism is, we cannot point to what’s wrong or what’s different with each one of these protocols.
Ari: Would it be fair to say that from the end consumer’s perspective, the user of these devices, what they care about is more the end effect, the ultimate effect, whereas from a research perspective, it’s really critical for the scientific legitimacy of this field, as well as to facilitate further knowledge, further exploration in a way that is helpful and makes sense? It’s really important to elucidate the mechanisms.
Dr. Arany: The mechanism is not merely an academic exercise. I think a lot of people think people who do cells and mice and flies and frogs are trying to do things in a very academic and didactic way, a very intellectual way. If you think about what we practice in the clinic today, it actually comes from all this research. All the research advances that help our understanding actually make it to clinical practice.
Anyone you talk to in medicine will talk about the pyramid of evidence, has it reached the highest level of evidence, which is a systematic review and meta-analysis, which is based on many clinical studies that have been done very carefully? Yes, the research is very academic and very important for our understanding, but that understanding has led to a better form of treatment and the consistency of the treatment.
The reason you’re hearing so much about PBM now– It’s been around for the last 40, 50 years, right? From the ’60s, it was around, but suddenly there’s so much buzz about this treatment. It’s largely because our understanding and the technology associated with that understanding has actually improved.
Why photobiomodulation works on multiple diseases
Ari: Yes. Okay. Are there any other mechanisms that you think are really important to mention here?
Dr. Arany: I mentioned the three mechanisms. One is the mitochondrial mechanism. The other one is the extracellular TGF-beta mechanism. The third one is the cell membrane transporters, which are light-sensitive, especially the pain receptor TRPV1. Those are the three major mechanisms. However, I think you pointed out in the early part of the talk, when you do light treatment, you’re exposing all the cells and all the constituents of the cells and tissues to light. It’s probably acting at multiple levels at the same time. We are back to the question, how can it work in so many different diseases, right?
When you think about the definition of photobiomodulation– Oh, by the way, the term photobiomodulation was coined not very long ago. It’s about 10 years old now. It is a PubMed MeSH term. This is how all of the scientific literature now is indexed in National Library of Medicine at the NIH. There are over 350 terms, everything from red light therapy to low-level light treatment to cold laser treatment. The fact that we now agree on a term is also a big deal because we now actually recognize this therapy.
The point I was trying to make is that although the treatment has improved in its rigor and understanding, the fact that it’s working in so many different diseases is a little perplexing. How can it work in Parkinson’s, knee pain, arthritis, and wounds in your mouth? That intuitively doesn’t make sense. If you start thinking about what is common to all of these diseases, you will come to that conclusion that pain, inflammation, and aberrant immune response or a lack of healing is what is different, which is common in all of these diseases. Those are the fundamental biological response that PBM addresses.
We know that it’s capable of modulating these responses. In many cases, photobiomodulation should be used as an adjunct, not as a main line of treatment. That’s where there’s a lot of discrepancy in people who try it and do not see optimal results.
Ari: I think this question of why does it work in so many different diseases and what are the specific mechanisms of how it works is perplexing when we look at it through the lens of a conventional medical paradigm that is very focused on finding the unique mechanisms of how something works and the unique mechanisms of a particular disease process. We can look at it through that lens of evaluating it relative to a drug and say a drug acts in a very targeted way on this specific mechanism and therefore affects this specific disease or problem.
If we shift the comparison and we were to compare it to, let’s say, exercise or eating a healthy diet, why is it that eating a healthy diet is also broadly protective against dozens of different diseases from neurological diseases to heart disease to lung diseases to immune-related diseases and so on and so forth? Why is exercise protective, even doing physical work for your muscles, why is it protective against brain diseases and all kinds of many dozens of different diseases in different systems of your body? It’s because these things are affecting hundreds of mechanisms that affect overall health of the system in many different ways.
They’re not acting like a drug trying to block a specific mechanism of a specific disease. If we were to, in light of what we were discussing earlier about the fact that this whole mechanism of photobiomodulation evolved as a result of hundreds of thousands of years, millions of years of our ancestors being exposed to sunlight, this is, I think, should be looked at more in the light of, excuse the pun, more in the light of that this is essentially a required nutrient for supporting human health in the same way that eating a healthy diet is or doing exercise is.
Dr. Arany: Right. You make a very good point about exercise and diet. I’m a big believer in the holistic approach, as you’re pointing out, which is actually better than the sum of the small parts.
Ari: Yes.
Dr. Arany: Let’s go back to those two examples. Exercise in the right amount on a daily basis is actually really good for you, both for your mental health as well as your physical health. However, we all know that if you are overworked or you’re pushed to your physical limits or you have mental stress, that will interfere with your performance. Other way around, it will undermine your health.
Similarly, with your diet, the food that we eat, the right amount, the right proportions at the right time is very helpful. However, we know that obesity is unfortunately a huge problem. When you think about all the malnutrition that exists, it is again, the other end of that spectrum. In an ideal world, you would give them the right amount of food and the right amount of exercise. Light is no different. That is how we should be thinking of it. I think it has a very important role in the holistic approach, which I think you’re also echoing, in terms of health. Whether you think of light as a supplement or you think of light as a drug, that’s up to you.
Ari: Or as a [crosstalk] necessary nutrient.
Dr. Arany: The definition of a drug is a substance that is absorbed and can change body function. Light satisfies that need.
Ari: Right. I would favor more conceptualizing it as a necessary nutrient for health rather than necessarily– In the sense of if you put people in a light-deprived environment, they will become unhealthy. You will see that, if they’re exposed to, let’s say, only artificial light of certain spectrums and that’s devoid of certain spectrums, they will quickly become unhealthy in much the same way that you would if you were deprived– I’m playing with words a little bit here– necessary nutrients in your diet or necessary nutrients in terms of human movement. You would quickly become unhealthy. Anyway, we’ll leave that discussion for another time.
As far as mechanisms, when I spoke with Dr. Hamblin about it, he basically conceptualized the cytochrome c mitochondrial-mediated pathway as– I don’t want to misrepresent here, the gist of it was like, “Well, for a long time, we thought that was the main mechanism, photons interacting with cytochrome c and the mitochondria. Mitochondria produce more energy. That’s the main thing going on.”
He made the case that he thinks that’s actually a fairly small portion of the overall effect and that it’s more about lasting changes in growth factor expression, in gene expression changes and so on that don’t just affect mitochondrial energy production in a very transient way for minutes or hours, but are long-lasting changes in gene expression that might last maybe days or sometimes longer. Do you agree with that?
Dr. Arany: I do agree with that. I think there are benefits to doing PBM, both as a prevention to improve performance, improve resilience, as well as a long-term benefit of getting repeated treatments. We should not be thinking of PBM and light therapy as only for treatment, therapeutic benefit, but also, like you’re pointing out, as a necessity part of our everyday life, just like we need to eat every day and preferably exercise every day, right? Not possible with all our routines, but we should be getting light on a regular basis.
Going on to the sunlight like we were discussing before has many, many benefits. However, if you can also supplement that with whether it’s an indoor lighting lamp or an actual PBM device, I think it has significant benefits.
Ari: Do you think, broadly, that it’s fair to summarize the end effect of photobiomodulation as being– If you were going to boil it down for a layperson and say, in very simple terms, here’s what red and near-infrared light therapy could do for you, would you say that the dominant effect is essentially about cellular growth and regeneration more than anything else?
Dr. Arany: Cellular growth, you’ve got to be careful when you use that term. Normally when you think of cellular growth, you’re thinking after development in an adult. That usually means a tumor.
Ari: Yes. Not abnormal cell growth. Not cancerous tumors, but growth in the sense of stimulating healing of damaged tissues.
Dr. Arany: There are several ways to think about this. If you think about what red light and infrared light does for a normal adult who’s functioning well, is healthy, is that it improves their resilience and improves their health overall, wellness overall. This has both psychological as well as physical benefits too.
Red Light Therapy and Redox balance
Ari: As far as the mechanism of improving resilience, would you conceptualize that more through the TGF beta pathway or would you conceptualize it more through reactive oxygen species activating the antioxidant response element, activating maybe the NRF2 pathway, and increasing internal antioxidant supplies?
Dr. Arany: That’s a great segue into actually discussing about Redox. Redox has always had multiple benefits to it, but also usually it’s associated with a bad outcome. When we think about ROS and Redox, we are normally thinking about aging and cancers, and poor skin health.
That’s how we think about Redox, which is why a lot of people like Anne are promoting antioxidants because they are beneficial over the longer term. What people don’t realize, unfortunately, is that the ROS that is present in the body is absolutely critical. If you think about your endothelial cells, which are the vessels, cells lining your blood vessels.
Ari: Real quick for those listening, ROS for people listening is reactive oxygen species. These are otherwise known as free radicals, the things that we’re often taught by various health experts are bad for us. Oxidative stress, oxidative damage, free radicals, reactive oxygen species. These are all under the same umbrella here.
Dr. Arany: To finish that thought, one of the best pro-oxidants is exercise, which is, again, very non-intuitive. If you’re using antioxidants and you’re exercising, both of them are great for you.
Ari: Which displays a lot of the oversimplistic thinking that’s been presented for decades now to the public on this topic, where we’re taught to think of free radicals as bad and antioxidants as good. The literature just really does not support that.
Dr. Arany: PBM has unfortunately been on both sides of that story. PBM has been used as preventing antioxidant stress. It actually can reduce oxidative stress. It can act as an antioxidant. Surely enough, if you do any PBM treatments in the lab and measure the levels of scavengers such antioxidants, such as superoxide dismutase, glutathione peroxidase, all these catalysts, all these anti-ROS species.
You will see them go up eventually. Right after PBM treatment, we actually have a big pulse of Redox that comes from the mitochondria as well as the ROS nitric oxide that is being generated. All of that shows you that you should be looking at both sides of the coin.
There is ROS in the initial phase, which is actually good for us because it helps with phagocytosis and all these processes, which are very important to clear the injury and the damage. Eventually, we do want the antioxidant response because we want that thing to stop.
We, again, make that analogy with the wound, right? If a wound does not have inflammation, that wound will never heal. It’ll get infected. It’ll basically fall apart. That inflammation has to stop, otherwise it becomes a chronic wound. That is why you need both sides of that coin. PBM and Redox has that story to say.
PBM and melatonin
Ari: With this in mind, another interesting segue here is Russell Ryder’s work on melatonin. This didn’t come up yet in our discussion of mechanisms. I assume you’re familiar with it, but I’m curious how you see the melatonin side of this story, which is little known, still, I think by most people, how that factoring into this equation or this story of mechanisms.
Dr. Arany: Melatonin has been extensively studied, and specifically with blue light. It is known that there is a very specific biosynthetic pathway involving the pineal gland. That is very well understood. However, when we are doing PBM, like you’re correctly pointing out, we have not tried to connect the dot between blue light PBM and the melatonin response.
If you talk to anyone who’s been getting even near-infrared light treatments for concussions, PTSD, the number one improved symptoms, including in our own clinical trial, is improved sleep. We know we are affecting that circadian rhythm, that biological clock.
However, we are using infrared light, which is not a conventional melatonin-inducing pathway. There is a lot more to that story than we are appreciating right now. We have to move away from some of the convention of melatonin biology, which is largely blue and green light.
Ari: What you said is interesting. What I’m referring to, I don’t know if you’ve seen Russell Ryder’s research on extra pineal melatonin, mitochondrial-derived melatonin. Where it’s been shown, I believe several studies now, that red and near-infrared, they use a red wavelength, but they refer to it as near-infrared, show inside of cells at the mitochondrial level supports mitochondrial-derived. Not pineal-derived, melatonin secretion. Have you seen that research?
Dr. Arany: I don’t believe so.
Ari: I’m going to have to share those studies with you.
Dr. Arany: There’s so much interesting work going on in so many different areas now, I’m not sure.
Ari: This is interesting. I’ll send that to you via email. I’d be very interested to hear your thoughts on that. Anything else to wrap up? We spent a lot more time on mechanisms than I anticipated, but anything else to wrap up the mechanisms side of this story?
Dr. Arany: No. I think it is important for people to realize that the popularity of photobiomodulation in red light therapy is largely being shepherded, if you will, without better understanding of how it works. That is why you see a lot of new devices, better technology, more colors that are available, and combination of colors. I think that’s a really, really important advance in the field, where people are using multiple wavelengths to do different treatments.
LED lights versus laser
Ari: Let’s go to LED versus laser. What are your thoughts on that?
Dr. Arany: There used to be a time when there used to be a lot of laser purists in the field who thought that LED has no role in PBM. Unfortunately or fortunately for us, the clinical data has shown that LEDs have a clear role. Now the question is, are they comparable and do they give you equal benefit?
In the lab where we can control all the parameters, we have seen no difference between the benefits from an LED and a laser. However, when we get to animal studies and we do our clinical trials, we know that a laser is less forgiving than an LED in the hands of an inexperienced clinician.
LED, you’ll have to do a lot more things wrong to end up overdosing. I think that’s one of your questions I saw about the Armstrong’s curve. We know that PBM cannot do damage. However, if you give too much dose, you will negate your benefit. That is more possible quickly with a laser than an LED device.
Ari: As far as the actual effects, all things being equal, do you think there’s an advantage for laser? I’ve had many discussions with what you referred to as laser purists and people who have been in the clinic many years using these, and they are convinced lasers are better.
I just did a podcast with Tom Kerber, who’s done extensive testing. I know you’ve had a discussion with him. He’s tested this in various ways with nice instruments and found, hey, you get similar diffusion of light in the tissues, you get similar penetration.
There isn’t plausible reason to think that they’re doing radically different things because even the collimated light diffuses once it enters the tissue. What’s your take on that?
Dr. Arany: A photon is a photon. It doesn’t matter what the source is. It’s the way it behaves in different media that is different, right? That’s where we should think about. At the cellular level, at the molecular level, when the energy transfer is occurring, there is no distinction between the two sources of light. However, as we discussed, and I’m sure your audience will appreciate, a laser is much more efficient at the energy transfer than an LED. However, when the photon enters the tissue, many of those properties are lost. Many of us do experiments on a single layer of cells.
In that case, as we have seen, no difference between LEDs and lasers. When we start making it more complex, that’s when we start seeing differences between the laser performance and the LED performance.
Ari: Other than that, you don’t think that this is a big issue. Is there any area where you would say, yes, for this specific benefit or this specific type of treatment, lasers are clearly superior or vice versa. That in this specific context, LEDs are vastly superior.
Dr. Arany: Not so much in the biological or the clinical context, but in terms of policy and regulations, I personally feel that lasers should be restricted to clinical units in the hands of a trained operator. It doesn’t matter what their qualification is.
My personal opinion is that everybody can be trained to do this treatment. If laser technicians can remove hair with very powerful lasers, I’m sure we can do PBM folks to get adequately trained. I’m not a big fan of take-home laser devices because of the potential for damage and the fact that you might actually–
The natural tendency is if 10 is good, then 200 is going to be better. That tendency, I think we can’t take away from people. I would rather have LED devices, which are take-home and laser devices in the clinic. The only place where I see LEDs in the clinic right away is when you’re trying to treat large surface areas, right?
Lasers in that spectrum is going to be very difficult if at all possible. That’s where all your beds and your large arrays are most likely going to be LED-based.
Ari: On the practical side of things, are there any big misconceptions that you feel, as you and I have discussed, this field has expanded, especially since I published my book on the subject in 2018. This field has exploded in popularity. It’s become mainstream now.
I remember a time 10 years ago where I was having to go through a marijuana-growing light company to make me custom lights because no company even existed that was making these devices. I was convinced it was going to go mainstream.
I should have started a business making these devices, and I would have been the first. Now it’s mainstream. It’s exploded in popularity. Given that and given that there’s so much discussion by so many people out there, so many different companies marketing their devices, are there any things, areas that you feel people are getting wrong, where they’re doing things wrong or they’re understanding things wrong?
Dr. Arany: I think using light as a main line of treatment for many diseases is not advisable, for two reasons. One, it has not been proven to have adequate efficacy in that specific disease. Two, you might be potentially withholding an effective mainline treatment. I gave the example of concussion.
Just because you have access to light therapy, some people are like, “I don’t want to go to a neurologist. I will be fine to do light treatment by myself.” That’s a dangerous place to go. My recommendation to the people who are hearing about this for the very first time is not to think of it as the main line of treatment for every disease.
There are specific diseases where we have proven efficacy. In many diseases, given the large list of things this can do, you should probably consult with a clinician and ensure that you’re getting standard of care. You can consider using light as an adjunctive treatment.
PBM cannot treat everything
Ari: Any other areas that jump out to you as far as myths, misconceptions?
Dr. Arany: It’s a good thing and a bad thing that it works in so many diseases. We have to start making that distinction where is PBM adjunctive or synergistic versus where should we be using it as the main line of treatment. There are very specific diseases where it can. Diseases and wellness, where it can be used to enhance performance, enhance resilience.
In many other cases, for example, going back to wound healing, if you have a diabetic, necrotic wound and you don’t get rid of that dead necrotic tissue, PBM is not going to heal that wound. You have to do standard wound management before you can use the light. Light is amazing in those contexts, but it will not work if you don’t get rid of that necrotic tissue and the biofilm and the infection.
Ari: The devices have changed a lot over the last 20 years. It used to be, as you said, mainly laser, and then LED technology came onto the scene. We’ve had this explosion of LED panels. That’s the dominant way that people are using these devices, which is different from actually–
The vast majority of the literature that’s been accumulated on the subject has used not necessarily LED panels from a distance, but has been using lasers or LED devices and pads oftentimes applied directly to the skin.
I’m curious how big of an issue? Do you see an issue there? Do you see an issue with the widespread use of panels that are being used in a non-contact way, not pressed in contact with the skin? What’s your take on that issue of contact versus non-contact light therapy?
Dr. Arany: This brings us to a bigger question on the dosimetry, which I think is the other big topic. Besides the mechanism topic, I think dosing in PBM is a whole separate topic by itself. We’ll have to come back-
Ari: Okay. We’ll have to cover it in depth in part two then.
Dr. Arany: Yes. We’re happy to come back for that. Very briefly, we have realized after doing a lot of studies, controlled studies in the lab and in clinical scenarios, that the amount of light that we provide to the patient or the biological target, we can only control what gets on the surface.
You can do very sophisticated Monte Carlo simulations and this and that to see where that light is going. At the end of the day, we are guesstimating how much light is going where. That’s the first problem. The second problem is we still don’t know how much light energy needs to go to which target.
Even if you could figure that out, that would be a huge advance in the field. Right now, we don’t even know how much light and mitochondria needs. We know mitochondria and epithelium need different energy. We know that fibroblasts need different energy.
We have done those studies where we have looked at different cell types, which are present in your skin and your different organs. Each one of them needs different amounts of energy. Now, we are getting to a point at which we will be more confident how much energy needs to go to which tissue.
Right now, we don’t have that answer. My recommendation is, as long as we are controlling the amount of light dose on the surface, we are doing as precise a treatment as feasible, even the current technology.
Ari: Given that, what distinction would you make between contact versus non-contact light therapy as far as the amount of light that is hitting the surface, but maybe bouncing off versus the amount of light that is actually entering through the skin to the deeper tissues?
Dr. Arany: If you want to be more efficient, obviously being in contact is great. I would recommend it. A lot of people have lots of success with using some kind of a contact mode for their light device, whether it’s a handheld probe or an LED, or a mat where they lay on.
My concern would go back to how much light is enough light, right? If you’re going to get enough light on the surface, how much light is going deeper inside? That would be a direct reflection of whether it’s in contact or some surface away. If you only care about how much light is on the surface, then that question is moot.
Ari: Meaning if you’re only interested in superficial treatment of skin versus treating deep tissues?
Dr. Arany: No, I wouldn’t say that. If you’re using near-infrared light, let’s say 1064 or 94980 or 810 for that matter, the amount of light that you increase by being in surface versus saying about, let’s say a foot away or a few centimeters away, is marginal compared to how much you can deliver.
It’s a question of just increasing the amount if your surface is some distance away. That’s very easy to do. I don’t think the benefits of being in contact justify any difference in the way you’re treating. Now, why would you want to be some distance away if you’re thinking about the throughput of your clinical care?
I’m not talking about home-use devices, which is your personal device. If you’re thinking about clinical care and you’re thinking about pushing patients through your clinic, you would rather not have to sterilize that head with a caustic agent and damage the electricals and stuff.
People use thin sleeves over their probes or some kind of a plastic clear wrap. If you don’t have to touch the patient, it is much easier to do those kinds of treatments. Practical value might oversee or supersede the minimal benefit you get from being in contact.
Ari: If you’re trying to treat deep tissues, you don’t see contact direct with the skin as being a big issue?
Dr. Arany: I don’t. I think that’s a misconception that people who feel that if you seal the amount of light, you’ll get more energy. Yes, you will, but there are easier ways of doing that.
Ari: What are the easier ways?
Dr. Arany: We gave the example of fractionated ionizing radiation. Those beams that get energy in. Before we used to expose the tumor from the outside and we used to put all the energy through one beam, which we realized was not a good idea because it used to burn everything on its way to its target.
Now, we use thousands of beams that have been angulated and get the right amount of energy only where it’s necessary. That is the next generation of PBM devices, which don’t rely on a single beam giving you enough energy.
If you have thousands of beams that are providing that energy– Think of the large LED arrays. If you use them in the right way, you can get enough energy in.
Ari: Interesting. Are there any devices like that exist now?
Dr. Arany: There are several in development. We are developing some of our own. That is the direction that the field is going in. I think another interesting question now that you brought it up, and this could be– We could go into a lot more detail in the next session.
When you’re doing light treatment, whether it’s in a way, but definitely when you’re in contact, what people are ignoring is the transit zone. If you’re putting a lot of energy on top, eventually less energy reaches the bottom.
That area and the bottom is where hopefully your target is, whether it’s your joint, whether it’s your knee, whether it’s your hip, whether it’s your back, whether it’s your spine. I think people are trying to put a lot of energy on top so that you get enough energy after your target. All that energy that is going through, people are being ignoring. That area potentially could be negating your benefit because that’s an area of higher energy.
Ari: Clarify that one more time. I didn’t quite get that.
Dr. Arany: As you’re pushing energy from the top into a deep tissue, all that energy in the transit zone, people have ignored because they don’t care about that energy.
Ari: The transit zone is the more superficial tissues?
Dr. Arany: Correct. The target is what they care about. People put class four lasers, super pulse lasers, which is great. I think there is a role for all of those in PBM. People have ignored that superficial tissue that they’re transitioning to.
Ari: What do you think is happening there that’s of importance? Meaning you’re saying that you could get a systemic benefit from that by erading the blood, or you’re saying that you’re overdosing those tissues?
Dr. Arany: You’re overdosing those tissues.
Ari: Having said that certain types of devices with non-contact can, if they’re designed correctly, the ones you’re referring to, can lead to deep penetration, do you think that’s the case for the panel-style devices that exist on the market today that are popular?
Are they actually delivering a lot of light to the deep tissues, or is it mostly staying pretty superficial if you’re using these devices from 6 or 12 inches away?
Dr. Arany: Again, let’s take the example of a spine. I wish the answer was yes or no. That would have made life easier. Let’s say you have a patient of MS, multiple sclerosis. You’re trying to do treatments for them with a light bed, which is very, very popular these days. You want a lot of energy at the level of the spine or the neural tissue, which have been demyelinated.
Getting that much energy into those areas is not very difficult with those large LED panels. You really don’t need high-power lasers and stuff to get that much energy there. If you just measure. The question we keep coming back to is how much energy is enough energy? If you can’t answer that question, then the light delivery system is a trivial part to solve technologically.
The biological question, going back to our original discussion, why do we care about mechanisms? How much energy do we need on the nerve to remyelinate? That’s the question we should be answering. If we can answer that question, we can very easily solve the light delivery problem.
Ari: Dr. Arany, I have about a hundred more questions that I’d love to ask you, but I know you have to run. We’ll leave it for part two. Thank you so much. This has been excellent. I’ll follow up with you via email and we’ll get the next part scheduled. Thank you for your time. I really appreciate it.
Dr. Arany: Thank you for having me, Ari. Look forward to the next one.
Ari: Okay, talk to you soon.
Dr. Arany: Bye-bye.
Ari: Bye.
Show Notes
00:00 – Intro
00:52 – Guest intro: Dr. Praveen Arany
05:49 – How red and near-infrared light impacts the body
12:06 – The UVB and Vitamin D connection
14:44 – Why sunlight is not enough when it comes to RLT
19:19 – Using photobiomodulation for stimulating healing
29:31 – Why one-size-fits-all treatments don’t always work in PBM treatment
32:27 – Why photobiomodulation works on multiple diseases
42:01- Red Light Therapy and Redox balance
46:46 – PBM and melatonin
48:11 – LED lights versus laser
54:36 – Why PBM cannot treat everything
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