Photobiomodulation’s Secret is in the Genetic Pathways
Our team investigated how photobiomodulation takes various genetic pathways to heal and achieve homeostasis. A large part of the findings are published in the following papers: Photobiomodulation on Stress, and Photobiomodulation‐ mediated Pathway Diagnostics. This article is a simplified presentation of the investigations. In principle, our body systems seek to restore homeostasis or internal balance by “detecting” dysfunction or imbalance in the systems (more accurately described as a “negative feedback” process).
Photobiomodulation ‐ the effect of light on modifying a cellular condition ‐ is a method that facilitates this process. More than that, the study implicates that through the expression of the genes during the photobiomodulation process, it may also enhance the health of the cells beyond their normal level. Many details (particularly the details on the study methodology) are left out; but these are available on request.
Some basics on cell proliferation and the experiments Our body is composed of cells that constantly proliferate under a complex interplay of various genes. Even the proliferation process has to be in homeostatic condition – otherwise there could be only partial growth or on the other hand, out‐of‐control growth such as cancer. Healing involves cell proliferation, but this is often compromised under stress (which can be defined as an environment that causes a dysfunction). The investigations simulated this stress by subjecting the cells in high glucose solution. In high glucose environment, the cells are found to have lower count than in a normal level glucose environment (a good case to control our sugar intake). See Figure 1 below. This suggests that under stress, the homeostatic process is only partially activated. In about 3 days(72 hours) in high glucose solution, it becomes clear that cellular proliferation is significantly lower relative to normal glucose, although cells continue to thrive in glucose. See Figure 2 below. The Effect of Low Intensity light When we subject the cells under low-intensity red light, the cells in high glucose (RLED – HG) recover their proliferation in about 3 days. See “RLED – HG” versus “HG” in Figure 3 below. “CON” in the figure stands for control(or cells in normal level glucose)
The response of stressed and dysfunctional cells The cells in our body collectively proliferate under pre-programmed settings to to restore their desired normal functions. These “programs” would be determiend by our genotype. The genes are grouped under categories that work in accordance with the programs and result in restored homeostasis. The group of genes can be classified as activators, inhibitors and regulators of proliferation. The genes are coded into working protein through messenger ribonucleic acids(mRNA). For the investigations, the research group examined the mRNA of the activators, manganese superoxide dismutase (MnSOD) and insulin-like growth factor 1(IGF-1)); inhibitors, forkhead box O3 a(FOXO3a), B-cell lymphoma-2 interacting mediator of cell death(BIM), and p27 gene; and a regulator, sirtuin (SIRT1). The studies found that cells stress have high mRNA expressions for inhibitors and low mRNA for activators, explaining how these stressed cells have lower proliferation. When these stressed cells(under prolonged high glucose environment), are illuminated with low intensity red light, they start to restore the levels of mRNA to restore the respective correct level of genetic activation for proliferation. See Figure 4. Thus, red light of low intensity over a certain period of time has the uncanny ability to restore dysfunctional cell condition. This is reflected as a healing process, which can be recognized in the healing of wounds, alleviating pain, cellular rejuvenation, or in a more systemic sense, overcoming numerous ailments and diseases.
The potent proliferation activator, IGF-1 seems to thrive in glucose and to thrive even further with the input of photobiomodulation. The infusion of a potent control inhibitor, LY294002 does not appear to have significant impact on reducing IGF-1 expression. See Figure 5.
Enhancement of normal cell functions
What may be surprising is that when normal cells in normal level glucose solution are exposed to low intensity red light, the proliferation continues. It gets into the mode when homeostasis that is specific to proliferation is achieved( proliferation -specific homeostasis or “PISH”). See Figure 6. In the body there are other regulatory components to limit overactive proliferation. For example compromised inhibitor BIM needs to have mutated myc gene present to produce aggressive malignancies.
Figure 7 below is telling. The mRNA of inhibitor genes for non-stressed cells in normal glucose respond to photobiomodulation in a similar manner to stressed cells. Low intensity red light limits the activity of the mRNA inhibitor FOXO 3a, BIM and p27 genes. There was no significant change in the expression of mRNA for the activator gene mSOD as well as SIRT 1. On the other hand, activator IGF-1 responded strongly to photobiomodulation.
In layman’s terms, photobiomodulation supports cellular proliferation by limiting the genetic activities that put the brakes on it. In addition, it opens the gates for for the activities that encourages more proliferation.