Sunday, November 7, 2010

Grow Taller with Low Intensity Light Therapy?

Low Intensity Light Therapy(or LILT for short) has been linked to biophotonsElectromagnetic Fields alter biophoton emissions as well.  Since PEMF affects biophotons which effect genetic expression(upregulating specific genes may increase height) and LILT affects biophoton emissions as well perhaps LILT affects genetic expression as well.  We already know that ultraviolet light has an affect(it causes DNA damage which can cause skin cancer) and we know that the lack of light is involved in melatonin signaling.

We have a lot of information about how interstitial fluid flow can manipulate the actin cytoskeleton and cause cellular proliferation + differentiation(this can cause height growth).  Biophotons, electromagnetic fields, and light are a new form of genetic signaling that we can study in an attempt to grow taller.  What insights does Low Intensity Light Therapy provide in the genetic signaling of electromagnetic fields?

Low-intensity light therapy: exploring the role of redox mechanisms.

"Low-intensity light therapy (LILT) appears to be working through newly recognized photoacceptor systems. The mitochondrial electron transport chain has been shown to be photosensitive to red and near-infrared (NIR) light. Although the underlying mechanisms have not yet been clearly elucidated, mitochondrial photostimulation has been shown to increase ATP production and cause transient increases in reactive oxygen species (ROS). In some cells, this process appears to participate in reduction/oxidation (redox) signaling. Redox mechanisms are known to be involved in cellular homeostasis and proliferative control. In plants, photostimulation of the analogous photosynthetic electron transport chain leads to redox signaling known to be integral to cellular function. In gene therapy research, ultraviolet lasers are being used to photostimulate cells through a process that also appears to involve redox signaling. It seems that visible and near visible low-intensity light can be used to modulate cellular physiology in some nonphotosynthetic cells, acting through existing redox mechanisms of cellular physiology. In this manner, LILT may act to promote proliferation and/or cellular homeostasis. Understanding the role of redox state and signaling in LILT may be useful in guiding future therapies, particularly in conditions associated with pro-oxidant conditions."

So LILT has good effects increase in ATP production and cellular proliferation but bad effects like an increase in reactive oxidative species and possible DNA damage from ultraviolet light.  Hence why it's low intensity.  Then there's the matter of actually getting through to the chondrocytes and osteoblasts.  Electromagnetic fields have that ability but being out in the sun a long time can cause skin cancer but not bone cancer.  This indicates that light only affects the cells that it directly hits.

The effect of 904 nm low level laser on condylar growth in rats.[This is infra-red light]

"A growth center of the mandible that contributes to its length and height is the mandibular condyle. Proliferation of prechondroblasts, followed by synthesis of the extracellular matrix and hypertrophy of the cartilage cells, governs the major part of condylar growth. The sample consisted of 54 male rats, weighing between 60 g and 80 g, divided randomly into three groups. Group I was the control group, group II was irradiated bilaterally, and group III was irradiated on the right side. Laser irradiation (lambda = 904 nm, 2000 Hz, pulse length 200 ns and output power 4 mW) was performed, and the procedure was repeated after a 50-day interval. Two months later, the rats were killed. In a single blind manner the lengths of denuded mandibles and the lengths of mandibles on soft tissue were measured. The growth of the mandibles in the unilaterally irradiated group (P < 0.001) and the bilaterally irradiated group (P < 0.05) was significantly more than that in the control group. There was no significant difference between right and left condylar growth in the bilaterally irradiated group (P = 0.3). Soft tissue analysis also verified these results (P < 0.001). Histomorphometric results also revealed a significant difference between laser-irradiated groups and the control group (P < 0.01). We concluded that particular laser irradiation with the chosen parameters can stimulate condylar growth and subsequently cause mandibular advancement. These findings might be clinically relevant, indicating that low level laser irradiation can be used for further improvement of mandibular retrognathism."

So you can grow taller with infrared light.  What about ultraviolet light which is at the other end of the electromagnetic spectrum...

Safety and efficacy of ultraviolet-a light-activated gene transduction for gene therapy of articular cartilage defects.

"Gene therapies for articular cartilage defects are limited by the absence of an in vivo delivery system that can mediate site-specific transduction restricted to within the margins of the defect during routine arthroscopy. We have proposed the use of ultraviolet light to stimulate gene expression following infection by recombinant adeno-associated virus (rAAV). However, research has demonstrated that short-wavelength ultraviolet light (ultraviolet C), while effective, is neither safe nor practical for this purpose. We evaluated the safety and efficacy of long-wavelength ultraviolet light (ultraviolet A) from a laser to induce light-activated gene transduction in articular chondrocytes in vitro and in vivo.
The effects of ultraviolet A from a 325-nm helium-cadmium laser, delivered through a fiberoptic cable, on cytotoxicity, mutagenesis, intracellular reactive oxygen species, and light-activated gene transduction of human articular chondrocytes were evaluated in dose-response experiments of primary cultures. Cytotoxicity was determined by trypan blue exclusion. The presence of pyrimidine dimers in purified genomic DNA was determined by enzyme-linked immunosorbent assays. Intracellular reactive oxygen species levels were determined by flow cytometry at one hour and twenty-four hours. In vitro light-activated gene transduction with rAAV vectors expressing the green fluorescent protein (eGFP) or beta-galactosidase (LacZ) was determined by fluorescence microscopy and bioluminescence assays, respectively. In vivo light-activated gene transduction was quantified by stereotactic immunohistochemistry for beta-galactosidase in rabbit articular cartilage defects in the patellar groove that had been irradiated with +/-6000 J/m2 of ultraviolet A one week after direct injection of 10(7) transducing units of rAAV-eGFP.
Ultraviolet A failed to induce significant cytotoxicity at all fluencies below 6000 J/m2. Dose-dependent cytotoxicity was observed at greater fluencies. In contrast to ultraviolet C, which induced significant (p < 0.05) pyrimidine dimer formation at all fluencies in a dose-dependent manner, ultraviolet A failed to induce DNA modifications. Conversely, ultraviolet C proved to be a poor inducer of intracellular reactive oxygen species, while ultraviolet A immediately induced high levels of intracellular reactive oxygen species, which were completely resolved twenty-four hours later. Ultraviolet A demonstrated significant light-activated gene transduction effects in vitro, which were dose-dependent (p < 0.05). In vivo, ultraviolet A mediated a tenfold increase in transduction in which 40.8% of the superficial chondrocytes adjacent to the defect stained positive for green fluorescent protein compared with 5.2% in the knees treated with no ultraviolet A (p < 0.006).
These results provide what we believe is the first formal demonstration of an agent that can induce rAAV transduction in the complete absence of cytotoxicity and DNA modification. They also suggest that the mechanism by which long-wavelength ultraviolet light mediates site-specific gene expression is by means of the induction of intracellular reactive oxygen species. Finally, laser-derived ultraviolet A can be readily transferred through a fiberoptic cable to mediate light-activated gene transduction in vivo."

So Ultraviolet light can induce gene modification but as a result of reactive oxygen species which can cause DNA damage.

So infrared light can induce height growth but there is no way to get it there(for us).  The best solution is to generate electromagnetic fields in the infrared frequency (above 700nm) and place that against the epiphysis of bones. 


  1. Very interesting but as far as I know the mandible bone is different from the leg bones and could present a different behaviour. Would this technique be also effective in leg bones?

    Would infrared light create growth in "fused" epiphysis? Where non fused rats or where they adult rats?

  2. What do you think about this Tyler?

  3. Tyler this xcrunner seems to have quite a few options for height growth. The Methylprotodioscin and dimethylicaritin are VERY expensive however...but his other method I think is worth a look too. I don't have a link but it's basically:

    sam-E 2 gs daily
    GH stimulators (arginine, lysine etc)
    stretching exercises

    What do you think?