Grow Taller with Low Intensity Light Therapy?

Low Intensity Light Therapy(or LILT for short) has been linked to biophotons.  Electromagnetic 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. 

Stature Gain with Meditation?

In the post about biophotons, Jory expressed his doubts about the possibility of biophotons being able to manipulate height.  Jory has grown several millimeters by lateral synovial joint loading which by best estimation works by mechanotransduction through the actin cytoskeleton of various cell types in the bone(chondrocytes, osteoblasts, and stem cells).  Lateral Synovial Joint Loading works by inducing interstitial fluid flow which brushes past the actin fibers on these cell types causing adaptations.  Several exercises induce interstitial fluid flow but not to the degree that LSJL does; these exercises induce a stature gain that is minor enough not to be detectable.   This interstitial fluid flow works to increase height either by triggering new bone deposition of surface osteoblasts or by organic development of chondrocytes.

Biophotons are a similar signaling mechanism as to mechanotransduction but instead of operating by mechanisms of shear strain, interstitial fluid flow, and hydrostatic pressure; biophotons function based on light and electromagnetic fields.  Like mechanical loading, biophotons have the ability to alter genetic expression.  Which means that biophotons have the ability to increase height.  Like mechanical loading, the genetic expression change generated by things like hypnosis, meditation, etc. may not be enough and more powerful biophoton generating mechanisms may need to be used like Pulsed Electric Magnetic Fields.

Meditation, Hypnosis, Positive Thinking, etc. may be effective in altering biophoton emissions but only to a minor degree and more powerful tools may be needed like PEMFs to get a really effective height or stature gain.

Effect of meditation on ultraweak photon emission from hands and forehead.

"Various physiologic and biochemical shifts can follow meditation. Meditation has been implicated in impacting free radical activity. Ultraweak photon emission (UPE, biophoton emission) is a constituent of the metabolic processes in a living system. Spectral analysis showed the characteristics of radical reactions.
 Recording and analysing photon emission in 5 subjects before, during and after meditation.
UPE in 5 subjects who meditated in sitting or supine positions was recorded in a darkroom utilising a photomultiplier designed for manipulation in three directions.
Data indicated that UPE changes after meditation. In 1 subject with high pre-meditation values, UPE decreased during meditation and remained low in the postmeditation phase. In the other subjects, only a slight decrease in photon emission was found, but commonly a decrease was observed in the kurtosis and skewness values of the photon count distribution. A second set of data on photon emission from the hands before and after meditation was collected from 2 subjects. These data were characterised by the Fano factor, F(T), i.e. variance over mean of the number of photoelectrons observed within observation time T. All data were compared to surrogate data sets which were constructed by random shuffling of the data sets. In the pre-meditation period, F(T) increased with observation time, significantly at time windows >6 s. No such effect was found after meditation, when F(T) was in the range of the surrogate data set.
The data support the hypothesis that human photon emission can be influenced by meditation. Data from time series recordings suggest that this non-invasive tool for monitoring radical reactions during meditation is useful to characterise the effect of meditation. Fano factor analysis demonstrated that the time series before meditation do not represent a simple Poisson process. Instead, UPE has characteristics of a fractal process, showing long-range correlations. The effect of meditation waives out this coherence phenomenon, suggesting a weaker and less ordered structure of UPE. In general, meditation seems to influence the complex interactions of oxidative and anti-oxidative reactions which regulate photon emission. The reason for the statistical changes between pre- and post-meditation measurements remains unclear and demands further examination."

Now the reason that the photon emissions went down could be because they were no longer moving and weren't performing as many redox reactions.  Also, this study seems to suggest that the mind has the power to influence the oxidative reactions themselves.

During meditation, people control their breathing and breathe slowly thus making it less likely that they perform redox reactions.  Meditation did not change the frequency or color of the biophoton emission making the ability of meditation to alter genetic expression unlikely. 

Gene expression profiling in practitioners of Sudarshan Kriya[An Indian Form of Meditation]

"The rapid pace of life, eating habits, and environmental pollution have increased stress levels and its related disorders. The complex molecular response to stress is mediated by stress genes and a variety of regulatory pathways. Oxidative stress is internal damage caused by reactive oxygen species[oxidative stress can cause damage to height related genes]. Increasing evidence suggests that chronic psychosocial stress may increase oxidative stress, which in turn may contribute to aging, and etiology of coronary diseases, cancer, arthritis, etc. Psychophysiological concomitants of meditation have been extensively researched, but there are very little data available on biochemical activity leading to relieving stress by causing a relaxation response by Sudarshan Kriya (SK). SK is a breathing technique that involves breathing in three different rhythms. It is preceded by Ujjayi Pranayam (long and deep breaths with constriction at the base of throat) and Bhastrika (fast and forceful breaths through nose along with arm movements)[You'd expect this sort of activity to increase biophoton emissions].
Forty-two SK practitioners and 42 normal healthy controls were recruited for our study. The practitioners had practiced SK for at least 1 year. Selected normal healthy controls did not perform any conventional physical exercise or any formal stress management technique. Whole blood was used for glutathione peroxidase estimation and red blood cell lysate was used for superoxide dismutase activity assay and for glutathione estimation. White blood cells were isolated from fresh blood and assayed for gene expression using reverse transcriptase-polymerase chain reaction. The parameters studied are antioxidant enzymes, genes involved in oxidative stress, DNA damage, cell cycle control, aging, and apoptosis.
A better antioxidant status both at the enzyme activity and RNA level was seen in SK practitioners. This was accompanied by better stress regulation and better immune status due to prolonged life span of lymphocytes by up-regulation of antiapoptotic genes and prosurvival genes in these subjects[These antiapoptotic genes may express themselves in chondrocytes as well].
Our pilot study provides the first evidence suggesting that SK practice may exert effects on immunity, aging, cell death, and stress regulation through transcriptional regulation."

What's interesting is that you'd effect some of these studies to increase the amount of redox reactions like the fast and forceful breaths.  What is uniform between SK and Meditation is that you are learning to control your breathing.  This could possibly lead to you controlling redox reactions which in turn controls biophoton emissions.  These biophoton emissions increase expression of antiapoptotic genes which would express expression in all areas including growth plate chondrocytes.

So the important thing isn't the meditation, it's the breathing.  Developing breathing control whether through exercise, singing, etc. will probably result in a small stature gain during development by improved biophoton emissions increasing expression of antiapoptotic genes and reducing DNA damage from reactive oxidative species.

Regulation of gene expression by yoga, meditation and related practices: a review of recent studies.

Review study that mentions the following studies:

Genomic Profiling of Neutrophil Transcripts in Asian Qigong Practitioners: A Pilot Study in Gene Regulation by Mind–Body Interaction

"Six (6) Asian FLG practitioners and 6 Asian normal healthy controls were recruited for our study. The practitioners have practiced FLG for at least 1 year (range, 1–5 years). The practice includes
daily reading of FLG books and daily practice of exercises lasting 1–2 hours. Selected normal healthy controls did not perform Qigong, yoga, t’ai chi, or any other type of mind–body practice, and had not followed any conventional physical exercise program for at least 1 year. Neutrophils were isolated from fresh blood and assayed for gene expression, using microarrays and RNase protection assay (RPA), as well as for function (phagocytosis) and survival (apoptosis).
The changes in gene expression of FLG practitioners in contrast to normal healthy controls were
characterized by enhanced immunity, downregulation of cellular metabolism, and alteration of apoptotic genes in favor of a rapid resolution of inflammation. The lifespan of normal neutrophils was prolonged, while the inflammatory neutrophils displayed accelerated cell death in FLG practitioners as determined by enzyme-linked immunosorbent assay. Correlating with enhanced immunity reflected by microarray data, neutrophil phagocytosis was significantly increased in Qigong practitioners. Some of the altered genes observed by microarray were confirmed by RPA.
Qigong practice may regulate immunity, metabolic rate, and cell death, possibly at the transcriptional level. Our pilot study provides the first evidence that Qigong practice may exert transcriptional regulation at a genomic level. New approaches are needed to study how genes are regulated by elements associated with human uniqueness, such as consciousness, cognition, and spirituality."

A spot analysis of the genes revealed no overtly height increasing genes with the exception of some apoptosis genes.

 Genomic Counter-Stress Changes Induced by the Relaxation Response

"We assessed whole blood transcriptional profiles in 19 healthy, long-term practitioners of daily RR practice (group M), 19 healthy controls (group N1), and 20 N1 individuals who completed 8 weeks of RR training (group N2)."

Gene expression ontology mostly revealed that the gene alteration was anti-catabolism.  Nuclear messanger RNA splicing genes were also altered.

A full gene list was not available.

Genome-wide expression changes in a higher state of consciousness.

"We assessed the whole genome gene expression analysis of long-term meditators in four separate trials and detected significant differential gene expression in association with higher states of consciousness."

A full gene list is given.

A spot analysis for any of the meditators looking for genes related to height revealed that HIF1A was downregulated.  No other overtly pro-chondrogenic or pro-height genes were revealed.

Blood samples were taken so pro-chondrogenic genes directly in the bone marrow may not have been detected.

Mental Height Increase with Biophotons?

Previously, in an article about growing taller with hypnosis, I reported on biophotons being a possible mechanism for how the brain can influence height growth.  We learned that biophotons are stored in DNA and that thoughts can produce electric and magnetic energy which creates an ordered flux of photons.  Pulsed Electric Magnetic Fields alter the expression of certain genes and that expression may be via biophotons.  Maybe it's possible to generate similar magnetic fields only with the power of thought(PEMFs were found to be able to increase cellular proliferation and differentiation).

Biophotons may be a way to control cell growth in cancer and as a corollary may be able to increase cellular proliferation in certain areas(like the growth plate).  Certain genes affect cell growth so for instance a certan biophoton frequency may inhibit myostatin thus stimulating cell growth and another biophoton frequency may upregulate myostatin which would inhibit cell growth.

Biophotons(biological photons) are different colors on the electromagnetic spectrum so thinking with certain colors may be a way to mentally induce height growth by thinking certain colors that upregulate certain genes(biophotons travel through neurons). 

Estimation of the number of biophotons involved in the visual perception of a single-object image: biophoton intensity can be considerably higher inside cells than outside.

"The retina transforms external photon signals into electrical signals that are carried to the V1{You can detect the biophoton signatures of other people; if you often see tall people will you pick up their tall biophoton emissions and grow taller?} (striatecortex). V1 retinotopic electrical signals (spike-related electrical signals along classical axonal-dendritic pathways) can be converted into regulated ultraweak bioluminescent photons (biophotons) through redox processes within retinotopic visual neurons that make it possible to create intrinsic biophysical pictures during visual perception and imagery. biophotons are not by-products [of cellular metabolism], other than originating from regulated cellular radical/redox processes. The biophoton intensity can be considerably higher inside cells than outside. The real biophoton intensity in retinotopic neurons may be sufficient for creating intrinsic biophysical picture representation of a single-object image during visual perception."

So the external biophotons of those around you could possibly alter your own biophoton emissions.  Your retina detects external photon signatures and then those photon signatures are transmitted to your cells by neuronal pathways.  Could you also grow taller by looking at certain frequencies of light? 

Biophoton detection and low-intensity light therapy: a potential clinical partnership.

"Low-intensity light therapy (LILT) [can accelerate] ATP production and [mitigate] oxidative stress. Cellular reduction/oxidation (redox) state may play a central role in determining sensitivity to LILT and may help explain variability in patient responsiveness. In LILT, conditions associated with elevated reactive oxygen species (ROS) production, e.g. diabetic hyperglycemia, demonstrate increased sensitivity to LILT.  The production of [biophotons] is associated with cellular redox state and the generation of ROS."

Cellular reduction/redox state is what determines how sensitive a cell is to biophotons.  How sensitive are chondrocytes? 

Low oxygen reduces the modulation to an oxidative phenotype in monolayer-expanded chondrocytes.

"Autologous chondrocyte implantation requires a phase of in vitro cell expansion, achieved by monolayer culture under atmospheric oxygen levels[chondrocytes like low oxygen environments]. Chondrocytes reside under low oxygen conditions in situ and exhibit a glycolytic metabolism. oxidative phosphorylation rises progressively during culture, with concomitant reactive oxygen species production. We determine if the high oxygen environment in vitro provides the transformation stimulus. Articular chondrocytes were cultured in monolayer for up to 14 days under 2%, 5%, or 20% oxygen. Expansion under 2% and 5% oxygen reduced the rate at which the cells developed an oxidative phenotype compared to 20% oxygen. However, at 40 +/- 4 fmol cell(-1) h(-1) the oxygen consumption by chondrocytes expanded under 2% oxygen for 14 days was still 14 times the value observed for freshly isolated cells. Seventy-five to 78% of the increased oxygen consumption was accounted for by oxidative phosphorylation (oligomycin sensitive). Expansion under low oxygen also reduced cellular proliferation and 8-hydroxyguanosine release, a marker of oxidative DNA damage. These parameters remained elevated compared to freshly isolated cells. Expansion under physiological oxygen levels reduces, but does not abolish, the induction of an oxidative energy metabolism. Simply transferring chondrocytes to low oxygen is not sufficient to either maintain or re-establish a normal energy metabolism. A hydrophobic polystyrene culture surface which promotes rounded cell morphology had no effect on the development of an oxidative metabolism. The shift towards an oxidative energy metabolism is often accompanied by morphological changes."

Low Intensity Light Therapy(which most likely operates by biophotons) has been shown to reduce oxidative stress.  Maybe the low oxidative levels found in chondrocytes is due to the high oxygen consumption of them(the tendency to observe chondrocytes under hypoxia is due to chondrocytes liking to consume oxygen not by them liking to grow under hypoxic conditions).  Low oxygen does reduce the likelihood to acquire an oxidative phenotype and maybe an oxidative phenotype reduces height growth(but low oxygen does induce DNA damage). 

"The increased oxygen consumption of expanded cell populations cannot be accounted for by the utilization of existing mitochondrial reserve function. Rather, the maximal oxidative capacity of these cells is increased[Maybe chondrocytes can adapt to non-hypoxic[above 5% oxygen] environments]. Mitochondrial biogenesis [occurs] during monolayer culture of primary chondrocytes. Together, these data suggest a fundamental adaptation of the chondrocytes towards an oxidative metabolic phenotype, with significant implications for the functionality and longevity of the resulting cell population. Mitochondria [is] a key source of ROS generation. Excessive ROS generation [augments] the formation of altered bases such as 8-hydroxyguanosine in the cellular DNA and promote premature proliferative senescence in a wide range of cells{why reactive oxidative species can reduce height growth and therefore why anti-oxidants can enhance height growth}"


"By culturing chondrocytes using systems which inhibit cell adhesion and maintain a rounded cell morphology, the loss of native synthetic phenotype is inhibited[chondrocytes stay chondrocytes]"<-inhibiting chondrogenic cell adhesion[you need mesenchymal adhesion though to initially form the growth plate] may help height growth by preventing chondrocytes from acquiring a fibroblastic phenotype.

"culture under low oxygen conditions is reported to influence both the maintenance of the native chondrocytic phenotype and its re-expression following monolayer culture"<-lower than 5% oxygen is important but vascularity is needed too at some stages

Transforming growth factor Beta1 induction of tissue inhibitor of metalloproteinases 3 in articular chondrocytes is mediated by reactive oxygen species.

"Transforming growth factor beta1 (TGF-beta1) stimulates cartilage extracellular matrix synthesis but, in excess, evokes synovial inflammation, hyperplasia, and osteophyte formation in arthritic joints. TGF-beta1 induces tissue inhibitor of metalloproteinases 3 (TIMP-3), an inhibitor of cartilage-damaging matrix metalloproteianases and aggrecanases. In primary human and bovine chondrocytes, ROS scavenger and antioxidant N-acetylcysteine (NAC){Even though NAC is an anti-oxidant you don't want to take it as it inhibits NADPH oxidase which is needed for chondrogenic differentiation} inhibited TGF-beta1-induced TIMP-3 mRNA and protein increases. Ebselen and ascorbate also reduced this induction. TGF-beta1 time-dependently induced ROS production that was suppressed by NAC. Hydrogen peroxide, a ROS, induced TIMP-3 RNA. The TIMP-3 increase induced by TGF-beta1 was partly Smad2-dependent. TGF-beta1-stimulated Smad2 phosphorylation was inhibited by NAC{Another reason why NAC is bad for height growth Smad2/3 phosphorylation help height growth}. Reduced glutathione and L-cysteine also blocked Smad2 and TIMP-3 induction by TGF-beta1, whereas a nonthiol, N-acetylalanine, did not. Smad2 was not activated by H2O2. Smad2 phosphorylation was independent, and TIMP-3 expression was dependent, on new protein synthesis. TGF-beta-stimulated ERK and JNK phosphorylation was also inhibited by NAC. However, inhibitory actions of NAC were not mediated by ERK activation. ROS mediate TGF-beta1-induced TIMP-3 gene expression. Blocking TGF-beta1-induced gene expression by modulating cellular redox status with thiols can be potentially beneficial for treating arthritic and other disorders caused by excessive TGF-beta1."

MMP-3 plays a role in the formation of cartilage canals.  Too much vascularity like by FGF or VEGF has been shown to reduce final height growth.  Appropriate levels of TIMP-3 may prevent too much vascularity which has the ability to reduce height gain.  Reactive Oxygen Species which are mediated by biophotons mediate TIMP-3 which may affect height growth.  The problem is that reactive oxygen species are needed so you don't want to shut off their production entirely by a mechanism such as NAC.  You just want to get rid of the excess.

Biophotons are neurological signals that can be induced by mental thought or by lights.  These signals may affect redox reactions which may alter gene expression which could alter height growth.  Maybe mental height increase is possible after all.