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.