Monthly Archives: October 2013

Update #7 – Nothing Happened This Month – October 2, 2013

Update #7 – Nothing Happened This Month – October 2, 2013

Bronica SQ-A | Zenzanon-S 40mm F/4 | Kodak BW400CNThe month of September was a complete loss. There was absolutely no headway into this endeavor. It is partly due to the fact that so many other issues in my life have come up.

Things that are currently happening has included

  • Multiple fines over issues in my past
  • A dramatic increase in living costs over unexpected issues.
  • Housing repair issues
  • Legal issues with my other businesses
  • Possible terminal illness risks
  • Strange Illnesses which the physicians I have met with can’t even diagnose properly.
  • and one other, life altering issue that has turned my life completely upside down

As for my measured height, I have not been able to get even that done. However I have noticed that I seem to have lost weight. As for health problems, my personal lower back pain seems to have plateaued and not gotten worst.

I hope the readers can put up with this thing for a little while longer. I don’t expect to get back into doing any type of serious research at least until maybe even December.

There is nothing else I would wish to discuss or reveal any further to the regular readers.

Comparing the Differences Of LIPUS To Low Level Laser Therapy LLLT On How They Increase Bone Growth

Comparing the Differences Of LIPUS To Low Level Laser Therapy LLLT On How They Increase Bone Growth

At some point in the website, I have mentioned and did some research on both LIPUS aka Low Intensity Pulsed Ultrasound and LLLT aka Low Level Laser Therapy as a possible ways to accelerate the rate of long bones to grow. At this current time, I feel that LIPUS as a technique has no effect at all on bone growth. As for LLLT, it is also not effective, but there seems to be at least one study which contradicts my opinion.

What I am willing to accept about the LIPUS technology, is that there is some evidence that using LIPUS on bone fractures to stimulate healing seems to have been validated by just a few studies. It will work in increasing osteogenesis but not chondrogenesis, which is what we should be looking for. The same can be said of LLLT, but so far I have not personally found any studies or evidence to support the idea that LLLT can be used to heal bone fractures and increase the rate of osteogenesis or bone healing.

However, recently I did find two studies which made me look at the evidence. They are…

  1. Comparative study of how low-level laser therapy and low-intensity pulsed ultrasound affect bone repair in rats.
  2. Comparative study of the effects of low-intensity pulsed ultrasound and low-level laser therapy on bone defects in tibias of rats.

From the 1st study, it is revealed that LLLT seems to have some effect on at least making the bones stronger. The experimenters created 3 groups of lab rats, ones getting LIPUS, another group getting the LLLT, and a 3rd control group. The LLLT group showed that when the long bones which were cut beforehand were bent, the loading was higher than the other 2 groups. It seems that the process for bone growth is different between the LIPUS and the LLLT. Whereas the LLLT could cause actual bone growth by inducing more osteoblast and osteoid surfaces, the LIPUS group supposedly could increase the formation of of osteoclasts, thus causing the bones cells which is responsible for resorption to be increased.

We were however confused by the conclusion, since these researchers seemed to have contradicted themselves. They are saying that LIPUS could prevent bones from becoming resorbed but our interpretation of the abstract is that they actually increased resorption of the bone, thus making the bones weaker. 

Our opinions were validated by the 2nd study which we have referenced above.

The procedure the researchers did was almost exactly the same, using the same 3 groups. The results for this experiment actually made much more sense.

We quote the following…

The results showed intense new bone formation surrounded by highly vascularized connective tissue presenting a slight osteogenic activity….

The issue is that this new bone formation was only seen in the group of lab rats after a few weeks getting the LLLT treatment. For the rats getting the LIPUS, there was no sign of bone formation.

The conclusion

I think it is time to state that not only is LIPUS not chondrogenic, it is not osteogenic either. Compared to something like LLLT, it showed no effects. If LIPUS compared to LLLT shows no effect, then it definitely won’t hold water against something much more effective like PEMF technology.

Using Low Level Laser Therapy To Increase Height And Grow Taller

I have personally been working on multiple different projects in the last few months and that is for financial reasons. This project is never supposed to be very profitable. However, those other projects are in the field of medicine, specifically bioelectrical medicine which most people have probably never looked into before.

In my research for these other projects, I would again come across the research of Dr. Robert O. Becker, whose book “The Body Electric” was a very big eye opener for me. I managed to get a PDF of his book and printed it out at the local copier place close to where I live. I wanted to look at what other people have been able to propose and create who referenced Robert’s Work.

(Note: Back in the 1980s-1990s there were actually TWO different people with similar names doing this type of biomedical research on the therapeutic effects of fringe sciences. There is Robert (Bob) C. Beck Sc. D. ,the physicist who created the Beck Protocol promoting injecting colloidal silver, drinking ozone water, and using magnetic pulsers (like the Soma Pulser) and Robert O. Becker M.D., who is a Medical doctor or surgeon who did his research in almost the exact same area, but focused on the effect of electricity on bone and limb regeneration. Both of the researchers did researchers worked on the effects of iontophoresis.)

Publications by the Physicist Bob Beck

  1. Alternating current supplied electrically conductive method and system for treatment of blood and/or other body fluids and/or synthetic fluids with electric forcesPatent #: US 5188738 – Authors: Steven Kaali, Peter M. Schwolsky

Publications by the Medical Doctor Robert Becker (source) –

  1. US Patent # 5,814,094 – Iontopheretic System for Stimulation of Tissue Healing and Regeneration
  2. Robert O. Becker – The Discovery of Silver
  3. R. O. Becker, et al., “Experience With Low-Current Silver Electrode Treatment of Nonunion,” in Electrical Prop. Bone & Cartilage (ed. C. T. Brighton, et al.), Grune & Stratton (1979), USA.
  4. R. O. Becker, et al., “Clinical Exp. With Low Intensity Direct Current Stimulation of Bone Growth,” Clin. Orthop. & Rel. Res., vol. 124, pp. 75-83 (1977) . USA.
  5. Silver Helps Regrow Tissues in Hundreds of Patients – Destroyed Cells Regenerate With Silver-Based Procedure

After going through the Google Patents database, and doing all the research, I found what I think is another breakthrough, which is a similar type of technology. This is known as Low Level Laser Therapy. Low Level Laser therapy is believed by its proponents to have benefits benefits (at least temporarily) against the symptoms of arthritis, osteoarthritis, and tendinopathy, and lower back pain.

Note: The therapy is extremely controversial, with quite a few medical professionals who discredit the efficacy of the idea.

This post is just an extension on the post Tyler wrote a while back where he referenced the study Effects of laser acupuncture on longitudinal bone growth in adolescent rats.. He managed to find a PubMed article showing that Laser Acupuncture has an effect on the longitudinal growth rate of long bones in lab rats. That is good news.

Now I have found a few studies which correlate the application of Low Level Lasers to increased cartilage generation in the epiphyseal growth plates as well as decreased degeneration of

I also like to refer to the study Effect of GaAlAs laser irradiation on the epiphyseal cartilage of rats. This study seems to sort of validate the idea that laser irradiation on the developing bones do seem to have some type of positive, stimulating effect.

We do know that there are anti-degenerative properties for Articular Cartilage from studies like “The effect of low-level laser to apoptosis of chondrocyte and caspases expression, including caspase-8 and caspase-3 in rabbit surgery-induced model of knee osteoarthritis.” and “The effect of different treatment time of millimeter wave on chondrocyte apoptosis, caspase-3, caspase-8, and MMP-13 expression in rabbit surgically induced model of knee osteoarthritis.

However this conclusion and theory on using LLLT to increase bone longitudinal growth seems to be completely negated by the study The effects of low-level laser therapy, 670 nm, on epiphyseal growth in rats.

At this point, the conclusion I can make is that if you manage to emit a specific type of electromagnetic pulse of a certain type of frequency, impulse time, and intensity, there seems to be a lot of evidence in showing that the growth of growth plates can be stimulated, and the degeneration of articular cartilages can be decreased. It can be from a variety of electrical and photo stimuli, including lasers.

Impact of Growth Factors and PTHrP on Chondrogenic Differentiation of Human Mesenchymal Stem Cells

Impact of growth factors and PTHrP on early and late chondrogenic differentiation of human mesenchymal stem cells
  1. S. Weiss,  T. Hennig,  R. Bock,  E. Steck,  W. Richter*

Article first published online: 4 JAN 2010        DOI: 10.1002/jcp.22013        Copyright © 2009 Wiley-Liss, Inc.

Journal of Cellular Physiology

Volume 223, Issue 1,  pages 84–93, April 2010


Common in vitro protocols for chondrogenesis of mesenchymal stem cells (MSCs) induce an inadequate, hypertrophic differentiation cascade reminiscent of endochondral bone formation. We aimed to modify chondrogenic protocols in order to identify potent inducers, promotors, and inhibitors to achieve better chondrogenesis. Nine factors suspected to stimulate or inhibit chondrogenesis were used for chondrogenic in vitro induction of MSC. Differentiation was assessed by immunohistochemistry, alcian-blue staining, qRT-PCR, and quantification of alkaline phosphatase (ALP) activity. Pre-differentiated pellets were transplanted subcutaneously into SCID mice to investigate stable cartilage formation. Transforming growth factor (TGF)-β was always required for chondrogenic differentiation and deposition of a collagen-type-II-positive extracellular matrix, while bone morphogenetic protein (BMP)-2, -4, -6, -7, aFGF, and IGF-I (10 ng/ml) were alone not sufficiently inductive. Each of these factors allowed differentiation in combination with TGF-β, however, without preventing collagen type X expression. bFGF or parathyroid hormone-like peptide (PTHrP) inhibited the TGF-β-responsive COL2A1 and COL10A1 expression and ALP induction when added from day 0 or 21. In line with a reversible ALP inhibition, in vivo calcification of pellets was not prevented. Late up-regulation of PTH1R mRNA suggests that early PTHrP effects may be mediated by a receptor-independent pathway. While TGF-β was a full inducer, bFGF and PTHrP were potent inhibitors for early and late chondrogenesis, seemed to induce a shift from matrix anabolism to catabolism, but did not selectively suppress COL10A1 expression. Within a developmental window of collagen type II+/collagen type X cells, bFGF and PTHrP may allow inhibition of further differentiation toward hypertrophy to obtain stable chondrocytes for transplantation purposes.

My Interpretation:

You need TGF-beta to always be there in combination for the other growth factors to work. The others are BMP 2,4,6,7 aFGF, and IGF-1.

You want to avoid Collagen type X because collagen type X is produced by the chondrocytes after the chondrocytes have hypertrophied and by that time, it is already too late for them to proliferate which is what actually causes bone lengthening which is really just stacking of condrocytes in column fashion along the axis. Hypertrophy will always happen but proliferation will not. You want to focus on the layers closer and closer to the resting zone.

Also, you want to avoid matrix catabolism and desire matrix anabolism. The matrix they are referring to is the growth plate cartilage matrix, not the bone matrix. Catabolism is bad because that means it is going throughout process of breaking apart. You want to keep the growth plates intact strong, and multiplying.

It seems the bFGF and PTHrP inhibits early and late chondrogenesis which is a way to control hypertrophy. I am not sure if that means we should be striving to increase or decrease PTHrP.

{Tyler-I found the text file and have comments:

“Bone marrow samples for the isolation of MSC were obtained from 10 patients (range 34–73 years, 6 male/4 female) undergoing total hip replacement”

“Pellets of 4–5 × 105 MSCs were formed by centrifugation at 300g in 1.5 ml microcentrifuge tubes (Eppendorf, Hamburg, Germany). After incubation at 37°C, 6% CO2 for 4 days pellets were transferred to 96-well U-bottomed plates. Cells were kept in induction medium for 2, 4, 7, 14, 21, 28, or 42 days. Chondrogenic basal medium consisted of DMEM high glucose supplemented with 5 µg/ml insulin, 5 µg/ml transferrin, 5 ng/ml selenous acid, 0.1 µM dexamethasone, 0.17 mM ascorbic acid-2-phosphate, 1 mM sodium pyruvate, 0.35 mM proline, and 1.25 mg/ml BSA”

It seems that the default state for MSC pellet culture is to express type I collagen.  And TGF-Beta is needed to induce expression of Col2 unless in the presence of bFGF or PTHrP.  The other proteins tested were: BMP 2, 4, 6, 7. aFGF.  bFGF.  PTHrP. IGF-1.  Now other non-protein factors are able to induce chondrogenic differentiation without growth factors like mechanical factors.

“0.1 ng/ml of PTHrP allowed differentiation according to positive staining for collagen type II and alcian blue, 1 ng/ml PTHrP suppressed chondrogenic differentiation in MSC from three of four of the donors”

“PTH1R mRNA appeared not before day 21 of chondrogenic culture with TGF-β. This argued in favor of a receptor-independent action of PTHrP in the early phase of chondrogenic induction.”<-So this means that supplemental means that elevate PTHrP could inhibit chondrogenesis as PTHrP can inhibit growth plate action regardless of the presence or absence of receptors.