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 forces – Patent #: 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.

• Low-level laser on femoral growth plate in rats.
• The effect of low level laser on condylar growth during mandibular advancement in rabbits.
• The effect of 904 nm low level laser on condylar growth in rats.

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.

This has been my first finger progress update for one year:

Here’s the before picture:

You can see a definite increase in the epiphysis of the middle of the fingers.  Looking at the before video the finger was already slightly curved like that.  I don’t know why only the middle of the finger has responded so drastically maybe it involves blood vessels and hypoxia and clamping in the middle is just more efficient at cutting off those blood vessels then the other areas.

Loading regime has been 500 counts of LSJL on each of the three joint regions on the finger for 4 days and then alternate to loading the legs with LSJL.

Maybe the enhanced force relative to the size of the finger than relative to the leg has resulted in more epiphyseal width growth stimulation in the finger than in the leg.  Maybe a larger clamp is needed for the leg.

I believe an increase in finger length can be seen but a different ruler is used.  And the finger appears to be significantly longer than the earlier one even if the ruler was placed at a different point.  I will continue to work on lowering bodyfat percentage to try to make the bone more noticeable.

Here’s a link to a rock climbing thread to someone who had similar growth in the knuckle.  Now I can’t feel his knuckle to compare to mine.  But there are some differences:  The finger does not look inflammed and does not feel inflammed.  I have no finger pain and there is no restriction in joint movement which is typical of bone spurs.  Another key difference is that in his incidence the whole synovial joint area is enlarge whereas in mine it’s just the epiphysis if you look at mine you can see an indentation between the two epiphysis’.  Torwards the bottom of this page on arthritis you can see a picture of bony spurs: This is not consistent with the growth here as the growth is on the lateral ends of the bone rather than the top.

According to Factors influencing osteological changes in the hands and fingers of rock climbers, rock climbing does not increase osteoarthritis incidence and it does increase finger width.  “Analyses of total width and medullary width reveal that bone is being deposited on the subperiosteal surface, but not endosteally.”

Conclusion:  LSJL has a proven, undisputable effect on bone morphology as shown by the dramatic increase in epiphyseal width.  Those are not calluses.  That is bone.  It is likely not bone spurs nor the same sort of adaptation you might get from rock climbing. LSJL has a highly probable effect on increasing finger length that could become more drastic as alterations and honing of technique is made.

Recently while I was walking with my gf she told me an interesting anecdote about certain people in her extended family which seems to have the height gene which is expressed at a very high level.

While she herself if not tall, maybe even short, she seems to have some really big relatives. Repeatedly she has told me that her male cousin and his dad are of extreme height. There is also a equally tall grandmother of the cousin involved.

While there is not doubt that the standards of what is considered ‘tall’ in an Asian country would be different than in America, her claims seems to be very extreme.

The way she explains it is that her step-mother has around 5 biological siblings. She is not sure but the step-mother has around 3 sisters and 2 brothers. One of the sisters while not tall herself seems to be married to a very, VERY tall guy and the result is a very tall male step-cousin (through marriage).

Technically the relationship will be like step-cousins and step-uncles by marriage. The claim is that either the step-uncle by marriage or the step-cousin by marriage has a height that is reaching nearly as high as the ceiling.

Technically the ceilings in most buildings and places in South Korea are around 8 feet tall. She claims that these relatives have height that are only around 1 inch shorter than before scraping against the ceiling.

If we account for the shoes and a little bit of height due to hair, I would guess that she claims that these family members are around the 7′ 7″ – 7′ 9″ mark.

Apparently the cousin is so tall that he was recruited to play for some basketball team. I am not sure whether it is for a national team or not.

Based on my research, I don’t believe that her claims can be accurate. I don’t believe that there are anyone who can possibly be in the 7′ 7″ – 7′ 9″ height range in South Korea.

There is Ri Myung Hun who would be in the 7′ 9″ mark but he is in North Korea. The tallest person in South Korea should be the former Portland TrailBlazer Ha Seung Jin who is around 7′ 3″ – 7′ 4″. I told the story about the strange unknown tall korean guy I saw when I took the trip to Osaka in the post A 7 Feet Tall Korean Man Walks Through The Busan International Ferry Terminal Going To Japan

Besides these people, there are really no other contenders for anything in terms of giants found on the Korean Peninsula. What is generally well accepted about the demographics of the Korean ethnicity and the people who are from the Korean peninsula is that they are a very homogeneous group of people. There is a very low percentage of minorities and foreigners in both North Korea and South Korea. In addition, at least in South Korea people are very healthy an have a good health care system.

When we look at it that way, there should NOT be a very large long tail when looking at the bell distribution curve of the korean population. I have suspected for a long time that the reason why there seem to be a lot of Acromegalic Giants in places like China, Pakistan, and India is due to bad healthcare systems (as well as the extremely large population). The height distribution curve of these countries with below average healthcare systems will produce many more people in the long tail of the extreme height range. I note that almost everyone who has ever developed gigantism due to overactive pituitary systems and pituitary adenomas are not from the wealthy class.

South Korea should NOT be able to produce more than maybe 2-3 people over the 7′ 3″-7′ 4″ range. The reason is because the demographics of the society is extremely well documented and very uniform with the effect of minorities heights being negligeble effecting it. In the post Average Height Of Korean Men And Average Height Of Vietnamese Men the main reference I used was study done on a 1000 subject group of both college aged Korean and Vietnamese females and males. That revealed that that the average height of college aged Korean male students was around 5′ 9″.

Ha Seung Jin should be the tallest person in South Korea. Maybe he is not and there is some poor family located in the countryside of this Asian Peninsula where there is a case of acromegalic gigantism which is expressed in family members. We know that the gigantism due to pituitary adenoma can be completely genetic, due to our research on the Irish Giant Charles Byrne. However, it is extremely hard to believe that there is someone that tall that both I am not aware of or to the people at TheTallestMan.com website.

My girlfriend is claiming that one of her relatives which she has seen is supposed to be maybe 6 inches taller than Ha Seung Jin, around the 7′ 9″ – 7′ 11″ range. Can this be accurate?

I was going through this YouTube video entitled A brief discussion of Endometrial Cancer of Uterus and the lecturer revealed something at the time range of 19:45-20:00 of the video which explained and might have resolved an issue which I have been trying to figure out for a while now.

In the older post Increase Height Using Tamoxifen, Where Scientific Sources Contradict Each Other I had shown that there seems to be contradictory information on the effect of Tamoxifen on longitudinal bone growth. While Tamoxifen is supposed to be an aromatase inhibitor, preventing estrogen from turning into testosterone, there are a few cases which say that tamoxifen is bad for bone growth.

The Lecturer would reveal the following clue…” Tamoxifen is a selective estrogen receptor modulator that has an estrogen antagonist effect on the breast but has an estrogen agonist effect on the endometrium”

This shows that for different areas of the body, Tamoxifen can help increase estrogen or help decrease it.

Translation: Tamoxifen doesn’t just decrease the estrogen rate, but could increase it in other places. This means that tamoxifen is a horrible compound to take or inject to be used as some type of aromatase inhibitor like Letro or Anavar.

ATF6 is activated in response to ER stress.

Transmission of ER stress response by ATF6 promotes endochondral bone growth.

“X-box binding protein1 spliced (XBP1S), a key regulator of the unfolded protein response (UPR), as a bone morphogenetic protein 2 (BMP2)-inducible transcription factor, positively regulates endochondral bone formation by activating granulin-epithelin precursor (GEP) chondrogenic growth factor. Under the stress of misfolded or unfolded proteins in the endoplasmic reticulum (ER), the cells can be protected by the mammalian UPR. However, the influence of activating transcription factor 6 (ATF6), another transcriptional arm of UPR, in BMP2-induced chondrocyte differentiation has not yet been elucidated. In the current study, we investigate and explore the role of ATF6 in endochondral bone formation, focus on associated molecules of hypertrophic chondrocyte differentiation, as well as the molecular events underlying this process.
High-cell-density micromass cultures were used to induce ATDC5 and C3H10T1/2 cell differentiation into chondrocytes. Quantitative real-time PCR, immunoblotting analysis, and immunohistochemistry were performed to examine (1) the expression of ATF6, ATF6α, collagen II, collagen X, and matrix metalloproteinase-13 (MMP13) and (2) whether ATF6 stimulates chondrogenesis and whether ATF6 enhances runt-related transcription factor 2 (Runx2)-mediated chondrocyte hypertrophy. Culture of fetal mouse bone explants was to detect whether ATF6 stimulates chondrocyte hypertrophy, mineralization, and endochondral bone growth. Coimmunoprecipitation was employed to determine whether ATF6 associates with Runx2 in chondrocyte differentiation.
ATF6 is differentially expressed in the course of BMP2-triggered chondrocyte differentiation. Overexpression of ATF6 accelerates chondrocyte differentiation, and the ex vivo studies reveal that ATF6 is a potent stimulator of chondrocyte hypertrophy, mineralization, and endochondral bone growth{ATF6 may increase height, sometimes accelerators of growth increase height sometimes not}. Knockdown of ATF6 via a siRNA approach inhibits chondrogenesis. Furthermore, ATF6 associates with Runx2 and enhances Runx2-induced chondrocyte hypertrophy. And, the stimulation effect of ATF6 is reduced during inhibition of Runx2 via a siRNA approach, suggesting that the promoting effect is required for Runx2.
Our observations demonstrate that ATF6 positively regulates chondrocyte hypertrophy and endochondral bone formation through activating Runx2-mediated hypertrophic chondrocyte differentiation.”

“BMP2 can activate unfolded protein response (UPR)-signaling molecules, such as BiP (binding immunoglobulin protein), CHOP (C/EBP homologous protein), ATF4 (activating transcription factor 4), and IRE1α (inositol-requiring enzyme-1α). ”

“The UPR is divided into three arms, including the PKR-like ER-resistant kinase (PERK), activating transcription factor 6 (ATF6), and IRE1α; the three together act to restrict new protein synthesis and increase the production of chaperones.”

“. BMP2 induces mild ER stress, and then ATF6, as a 90-kDa protein (p90ATF6) in previous non-ER stress environment, is directly converted to a 50-kDa protein (p50ATF6, ATF6a) in ER-stressed cells.  ATF6 undergoes proteolysis and splicing after BMP2 stimulation. ATF6a protein was not detected until day 5 in BMP2-induced chondrocyte differentiation of ATDC5 cells. The expression of collagen X was also immune positive at day 7, indicating that ATF6a expression is prehypertrophic and hypertrophic chondrocyte-specific. The ER stress-induced ATF6 proteolysis occurs in BMP2 stimulation day 5. More significantly, ATF6a expression was 2 days earlier than that of collagen X.”

“ATF6 significantly stimulated chondrocyte hypertrophy, mineralization, and bone length.”

“ATF6 associates with Runx2 in chondrogenesis and ATF6 enhances Runx2-mediated chondrocyte hypertrophy”