How To Plan and Strategize To Use Amara’s Law and Kurzweil’s Law Of Accelerating Return To Our Advantage To Cancel Out Hofstadter’s Law and Murphy’s Law Effects

Originally I had wanted to give this post a different name entirely, “Why Height Increasing Technology Is Two Decades Too Early”- This was the original working title for this post. I wanted to through some key phrases in so that the readers may be more aware of what is coming in their future.

Here is the main point of this post: I believe that what we are trying to do, we are at least 20 years too early. The technology is just not there yet. However, that doesn’t stop us from going through the current data, and studies to write a complete guide for the next generation of researchers.

Before me and Tyler, there was Hakker and Sky. They failed because they were missing crucial information. They didn’t know what they didn’t know. They weren’t even aware of what they were ignorant about. The information we are lacking, is not here yet, or at least not revealed to the general public. However, there is something good that is coming. That is accelerated change in terms of scientific breakthroughs.

These days, things are changing so fast but that could be a good thing. It might be horrible for our current career prospects since it feels like we need to do more and more these days to even hold down a steady job and get our bi-monthly deposit into our bank account. However, if we can fully accept that overall, in the long run as long as we don’t kill ourselves through destroying the earth and the ecosystem, and barring any horrible natural catastrophe, where we will be in 40-50 years will be light years better. The same thing can be said about biotech innovation and the amazing breakthroughs happening everyday in labs around the world.

The fact is that height increase technology (or more specifically, cartilage regeneration and transdifferentiation technology) is probably at least 20 years too early of where we wish it could be – My guess is that it will become possible in 3 decades before we reach the next phase in the natural progression.

What Sky and Hakker tried to do, they were too early, and got the timing of the technology wrong. That is why I plan to play this game for the long term. Instead of putting effort into this endeavor for just 1-2 years, I am planning on focusing on this effort for at least 10 years.

What we might be seeing happening across the world and in our every day lives with IT, and computers, and automatization of everything that can be digitalized, is the result of software. What has been traditionally just information can now all be derived from a software engineer who writes in computer language to create an algorithm. The same thing can not be done with biology. What is happening with computers and software is not happening with biology or genetics.

The problem with Biotech, the Biological Sciences, Chemical related, and Anything Related to Medicine, Pharmaceuticals, is because those types of sciences can not be completely fitted into just a data file on a computer. With the biological sciences you need to actually do real experiments, requiring a real lab with laboratory equipment.

Amara’s law says that one greatly overestimates what they can accomplish in 1 year and underestimates what they can do in 10 years.

Our cognitive biases which causes people to become overly optimistic makes us become bad forecasters of the future. We are almost blind to all the factors which will impeded on our progress. We forget to consider just how hard some things will take.  We make a prediction on how fast something takes to be finished, we never consider unknown problems that crop up (That is Murphy’s Law).

The result is that what we thought might be simple and quick takes at least 50% longer in time to work out than we ever anticipated, even when we account for mistakes and poor judgement. That is Hofstadter’s Law.

The way nature works is not linear, but exponential. Let’s first accept the idea that for the next few years, things are just going to go very slowly, VERY SLOWLY. We are not going to see that much traction, not for a long time. I think this is what some people call the Plateau in our research. We have hit a level which we can’t cross without some major initial capital funding into the project, to get lab equipment.

When we are looking at progress in a short time frame, say 2-5 years, progress may look slow, and linear, with 10-30% increases annually. The result is that scientists and data analysts think that in the future, the trend will stay in that growth pattern, when in fact, things almost never grow linearly. It is exponentially.

That is Kurweil’s Law of Accelerating Returns. We have not reached that inflection point yet, when thing really take off. I am betting that after 10-15 years, then things really start to take off for us.

That is the time when we finally start to see some real results, when all of our hard work starts to really pay off and we see not just returns, but massive returns.

So Amara’s Law + Kurzweils’s Law of Accelerating Return will be eventually, after maybe 10-15 years, finally manage to over come all the trappings involved with Murphy’s Law and Hostadter’s Law.

Now obviously, if walking was able to increase height people would be a lot taller?  But if repetitive stress can induce plastic changes in cortical bone that could possibly contribute to height gain.  More on plastic deformation here.  Michael talks about the definition of Plastic deformation here and he talks about the values needed to induce plastic deformation here.

One possibility as to why inducing microcracks to cause plastic(permanent) changes in bone length is that most microcracks such as those induced by walking would be more compressive microcracks rather than tensile strain microcracks which would be what would be needed to make a bone longer.  One study finding longitudinal decrease in height in the lower legs would be consistent with the fact that typical athletic stimuli induces compressive changes rather than lengthening changes. Although another study also mentioned in the same post found that exercise increased height slightly in the spine. Although it would be logical to think that kicking with ankle weights would be one such stimuli to induce longitudinal plastic deformation of the bone.

Effects of fatigue induced damage on the longitudinal fracture resistance of cortical bone.

“As a composite material, cortical bone accumulates fatigue microdamage through the repetitive loading of everyday activity (e.g. walking). Twenty longitudinally orientated compact tension fracture specimens were machined from a single bovine femur, ten specimens were assigned to both the control and fatigue damaged groups. The damaged group underwent a fatigue loading protocol to induce microdamage which was assessed via fluorescent microscopy. Following fatigue loading, non-linear fracture resistance tests were undertaken on both the control and damaged groups using the J-integral method. The interaction of the crack path with the fatigue induced damage and inherent toughening mechanisms were then observed using fluorescent microscopy.  Fatigue induced damage reduces the initiation toughness of cortical bone and the growth toughness within the damage zone by three distinct mechanisms of fatigue-fracture interaction. Further analysis of the J-integral fracture resistance showed both the elastic and plastic component were reduced in the damaged group. For the elastic component this was attributed to a decreased number of ligament bridges in the crack wake while for the plastic component this was attributed to the presence of pre-existing fatigue microcracks preventing energy absorption by the formation of new microcracks.”

“The composite structure of bone consists of three main components, this includes: collagen type I (organic phase), calcium hydroxyapatite (inorganic or mineral phase) and water [8]. These components are arranged hierarchically from macro to nano scale giving bone distinct material behaviour at each characteristic scale. This composite structure causes bone to form microdamage due to fatigue loading. In bone there are two main types of fatigue damage observed (linear microcracks and diffuse damage), which can be linked to different modes of loading. Another consequence of the composite structure of bone is that it exhibits rising fracture toughness with crack extension (i.e. a rising fracture resistance curve). As a macrocrack propagates through bone, microcracks form in the process zone at the tip of the main propagating crack. This damage can act to reduce the driving force available for crack growth by dissipating energy away from the main crack extension and also provides initiation sites for toughening mechanisms, such as uncracked ligament bridges and crack deflection. Pre-existing fatigue microdamage in the crack path can potentially interact with these mechanisms and alter the fracture resistance.”

In the study a microcrack was induced with a drill so it’s hard to extrapolate the results here to what would happen in various of forms of mechanical stimuli.

This image shows microcracks in bone.  You can see the drill induced crack on the part of a directly above c.

“a crack path of a typical control specimen showing various toughening mechanisms along the crack path: b microcracking ahead of the tip of the main crack, c several ligament bridges and d deflection and ligament bridge formation.”<-I think this kind of cracking could induce longitudinal bone growth however it would require an initial macrocrack such as that induced by the drill.  If you look at the a image directly above d the ligament bridging covers the entire length of the bone which could potentially result in total longitudinal bone growth.

“Typical damaged specimen following resistance curve testing. The approximate location of the pre-existing fatigue microcracks are marked using white lines. Scale bar is 250 µm”

Exercises like kicking with ankle weights can cause microcracks which can increase the likelihood of getting those macrocracks which can result in plastic deformation like longitudinal bone length increase.  But macrocracks are likely needed to induce that plastic strain in bone and only extreme ankle weight kicking is likely to induce that.

The bone constantly changes in length throughout the day by definition of microstrain.  Just cause a “macrocrack in bone” whole the bone is slightly lengthened and repeat and you should gradually grow taller.

Does LSJL only increase intermedullary pressure or does it have extra anabolic effects?  The next few studies address what happens only if intermedullary pressure is increased.  It’s possible that LSJL’s effects are due solely to an increase in vascularization which makes it less promising for adult height growth although it would still be possible to induce adult height growth.  These studies are performed on rats much older than those used in LSJL but no impact on longitudinal bone growth was studied.  However, it still shows even in aged individuals developmental genes like BMP-2 and TGF-Beta can be stimulated.

Dynamic hydraulic fluid stimulation regulated intramedullary pressure

“Physical signals within the bone, i.e. generated from mechanical loading, have the potential to initiate skeletal adaptation. Strong evidence has pointed to bone fluid flow (BFF) as a media between an external load and the bone cells, in which altered velocity and pressure can ultimately initiate the mechanotransduction and the remodeling process within the bone. Load-induced BFF can be altered by factors such as intramedullary pressure (ImP) and/or bone matrix strain, mediating bone adaptation. BFF induced by ImP alone, with minimum bone strain, can initiate bone remodeling.  To apply ImP as a means for alteration of BFF, it was hypothesized that non-invasive dynamic hydraulic stimulation (DHS) can induce local ImP with minimal bone strain to potentially elicit osteogenic adaptive responses via bone–muscle coupling. The goal of this study was to evaluate the immediate effects on local and distant ImP and strain in response to a range of loading frequencies using DHS. Simultaneous femoral and tibial ImP and bone strain values were measured in three 15-month-old female Sprague Dawley rats during DHS loading on the tibia with frequencies of 1 Hz to 10 Hz. DHS showed noticeable effects on ImP induction in the stimulated tibia in a nonlinear fashion in response to DHS over the range of loading frequencies, where they peaked at 2 Hz. DHS at various loading frequencies generated minimal bone strain in the tibiae. Maximal bone strain measured at all loading frequencies was less than 8 με. No detectable induction of ImP or bone strain was observed in the femur. This study suggested that oscillatory DHS may regulate the local fluid dynamics with minimal mechanical strain in the bone, which serves critically in bone adaptation. These results clearly implied DHS’s potential as an effective, non-invasive intervention for osteopenia and osteoporosis treatments.”

“bone fluid flow (BFF) with altered velocity or pressure acts as a communication media between an external load and the bone cells, which then regulate bone remodeling. In converse, discontinuous BFF can initiate bone turnover and result in osteopenia”

“Induced ImP possibly triggers the transformation of the bone nutrient vasculature, leading to the ultimate alteration in blood supply to the bone.”

“The ImP reached the peak at 2 Hz.” at about 15mmHg.

Dynamic fluid flow stimulation on cortical bone and alterations of the gene expressions of osteogenic growth factors and transcription factors in a rat functional disuse model

“Dynamic hydraulic stimulation (DHS) [is] a loading modality to induce anabolic responses in bone. To further study the functional process of DHS regulated bone metabolism, the objective of this study was to evaluate the effects of DHS on cortical bone and its alterations on gene expressions of osteogenic growth factors and transcription factors as a function of time. Using a model system of 5-month-old hindlimb suspended (HLS) female Sprague–Dawley rats, DHS was applied to the right tibiae of the stimulated rats with a loading frequency of 2 Hz with 30 mmHg (p–p) dynamic pressure, 5 days/week, for a total of 28 days. Midshafts of the tibiae were analyzed using μCT and histology. Total RNA was analyzed using RT-PCR on selected osteogenic genes (RUNX2, β-catenin, osteopontin, VEGF, BMP2, IGF-1, and TGF-β) on 3-, 7-, 14- , and 21-day. Results showed increased Cort.Th and Ct.BV/TV as well as a time-dependent fashion of gradual changes in mRNA levels upon DHS. While DHS-driven fold changes of the mRNA levels remained low before Day-7, its fold changes started to elevate by Day-14 and then dropped by Day-21. This study further delineates the underlying molecular mechanism of DHS-derived mechanical signals, and its time-dependent optimization.”

BMP2, IGF-1 and Tgf-Beta are all pro chondrogenic.

“Bone formation progresses over time after the initiation of mechanical loading. Within 24–48 hr after mechanical loading starts, new osteoblasts lay on the bone surface and contribute to bone formation that is observed after 96 hr of loading. Bone formation follows a time-dependent manner, in which it increases between 5 and 12 days of loading and returns back to baseline levels after 6 weeks of loading. These data suggest that the whole cycle of bone formation, including osteoblast recruitment followed by matrix production, lasts for about 5 weeks before declining back to baseline levels”<-new osteoblasts implies cell differentiation which could mean new chondrocytes as well.

Dynamic Hydraulic stimulation increased the periosteal surface.

At seven days interestingly the levels of the pro-chondrogenic genes IGF-1, BMP2, and TGF-Beta were low.  At 14 days they were all increased relative to control.

“HS may compress the veins within the skeletal muscle and increase the vasculature pressure gradient that promotes capillary blood flow in bone. Increase of capillary filtration may further increase ImP and induce BFF that ultimately promote bone regeneration”

I think LSJL does more than just pure Hydraulic stimulation does.

“Osteoblasts [orginiate] from MSCs”

“Our group previously presented a longitudinal study of bone marrow MSC quantification under DHS in a rat HLS model, where the MSC number was greatly increased in response to DHS by day 14 and diminished by day 21. MSCs may have completed proliferation and begun to differentiate towards osteoblastogenesis at this stage. In the meantime, the induced mRNA levels of the selected genes that we observed in the present study may couple the process of transforming MSC proliferation and differentiation into osteoblasts, which commit to the subsequent bone formation.”<-so maybe why the pro-chondrogenic genes were low at day 7 is that MSCs were proliferating rather than differentiating into chondrocytes.