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Metacarpal growth to prove LSJL

Below I will submit evidence of LSJL.  It is not perfect proof but with the resources available it is not possible to generate perfect proof.

However, I will submit the following facts as evidence that there is a very strong possibility that LSJL works.

The basis on whether this is proof of LSJL depends on the answers to the following questions:

    • What is the probability that every bone shaft on my left side of the body is longer than the right except for the one metacarpal which I performed LSJL?
    • What is the probability that my LSJL loaded finger is longer likely due to lengthening of the metacarpal when everything on my left side is longer(can provide additional evidence of my left side being longer if needed)?


Is this not reasonable proof that LSJL works?


So the current hypothesis is that LSJL lengthened my right index finger metacarpal.  The right index finger metacarpal is about 1% longer than the left and since my left bones are almost universally longer than my right bones(at least for all the bones that I have identified) that probably means about a 2% growth(with 1% being a correction of the discrepency).  The remaining bones of the index finger may have grown as well but not beyond the initial discrepency.


Here are my two hand images.  If I could proof that the fourth and fifth metacarpals were longer on my left side on my right that would provide evidence that the fact the index finger metacarpal is longer on my right side is an outlier and is due to loading from LSJL.  The middle finger is not taking into account because it is close to where I loaded with LSJL so there might be some byproduct lengthening of the middle finger.

hand bones

Here’s a labeling of the bones of the hand.  It would be easy to measure if it was like but the bones are not that organized.


Here’s a labeling of the bones on an actual skeleton.  You can see how the hamate mucks up with an accurate measurement.


4th metacarpal5th metacarpal

From these images you can see how hard it is to get an accurate measurement of the 4th and 5th metacarpal.  The shaft of the fourth metacarpal is definitely longer on the left side and eyeballing the shaft of the the 5th metacarpal the left bone looks like a little bit longer.  In terms on the exact beginning and end of the bone it is hard to tell because of the hamate.

Here’s the left and right index finger:


frontal index metacarpals

The shaft of the right bone looks longer in addition to the overall bone being longer.

I submit that the fact that the fourth and fifth metacarpal all have the left shaft as longer than the right like all the other bones I have compared with the exception of the right and left metacarpals of the index finger of LSJL induced lengthening.

Another potential LSJL design mentioned in a scientist paper

Todd Dodge is a scientist who works at Hiroki Yokota’s lab which developed the beginnings of LSJL.  Most of the paper is not relevant to LSJL except for his data that compares the inside of the control bone and an axial loaded bone.  The difference in the cracks is not as dramatic as the control and LSJL loaded bone.    This indicates that LSJL may alter bone structure more dramatically than typical loading and hopefully in such a way that facilitates neo-growth plate formation.  The key takeaway is the sample LSJL device provided in the picture at the end of this article and in the appendix of Todd Dodge’s paper.

Experimental and Computational Analysis of Dynamic Loading for Bone Formation<-Link to thesis at end of article

This paper is written by Todd Dodge who works closely with Hiroki Yokota who was involved in the initial ideas behind LSJL.

“Curvature in the structure of bone was hypothesized to enhance its damping ability and lead to increased bone formation through bending. In addition, loading at frequencies near the resonant frequencies of bone was predicted to cause increased bone formation, specifically in areas that experienced high principal strains due to localized displacements during resonant vibration“<-Is there a specific frequency for cartilage formation?

“Many types of applied mechanical loading of the skeleton have been proposed as potential treatments for osteoporotic conditions, including whole body vibration, axial loading or bending of long bones, and lateral joint loading. Each mechanical loading modality is thought to strengthen bone by causing dynamic fluctuations in intramedullary fluid pressure in areas that experience enhanced stresses and strains due to the applied load. This dynamic pressure gradient{This dynamic pressure gradient may also lead to stem cells differentiating into chondrocytes to form neo-growth plates} may cause fluid flow through the lacunocanalicular network of pores in the bone, causing a shear stress to be applied to osteocytes that inhabit those pores and channels. This shear stress may excite the osteocytes, causing activation of osteoblast activity and initiation of the bone remodeling process. Mechanical loading may also lead to application of force directly to osteocytes as strain in the bone matrix changes the shape of the lacunae and canaliculae{plastic changes in the bone matrix could lead to permanent lengthening?}, imposing deformations on the osteocyte and its processes”

Todd Dodge used lateral knee loading on OVX rats.  1N of load was used at 5Hz for 5 min for a group of rats that was tail suspended.  Loading was done once a day for five straight days.  For a group of rats that were OVX 15Hz for 3 min for 10 days(5 days on, then one off)  12 week-old female sprague dawley rats.  So sort of medium along in the growing process with it starting to taper off.

“The slight increase in BMD in hindlimb-suspended mice may be attributed to additional mechanical stress being applied to the lumbar section of the body, possibly increasing bone growth in that area.”

Unfortunately longitudinal growth was not measured.

Here’s the tibia response to axial loading:


tibia load

Compare this to the LSJL holes which are much bigger between control and loaded and are larger.

“Future studies may incorporate not only cortical bone but also trabecular bone and growth plates, as well as surrounding tissues such as muscle, skin, and joints.”<-We may need to wait for further studies to get the results we need for LSJL.

“the e ffects of loading may not only be localized to nearby bones, but may have remote impacts in the spine.”

Here’s the knee loading device that he recommends, note though it is designed for BMD not for lengthening:

Knee Load device

Creep strength and it’s applications to LSJL

If LSJL can physically deform the bone then perhaps it can deform the bone in such a way as to make it longer.

Creep of trabecular bone from the human proximal tibia

“Creep is the deformation that occurs under a prolonged, sustained load and can lead to permanent damage in bone{So to get creep with LSJL the duration of the loads should be longer}. Creep in bone is a complex phenomenon and varies with type of loading and local mechanical properties. Human trabecular bone samples from proximal tibia were harvested from a 71-year old female cadaver with osteoporosis. The samples were initially subjected to one cycle load up to 1% strain to determine the creep load. Samples were then loaded in compression under a constant stress for 2 h and immediately unloaded. All tests were conducted with the specimens soaked in phosphate buffered saline with proteinase inhibitors at 37 °C. Steady state creep rate and final creep strain were estimated from mechanical testing and compared with published data. The steady state creep rate correlated well with values obtained from bovine tibial and human vertebral trabecular bone, and was higher for lower density samples. Tissue architecture was analyzed by micro-computed tomography (μCT) both before and after creep testing to assess creep deformation and damage accumulated. Quantitative morphometric analysis indicated that creep induced changes in trabecular separation and the structural model index. A main mode of deformation was bending of trabeculae{stretchinig of the trabeculae would be what would make it longer although it’s possible that bending would make trabeculae longer if done in a certain way}.”

” One manifestation of creep damage is the decreased stature of elderly individuals due to the creep damage of vertebrae”

” trabeculae from vertebral areas are mostly rod-like, while in the metaphyses and epiphyses of long bones there is a more balanced mixture of plate-like and rod-like trabeculae. Furthermore, it was shown that these cellular structures degrade differently during the progression of osteoporosis, resulting in differences in the degree of anisotropy of mechanical properties”

” Creep occurs in three stages: primary, secondary and tertiary. Primary creep is the brief initial period during which the creep rate decreases and is accompanied with some material relaxation. In secondary creep, which is the longest and most studied regime, a steady state creep rate (dε/dt) is observed. Tertiary creep, occurring at the end of the secondary regime, is associated with an accelerated creep rate and more damage accumulation that results in eventual failure if the load is sustained. If the creep test is stopped during the secondary stage and the load removed, there is some elastic and viscoelastic strain recovery.”

creep strain

“under a prolonged load, microcracking of the bone matrix (and not fracture of the whole trabeculae) was the primary mode of deformation during creep. On the other hand, it was shown that even a small damage, barely distinguished on radiographs, to older vertebrae accelerates creep, and leads to a visible contribution to a vertebra deformity”

Here’s a paper that shows possible positive benefits of creep deformation:

In vitro torsion-induced stress distribution changes in porcine intervertebral discs.

“A cadaveric porcine spine motion segment experiment was conducted.

To test the hypothesis that small vertebral rotations cause increased stress in the anulus while decreasing stress in the nucleus through stiffening of the anulus.

Stress profiles of the intervertebral disc reportedly depend on degeneration grade and external loading. Increased stress in the anulus was found during asymmetric loading. In addition, depressurization of the nucleus combined with an instantaneous disc height increase was found when small (<2 degrees ) axial vertebral rotations were applied{So twisting could increasing height?}.

vertebral rotation

Seven lumbar porcine cadaveric motion segments consisting of two vertebrae and the intervening disc with ligaments were loaded in the neutral position with 340 N of compression. Stress profiles were obtained in the neutral position, then after 0.5 degrees and 1 degrees axial rotation of the bottom vertebral body. The distribution of compressive stress in the disc matrix was measured by pulling a miniature pressure transducer through the disc along a straight path in the midfrontal plane. Stress profiles were measured in vertical (0 degrees ) and horizontal (90 degrees ) orientation.

Deformation of the anulus by small axial rotations of the lower vertebra instantaneously decreased the horizontally and vertically measured stress in the nucleus while increasing stress in the anulus. A 1-hour period of creep loading decreased the stresses in the nucleus and the anulus 20% to 30%, depending on the orientation, but the effect of an increasing stress in the anular region after axial rotation persisted.

The compressive Young’s modulus of the composite anulus tissue increases instantaneously when small axial rotations are applied to porcine spine motion segments. This is accompanied by decreased stress in the nucleus pulposus, increased stress in the anulus fibrosus, changes in the stress profile superimposed on and independent of prolonged viscoelastic creep and dehydration, and changes in stress distribution independent of horizontal and vertical orientation.”

“the nucleus acts as a sealed hydraulic system, in which the fluid pressure rises substantially when volume is increased (by fluid injection) and falls when volume is decreased (by surgical excision or endplate fracture). “Stress” peaks in the anulus reportedly are increased by prior loading and degeneration.”

“[The] pressure reduction in the nucleus pulposus under torsion coincided with an increase of disc height ”

Magnitude of loads influences the site of failure of highly curved bones.

“The structure and material properties of bones along with applied boundary conditions determine the region of peak stresses, where fracture is expected to occur. As the site of peak stresses is not influenced by the magnitude of applied load, the fracture site is not expected to change during fatigue loading of whole bone at different loads. However, in a highly curved bone such as the rat ulna, the magnitude of applied loads was found to influence the fracture site. Fatigue loading was conducted under load control on intact rat forearms and on excised ulnae. The distance to the site of failure from the proximal olecranon process of ulnae was determined. In intact forearms, the site of failure demonstrated a linear progression distally, towards sites with lower moment of inertia (or sites exhibiting lower section modulus). Intact rat forearms and excised ulnae loaded to failure at low loads fractured 2-3mm distal to where they failed when applying high loads. This indicates a shift in the site of failure by approximately 10% of whole bone length just by varying the applied load magnitude. The site of failure in excised ulnae was similar when loading at 2Hz or at 4Hz, suggesting that this was frequency independent in this range and indicating that strain rate was not an important contributing factor. Creep loading of excised ulnae also demonstrated similar changes in the site of failure, indicating that magnitude of loads, and not type of loading were important in determining the site of failure.”

“the shape of whole bone can be such that failure occurs at sites other than the smallest cross-section and/or smallest moment of inertia. This is especially true for curved bones such as the ulnae and tibiae of commonly used rodent strains.”

“Loading was conducted by placing the excised ulnae between brass U-cups, with the load being applied in the direction parallel to the length of the ulna (left-to-right). During this loading, the natural curvature of the ulna causes bending induced tensile and compressive stresses on the lateral and medial surfaces, respectively”

“a gradual shift is observed as the site of failure of the ulna moves from 15.2 mm to 17.3 mm as the peak compressive load decreases from 26 N to 14 N”

“In excised ulnae, the site of failure shifted distally as the load was decreased, with failure occurring slightly distal to the mid-shaft at high loads and even more distally at lower loads, irrespective of the frequency of cyclic loading (2 Hz or 4 Hz) or the mode of loading (creep or cyclic).”

“Failure occurred at extremely short time scales at high loads, and at considerably longer time scales when loading at low loads. When loading at high loads, times to failure were not dependent on loading frequency or mode of loading (creep or cyclic). When loading at low loads, the time it took for the bones to fail decreased with increased frequency of cyclic loading  and was the shortest during creep loading. Dring cyclic loading, failure occurs in fewer cycles at greater loads, irrespective of the frequency of loading. At the same loads, loading at a higher frequency (2 Hz vs 4 Hz), there was no difference in the numbers of cycles to failure when loading was conducted at different frequencies (2 Hz or 4 Hz).”

“As expected, loading at high loads causes bones to fail in shorter times (within 30 s) as opposed to loading at low loads (periods of a week or two).”<-Loading for a week or two would be extreme.

I’m Writing A Book

I am currently working on writing a book that summarizes EVERYTHING that is on this website. All the important things will be added, and the extraneous information will not be. I will mention all the research and work that has been attempted in the last 15 years, from Sky, to Tyler, to Hakker, to Tim, and others who have tried to help out.

That is why I will not be posting on this website for at least another 4-6 months.

In addition, I have to focus on two other different businesses which are my primary sources of income.

  • Most of my time in the day is devoted to my companies and earning money, and keeping fit.
  • Most of my time at night will be devoted to finishing this book, as well as caring for my family members.

When the book is finally finished, probably in 2016, it will be released to the world, and this website will be transformed into something completely different.

I have decided to use the Natural Height Growth as one of the brand names under my primary umbrella corporation, and treat this website as a real asset. I will be coming back to make good on my promise to push the research much further.

This website will keep on going, and I will try to clean things up, and change dead links, and similar maintenance stuff now.

Anything new that comes out in the next few months will be from Tyler.

Resveratrol for height growth

I wrote about Resveratrol before and it is available for sale.

Resveratrol Supplementation Affects Bone Acquisition and Osteoporosis: Pre-Clinical Evidence Towards Translational Diet Therapy.

“Osteoporosis is a major public health issue that is expected to rise as the global population ages. Resveratrol (RES) is a plant polyphenol with various anti-aging properties. RES treatment of bone cells results in protective effects, but dose translation from in vitro studies to clinically relevant doses is limited since bioavailability is not taken into account. The aims of this review is to evaluate in vivo evidence for a role of RES supplementation in promoting bone health to reduced osteoporosis risk and potential mechanisms of action. Due to multiple actions on both osteoblasts and osteoclasts, RES has potential to attenuate bone loss resulting from different etiologies and pathologies. Several animal models have investigated the bone protective effects of RES supplementation. Ovariectomized rodent models of rapid bone loss due to estrogen-deficiency reported that RES supplementation improved bone mass and trabecular bone without stimulating other estrogen-sensitive tissues. RES supplementation prior to age-related bone loss was beneficial. The hindlimb unloaded rat model used to investigate bone loss due to mechanical unloading showed RES supplementation attenuated bone loss in old rats, but had inconsistent bone effects in mature rats. In growing rodents, RES increased longitudinal bone growth, but had no other effects on bone. In the absence of human clinical trials, evidence for a role of RES on bone heath relies on evidence generated by animal studies.”

“Resveratrol (RES) is a polyphenolic (3,4’,5-trihydroxystilbene) compound naturally present in red wine and a variety of plant foods such as grapes, cranberries, and nuts”

” human bone marrow-derived MSC with RES increased gene expression of the key osteogenic transcription factors, Runx2 and Osterix. RES was also demonstrated in vitro to act on various signal transduction pathways. RES activated the estrogen-mediated extracellular signal-regulated kinase 1/2 (ERK) signaling pathway regulating osteoblast differentiation and proliferation.  RES activated AMP-activated protein kinase (AMPK) which regulates osteoblast differentiation and inhibits bone resorption by acting as a negative regulator of RANKL. RES augmented Wnt signaling which stimulated osteoblastogenesis and bone formation. Treating human bone marrow-derived MSC with RES promoted differentiation of MSC towards osteoblasts by up-regulating Runx2 gene expression through the activation of Sirt1. Also, activation of Sirt1 by RES was shown to promote binding to PPARγ which repressed MSC differentiation into adipocytes. Additionally, RES suppresses osteoclastogenesis by acting through Sirt1 to bind to RANK which inhibited binding to RANKL”<-many of these processes should impact longitudinal bone growth as well.

Resveratrol stimulated tibial and vertabral length in new zealand white rabbits that were 12 weeks old.  200mg per kg of bodyweight were given.  Increased the amount of chondrocytes in the tibia and stimulated growth plate area while reducing fusion.  Decreased vascularization indicated by lower VEGF and laminin levels.

“RES supplementation delayed growth plate fusion by suppressing the replacement of avascular cartilage with vascularized bone indicated by the down-regulated gene expression of vascular endothelial growth factor, a signaling molecule in vascularization, and laminin, a cartilage protein.”

In 6 month old Fisher-Brown Norway rats, it increased tibia length and width.  Dosage was 12.5mg per kg of bodyweight.

“In vitro, RES treatment of chondrocytes obtained from an adult rat femur protected against the catabolic effect of pro-inflammatory cytokine, interleukin-1β”


Why Airborne Transmission Of The Ebola Virus Is Real – The CDC Is Not Telling The Full Truth

Airborne Transmission Of The EbolaNote: This post has nothing to do with the usual stuff we write about on this website. It is a post I wrote to express my own personal opinions on a recent medical topic and give the general public some extra information on the developments of the Ebola virus that is causing massive panic in the developed nations. I want the readers to make up their own minds on what they think the Ebola virus is capable of after reading this post. Am I right or am I wrong?

A few days ago I was having a nice talk with a friend of mine and the subject switched to the news about Ebola. All this recent talk about the disease made me realize that people need to be informed on the facts about Ebola, and not what just the media outlets and the news websites on the internet are telling them. Here is the truth.

The Ebola virus can be transmitted through the air. It is airborne.

This is my personal opinion, based on some initial research on the medical research, and scouring through the PubMed articles. Let me explain. I first became aware of the Ebola virus more than 2 decades ago, in 1997 in a middle school science class. The teacher in a rather unusual change of pace decided to show the class a documentary on the Ebola virus, to show us why biology was important and why we needed to understand this medical school course known as Epidemiology. (For those who might not know, the way modern medical school curriculum is broken down, 2 of the 4 school years are actually devoted to real textbook learning, which included courses on immunology, virology, pharmacology, physiology, and epidemiology. Refer to Stanford Med’s Curriculum here).

The first incident of an Ebola outbreak occurred in Zaire back in 1976. Almost 20 years after the first incident, Ebola broke out again in Zaire in 1995. It has around a 90-95% mortality rate for people who contract the virus. In that incident almost 400 people were killed.

It turns out that under some military/government order, the Ebola virus was brought into the USA back in 1989. A few dozen laboratory monkeys in a lab in Virginia started to die. Under orders, all the 60+ monkeys in a lab room were all killed to stop the contanmination. However, that did not stop the monkeys from dying. After the first room was cleaned and all the monkey’s killed, a second room that was not connected to the first room started to also have the monkeys inside drop dead. It turned out that the Ebola Virus was being transmitted through the air duct/ventilation shafts. This shows that more than 2 and a half decades ago, the virus was already airborne for monkeys.

To say the least I was scared to my core after finishing that little science lesson. (Ironically, I would be shown another Virus Outbreak Documentary, this time on the 1918 Spanish Influenza in 9th grade science class. Using science to scare young kids seems to be a common tactic in my school days.) Back then, the scientists and researchers studying up on this virus still weren’t sure about how the particular virus was being transmitted. However, here is what is known about it back then.

What was known back then was that the Ebola virus can be transmitted through the tears, the blood, and the surface of the skin. Since this virus is not like a flea which can jump from one host to the next using its legs, the only other way it can go to another host is if there is sweat as a medium on the surface of the skin. Viruses also are not like bacteria, which might have legs, known as flagella or cilia, which let them crawl around. The second person touches the skin with the finger surface touching the wet sweat and that goes to them. So now we know that the Ebola virus can be transmitted through 1. tears, 2. blood, and 3. sweat.

Pandemics comes from one of three different types of micro-organisms, 1. bacteria, 2. viruses, and 3. parasites. The Ebola is a type of virus, scientific name Ebolavirus zaire. Parasites are usually transmitted through the body by the intestinal tract, and the blood (ie Tapeworm). Bacteria usually are not transmitted through the blood because the White T-Cells would find them and kill them. That comes down to viruses. The question then becomes “How can a virus be transmitted through sweat, blood, and tears?” Sweat and tears makes sense, but blood as well? The most obvious common denominator would be water, since all fluid coming out of a human are predominantly composed of water, even urine which has a lot of urea/ammonia. I think it is safe to assume that this type of virus survives and is transmitted through water based fluids.

For humans at least, the way that the virus was being transmitted 2 decades ago was from one healthcare worker to the next. Let’s say that the first person gets sick and is lying in a hospital bed. They are too sick to do the basic functions so they have a caretaker who is right next to them to bring them food and take them to the bathroom. Over time the caretaker gets sick. Like a domino effect, that caretaker is then put into bed, and the caretaker’s caretaker gets sick as well, and the cycle continues.

Dr. William Close, who wrote the book “Ebola” showed that one cough is enough to transmit it. If I remember correctly, a cough is releasing one’s internal body liquid into the air in the form of liquid droplet, like the vapor you would find in a steam room/sauna.

We could even use influenza as a good example, to describe the way ebola would behave, since they are both virus based. When we look at the wikipedia article for the Flu/Influenza, “...Half of flu cases arise when people inhale tiny particles that float in the air, ” The Flu has multiple ways for transmission. If you look at the Wikipedia article on “Influenza Prevention”, it defines one of three ways to prevent Influenza “….the airborne route (when someone inhales the aerosols produced by an infected person coughing, sneezing or spitting)”  (Refer to http://www.journalofinfection.com/article/S0163-4453(08)00292-2/abstract)

If we look at this article “Influenza in the Hospital: Droplet or Airborne?” It seems that the difference between Droplet and Airborne is based on the 5 micrometer particle diameter cutoff point.

  • Large Droplet = greater than 5 micrometers
  • Airborne = less than 5 micrometers

If we then look at this article “Flu spreads via airborne droplets” we learn that the flu virus apparently is trapped in water droplets that are usually less than 5 micrometers on average, so  the illness is considered to be “airborne”. Hand washing would do nothing for the common Flu, since handwashing only removes the large sized droplets but not get the smaller airborne particles.

To further validate this point, If you refer to this study (http://cid.oxfordjournals.org/content/45/3/353.full), it shows that the definition on what constitutes an  “airborne” virus is based on the size of the microscopic parts, the AED, which is the diameter of the particles.

Also from the same study, “…At present, 3 major means of transmission of infectious organisms are generally recognized and form the basis of current recommendations for infection control. These differing sojourns and the survival of particles in aerosols have been better elucidated recently by new technology and help explain their capricious nature as effective vectors of infectious agents. of prime importance are the size of the particle, usually described as the particle’s aerodynamic equivalent diameter (AED), and its settling velocity. Particles of large AED settle quickly and, thus, are hazards primarily to those in close vicinity to an infected person. On the other hand, small particles are likely to remain airborne and destined for further spread. For example, particles with AEDs of 100 have settling times of 6.7 s (seconds), compared with 18.5 h (hours) for particles with an AED of 1

So the smaller the particle, the more time it will stay up in the air, since heavier particle will fall down on the ground due to gravity instead of get picked up by a draft of wind. What we need to do is scour through the PubMed database to find the AED (Particle diameter) of the ebolavirus zaire (scientific name) or the common flu virus, Influenza A.

Here was the first idea I had. – The Marburg Virus incident was like a precursor event which happened years before any of these nationally televised incidents, back in the 1960s in some town in Germany. The Marburg Virus was the first appearance of the Ebola virus, being very similar. Since they are similar in physiological function, we can assume that they would have similar mass, body shape, and form.

If you refer to the Wikipedia article on the virus, http://en.wikipedia.org/wiki/Marburg_virus, it says the following… “In general, the median particle length of marburg viruses ranges from 795–828 nm (in contrast to ebolavirions, whose median particle length was measured to be 974–1,086 nm” Source is http://www.sciencedirect.com/science/article/pii/0168170295000801.

I am not sure yet what the term “ebolavirions” mean, but if it means the individual virus unit, measured at around 1 micrometer each, then does it mean that the Ebola’s AED is also 1 AED? which would mean that it can stay in the air for up to 18 hours, which would definitely put it in the category of being “Airborne”.

Sure, we could say that the individual virus units, are likely would be clumped together, so maybe the AED of the virus might be much larger than we believe, but do they really clump together?

2nd Idea – Another way is if we can just compare the size of the influenza virus particle to the ebola virus particle, and if they are about the same size, then we will find out whether Ebola virus is airborne or not. The recent articles that have come out in recent years showed the Influenza A is airborne since the droplets that contain the virus is usually less than 5 micrometers in diameter.

From this John’s Hopkins’s Medical School’s Course PDF (http://ocw.jhsph.edu/courses/PrinciplesIndustrialHygiene/PDFs/Lecture4.pdf) , for the exact definition of AED, “The Aerodynamic Equivalent Diameter (AED) of a particle is the diameter of a unit density sphere that would have the identical settling velocity as the particle

It seems to calculate for AED, you have to take the particle, and use a droplet of water as the actual reference point. As it says in page 15 of the PDF, “…Referenced to spherical drop of water with identical settling velocity” – What we are actually calculating for when we are calculating the AED is to get the diameter for the droplet of water which would be falling at the same speed/velocity as this particle. So a micrometer diameter of lead (Pb) would have a truly large AED, since the drag force would do nearly nothing to slow it down as it is dropping and it has a high density. The ebolavirions may be 1 micrometer on average in size, but we have to account for the density, surface properties, drag force, and slip factor to get the “Settling Velocity” to be correct.

What I can say is that almost all microscopic living organic compounds are made from polymers, proteins, and RNA (collagen or amino acids), which are elastic, flexible, and have a lower density (specific gravity) than any type of sand/dust/solid particle, which would drop to the ground. It might be that the AED would be 1 magnitude larger (10X) than the actual diameter, but that would still make the AED around 10-20. If it is around that value, then the virus only reached the upper nasopharyngeal area, and not the tracheobronchial area, which is the lower respiratory area. (http://ocw.jhsph.edu/courses/PrinciplesIndustrialHygiene/PDFs/Lecture4.pdf) However, that is also a bad thing, since it would mean that coughing would be a very easy way to transmit what is in the upper tract area.

Based on that conjecture, if the medical definition of Influenza says it is technically a type of virus that can be transmitted through airborne pathways, then the Ebola virus must also based on medical technicality also be defined to be a type which can also be carried through airborne transmission, via microscopic water droplets, which is what causes the mist in saunas and water vaporizers. To validate this idea, we can just compare the size/diameter of the Ebola to the Influenza virus.

Concluding Thoughts

How can a virus spread so effectively among any local tribe/community if the natural automatic reaction among humans when there is a local outbreak is to stay indoors, and avoid contact with other humans in the area?

It can’t only be from human contact, and if we rule out it being airborne, as the CDC has claimed, then is it through the water. Maybe the low level of sanitation in Sierra Leone means that the entire village or area would be sharing/drinking from the same water source, but that would not explain why the doctors and helpers who treat the patients would develop them, since these are Western trained physicians. They would be drinking from bottles who were imported from other countries to make sure that the water supply is not contaminated.

Could it be that the virus is being transmitted through the skin surface, from sweat? Possible, but the medical staff is supposed to keep those gloves on at all times.

I personally hope that someone would be able to prove me wrong on all these main points, because I am just an amateur level researcher. If I am wrong, then this virus would be much less scary. If I am right though, god help us all.

You can refer to Nova’s Documentary on Ebola which is the source of half of the information that I present here