A recent post by Michael stated that one of the obstacles to LSJL success is that hydroxyapatite crystals have sharp edges and that could result in the damage to the cells of any microgrowth plate possibly induced by LSJL.

First, Shear Strain and Fluid Flow induced by LSJL may disrupt the crystals.  However, let’s look at the science of Hydroxyapatite crystals and cell death to chondrocytes.

Intracellular calcium oscillations in articular chondrocytes induced by basic calcium phosphate crystals lead to cartilage degradation.

“Basic calcium phosphate (BCP) crystals, including octacalcium phosphate (OCP), carbonated-apatite (CA) and hydroxyapatite (HA) crystals are associated with destructive forms of osteoarthritis.  We assessed the ability of BCP to induce changes in intracellular calcium (iCa(2+)) content and oscillations and the role of iCa(2+) in BCP-induced cartilage degradation.

Bovine articular chondrocytes (BACs) and bovine cartilage explants (BCEs) were stimulated with BCP or monosodium urate (MSU) crystals. iCa(2+) levels were determined. mRNA expression of matrix metalloproteinase 3 (MMP-3), a disintegrin and metalloprotease with thrombospondin-like motifs 4 (ADAMTS-4) and ADAMTS-5 was assessed. Glycosaminoglycan (GAG) release was measured in the supernatants of BCE cultures.

All three BCP crystals significantly increased iCa(2+) content. OCP also induced iCa(2+) oscillations. Rate of BACs displaying iCa(2+) oscillations increased over time, with a peak after 20 min of stimulation. OCP-induced iCa(2+) oscillations involved both extracellular Ca(2+) (eCa(2+)) influx and iCa(2+) stores. Indeed, OCP-induced iCa(2+) oscillations decreased rapidly in Ca(2+)-free medium. Both voltage- and non-voltage-dependent Ca(2+) channels were involved in eCa(2+) influx. BCP crystal-induced variation in iCa(2+) content was associated with BCP crystal-induced cartilage matrix degradation. iCa²(+) was not associated with OCP crystal-induced mRNA expression of MMP-3, ADAMTS-4 or ADAMTS-5.

BCP crystals can induce variation in iCa(2+) content and oscillations in articular chondrocytes. BCP crystal-induced changes in iCa(2+) content play a pivotal role in BCP catabolic effects on articular cartilage{and potentially possibly LSJL induced micro-growth plates}.”

“BCP crystal deposition in knee articular cartilage is associated with cartilage destruction, more severe clinical symptoms, and chondrocyte phenotype changes towards hypertrophy as suggested by increased expression of type X collagen and greater ability to produce BCPs in vitro”<-So the BCP crystals within the bone will encourage the chondrocytes to hypertrophy.

“BCP crystals may stimulate articular cells through two mechanisms. They can first activate cells as endocytosed or phagocytosed particles leading to intralysosomal crystal dissolution with subsequent elevation of intracellular Ca2+ levels and release of inflammatory cytokines. The other mechanism of cell activation by Ca2+ crystals involves a direct crystal–cell membrane interaction”

“In articular chondrocytes, BCP crystals induce increased DNA synthesis and cell division{this is anabolic}, IL-1β mRNA overexpression, nitric oxide and MMP-13 production, increased caspase-3 activity and chondrocyte apoptosis”

“iCa2+ was involved in OCP-induced proteoglycan degradation but not OCP-induced mRNA expression of MMP-3, ADAMTS-4 or ADAMTS-5.”

This next study relates to HA crystals and causing apoptosis in another type of cell in bone osteoblasts.

Effects of four types of hydroxyapatite nanoparticles with different nanocrystal morphologies and sizes on apoptosis in rat osteoblasts.

“Hydroxyapatite nanoparticles (nano-HAP) have been reported to cause inflammatory reactions. Here, we aimed to compare the effects of four types of nano-HAP with different nanocrystal morphologies (short rod-like, long rod-like, spherical or needle-shaped crystals) and sizes (10-20, 10-30 or 20-40 nm) on growth inhibition and apoptosis in primary cultured rat osteoblasts. The osteoblasts was treated with the four types of nano-HAP at various concentrations (20, 40, 60, 80 or 100 mg/l).  All four types of nano-HAP inhibited the growth of osteoblasts in a dose-dependent manner. These nano-HAP significantly induced apoptosis in osteoblasts. Nano-HAP with smaller specific surface areas induced lower apoptosis rates. The needle-shaped and the short rod-like particles induced greater cellular injury than the spherical and long rod-like particles, respectively. The increased apoptosis rates were accompanied by increased p53 and cytochrome c expression. nano-HAP inhibit the activity of osteoblasts and also induce the apoptosis of osteoblasts in vitro. The nano-HAP-induced apoptotic pathway is mediated by a mitochondrial-dependent pathway. Moreover, the sizes, morphologies and concentrations of nano-HAP have significant effects on the apoptotic level.”

“nano-HAP with diameters less than 100 nm can cause inflammatory reactions, especially when the particles are needle-shaped”

nano-HAP increases caspase 3 and 9 and increases Bax levels while decreasing Bcl2.  The first three being pro-apoptotic proteins and the last being anti-apoptotic.

If HA crystals affect osteoblasts it’s likely they would affect chondrocytes too.  However, osteoblasts manage to survive in bone tissue despite the existence of HA crystals.

Annexin 5 overexpression increased articular chondrocyte apoptosis induced by basic calcium phosphate crystals.

“Basic calcium phosphate (BCP) crystals (octacalcium phosphate (OCP), carbapatite (CA) and hydroxyapatite (HA)) are associated with severe forms of osteoarthritis. In advanced osteoarthritis, cartilage shows chondrocyte apoptosis, overexpression of annexin 5 (A5) and BCP crystal deposition within matrix vesicles.

Apoptosis was induced by BCP crystals, tumour necrosis factor (TNF)-alpha (20 ng/ml) and Fas ligand (20 ng/ml) in normal articular chondrocytes (control) and in A5 overexpressed chondrocytes, performed by adenovirus infection. Apoptosis was assessed by caspase 3 (Cas3) activity, and DNA fragmentation.

All BCP crystals, TNF-alpha and Fas ligand induced chondrocyte apoptosis as demonstrated by decreased cell viability and increased Cas3 activity and DNA fragmentation. TUNEL (terminal deoxyribonucleotide transferase-mediated dUTP nick end-labelling)-positive staining chondrocytes were increased by OCP (12.4 (5.2)%), CA (9.6 (2.6)%) and HA (9.2 (3.0)%) crystals and TNF-alpha (9.6 (2.4)%) stimulation compared with control (3.1 (1.9)%). BCP crystals increased Cas3 activity in a dose-dependent fashion. BCP-crystal-induced chondrocyte apoptosis was independent from TNF-alpha and interleukin-1beta pathways but required cell-crystal contact and intralysosomal crystal dissolution. Indeed, preincubation with ammonium chloride, a lysosomal inhibitor of BCP crystal dissolution[dissolved], significantly decreased BCP-crystal-induced Cas3 activity. Finally, overexpression of A5 enhanced BCP crystal- and TNF-alpha-induced chondrocyte apoptosis.

Overexpression of A5 and the presence of BCP crystals observed in advanced osteoarthritis contributed to chondrocyte apoptosis.”

So, Chondrocyte Apoptosis doesn’t occur unless the crystal is dissolved.  But it’s possible this may occur as a result of shear strain due to LSJL.    However, the apoptosis induced is not complete and wouldn’t totally inhibit micro-growth plate formation due to LSJL.

“Chondrocytes undergo apoptosis after exposure to NO or Fas ligand (Fas-L).”

“Annexins are ubiquitous proteins that can interact with acid phospholipids, membranes and cytoskeleton constituents in the presence of Ca2+. They are involved in regulating intracellular and extracellular activities such as endocytosis and exocytosis and Ca2+ fluxes. Chondrocytes produce annexins 2, 5 and 6 (A2, A5 and A6), whose levels are increased in OA cartilage. A2, A5 and A6 have been identified on matrix vesicles. A5 can form voltage-gated Ca2+ channels and mediates Ca2+ influx into matrix vesicles, which initiates extracellular mineralisation, and into cellular cytoplasm, which induces apoptosis of growth-plate chondrocytes”

” chondrocyte apoptosis induced by BCP crystals was independent from elevations in extracellular calcium and/or phosphate concentrations but required direct cell-crystal contact.”

“[BCP induced chondrocyte apoptosis requires] cell-crystal contact, crystal endocytosis and intralysosomal crystal dissolution responsible for intracellular Ca2+ elevation.

Hydroxapatite crystals require too many things to go wrong to induce apoptosis in cells to likely occur in a normal physiological environment.  And if they did they would cause apoptosis to a variety of cells not just chondrocytes so you would want to eliminate them regardless.

Thus, I do not believe that HA Crystals or BCP crystals are a hindrance of micro-growth plate formation.

Unfortunately, as of now there is no clear direction on how to manipulate the circadian clock to alter longitudinal bone growth.

Prolonged bioluminescence monitoring in mouse ex vivo bone culture revealed persistent circadian rhythms in articular cartilages and growth plates.

“we revealed a robust and extremely long-lasting circadian rhythm in ex vivo culture maintained for over six months from the femoral bone of a PERIOD2(Luciferase) mouse{How do we manipulate or re-initiate this circadian cycle for height growth?}. Furthermore, we also identified robust circadian clocks in flat bones. High- or low-magnification real-time bioluminescence microscopic imaging revealed that the robust circadian rhythms emanated from the articular cartilage and the epiphyseal cartilage within the growth plate of juvenile animals. Stimulation by forskolin or dexamethasone treatment caused type 0 phase resetting, indicating canonical entraining properties of the bone clock. Together, our findings from long-term ex vivo culture revealed that “tissue-autonomous” circadian rhythm in the articular cartilage and the growth plate of femoral bone functions for several months even in an organ culture condition, and provided a useful in vitro assay system investigating the role of the biological clock in bone formation or development.”

“the plasma PTH rhythm persisted under “constant routine” conditions where subjects were deprived of any exogenous time information, indicating that the rhythm is driven by the intrinsic circadian clock”

“At the molecular level, the circadian clock is composed of a set of clock genes forming cell-autonomous transcription/translation feedback loops; the molecular oscillators in turn drive the expression of output genes governing a variety of clock-controlled physiological processes. Specifically, two transcription factors, BMAL1 and CLOCK, heterodimerize and transactivate core clock genes such as Period genes (Per1 and Per2), Cryptochome1 (Cry1), and Rev-Erb genes (Rev-Erbα and Rev-Erbβ). Expressions of these genes (Bmal1, Per1, Per2, Cry1, Cry2, RevErbα and RevErbβ) show clear circadian rhythms with distinct peak times”

“circadian bioluminescence rhythms from long bones (proximal femoral ends and radiuses) and flat bones (calvariae and scapulae) showed similar period lengths”<-so the circadian rhythm may not be something that distinguishes between long and flat bones.

“both epiphyseal cartilage and articular cartilage in femoral trochlea  showed clear circadian rhythms for 4 days”

“expression of certain clock genes has been shown in growth plates”

” local circadian clocks in the epiphyseal cartilage may affect bone growth in juvenile animals.”

“Exogenous time cues (e.g. light) can reset internal clocks.”

“[The] phase of the bone clock [that] was strongly altered by forskolin, functions to increase intracellular cAMP levels through adenylate cyclase activation. Therefore, it is possible that in vivo circadian phase can be reset by endogenous substance(s) via the cAMP pathway in the bone. The hormone PTH increases intracellular cAMP levels via the PTH/PTHrP receptor, consequently inducing Per1 and Per2 expression through the cAMP–PKA–CREB pathway. In addition, sympathetic signaling stimulated by leptin has been shown to regulate bone remodeling in part through a β-adrenergic receptor (β-AR). The β-AR agonist isoproterenol also enhances intracellular cAMP levels and up-regulates Per1/2 and Bmal1 expression in primary mouse osteoblasts. In accordance, isoproterenol has been reported to stimulate the circadian rhythmic expression of Per1/2/3 and Bmal1 in human SaM-1 osteoblastic cells”

“DEX, synthetic glucocorticoids (GCs), was found to reset the bone circadian rhythm. GCs are secreted from the adrenal gland in a circadian manner. Although the SCN is not reset by GCs due to a lack of glucocorticoid receptor (GR) expression, circadian clocks in peripheral organs such as the liver, kidney, and heart are highly responsive to GCs. GCs are considered as internal time-cues which relay timing information within the body and synchronize the peripheral clocks, including bones, as shown here. At the molecular level, GCs bind to GR and regulate target gene expression via glucocorticoid response elements. Previous studies have identified Per1, Per2, and E4bp4 as direct targets of GRs in mice”

Forskolin alters Ca2+ and cAMP levels, I haven’t seen any studies regarding the effects of Forskolin on longitudinal bone growth.  Dexamethasone is widely known to inhibit longitudinal bone growth.  However, Dexamethasone is also known to help induce chondrogenic differentiation.

This is a response to the forum thread “Naturalheightgrowth Is wrong about LSJL” posted by longlegs. In this field and niche of research, there will always be doubters.

His/Her Original Post

The author of naturalheightgrowth.com made a publication on why LSJL would not work.

Source: Evidence That The LSJL Method Or Loading Is Ineffective In Post-Pubertal Adult Humans? (Important)

The author concludes that LSJL will not work because the the cartilage growth would need to work against the solid bone of the Periosteum. However the Periosteum has always covered the growth plate in the per-ossification stages.

Thus, if if the author of naturalheightgrowth is correct about this theory, then that would mean that it would be impossible for children to grow(which is clearly incorrect).

My Response To Their Claims

I note that every time someone puts up a link to the website anywhere, I am informed. I do spend some time to read all of the people’s concerns and questions. I will try to answer these people as well as I can.

• First, that posting was written last year, when my knowledge was not as advanced. My opinions have changed on that subject.

• Second, someone said that ‘a lot of success stories’ comes from using LSJL with results. Can any of you name even 9-10 people who have seen results at least by 2 cm? I make the cut off at 2 cms because 2 cms is probably enough of a gain to consider that it was not just from measurement error of the gain from hair, and different posture. For it to be “a lot” At least a dozen cases where something similar happened should be available.

• Third, I have asked Tyler to write for the website and you guys can notice that the 2nd to the most recent post about Acupuncture Lasers was his.

• Fourth, can any of you explain the exact mechanism how the chondrocytes can push in all 3 dimensions outwards due to hypertrophy and make the bones actually expand volumetrically. THIS EXACT ISSUE was (and still is) the main concern I have with the method. I wrote two  posts months ago playing devil’s advocate to make sure that I stay as objective and scientifically accurate as possible. Refer to them below…

• Post #1: How Lateral Synovial Joint Loading Works To Increase Height From Non-Distraction: FAQs and Concerns Answered (Guest Post)
• Post #2: Why LSJL Might Not Work, An Explanation Using Bone Mechanics And Bone Bridge Studies

Tyler made the correct point that children can grow because the chondrocytes expand and push the entire cartilage matrix upwards, and that has the cartilage pushing against bone tissue on both sides, but that is just in 2 directions out of a total of 6. One can simplify the bone-cartilage-bone schematic as a cylinder with three parts connected. However, in that configuration, the layer of cartilage is surrounded by bone on only 2 Directions, up and down.

When there is no cartilage, the MSCs in the epiphysis is essentially trapped and surrounded completely by bone. It would have to be pushing against cortical bone tissue in all 6 directions, up, down, left, right, front, back.

Think of it this way. Imagine that you are the growth plate itself. If there is only a wall of bone above you and below you, you can push upwards and whatever is on top of you would get raised up to a higher height since the upper wall is not connected to the lower wall.

Refer to the picture of Zydrunas Savickas from the Strongest Man Competition taken from VikingStrength.com. That log above him is indeed very heavy but he can push it up with great effort. Remember, imagine that you are the growth plate itself.

If however you are surrounded also by the same type of hard material that forms the wall that is above you and below you, and all the walls are connected, can you still push the wall above you and below you apart?

That is what happens when the growth plate gets fractured a bone bridge develops between the bones above and bellow the cartilage.

It would take probably at least 10X more power to push the bones apart from each other when the bone layers are connected, even with one bone bridge.

I don’t remember how to do the exact calculation to figure out what multiple of extra energy would be needed to push apart the external environment when one object is completely surrounded and trying to expand (ie hypertrophize). I do know that it is related to the Material Science principle of Surface Stress.

The first part of the calculation is very easy. You are calculating for energy, E, which is just Force times Distance in a cylindrical configuration, where the setup is solid-space-solid which actually represents bone-cartilage-bone in a very simplified physics model. Imagine yourself pushing upwards on a round surface. Multiple Force over a distance, assuming distance is just half a cm, 0.5 cm.

The 2nd part is the one I don’t know how to do. Imagine that you are pushing outwards in a spherical shell against a layer of the material, with a certain thickness (delta_r), material strength, and for the same change in distance, 0.5 cm. Never forget that you are calculating for something that is 3-Dimensional so the picture to the right is not completely accurate on the exact model you are trying to calculate for.

Based on my assumptions, if the MSCs did indeed differentiate into chondrocytes in the epiphysis (which we can induce in multiple ways), and they did start to expand in size (which we can probably also induc), what will most likely happen is that the cells won’t get too big. The moment the cells reach the cortical bone layer, they will come across randomly packed hydroxyapatite crystals which tend to have very sharp edges. The result is that a good proportion of the chondrocytes that are pushing outwards will have the outer membrane punctured by the hard crystal edges, like a knife to a balloon.

I am not saying that Tyler is a liar. I just can’t explain why or how he managed to get the height increase that he did using basic physics principles. If he did increase in height after he started to do the method, then somehow he has been succesful in an endeavor that millions of people around the world having been hoping for. I support him and his work for this website and all the work he has done. Very early on in the growth of this website, almost exactly a year ago, I thanked his effort and research which he has been doing for over half a decade “Thank You Tyler Christopher Davis aka Minigolf Of HeightQuest.Com“

Tyler’s Comments: I don’t think the hard crystal edges are an issue to LSJL as I mentioned in a post.  As for the statement that a microgrowth plate would have to work much harder against 6 directions than a standard growth plates 2, I’ve looked for information regarding the force required to push the tissue apart and I think a good model would be to look at adipose tissue as that is the most easily expanding tissue and is in the bone.  But I have not been able to find information on growth plates and how much force each cellular process generates and how much force is required to generate each percentage of growth.  That information would be ideal but I think adipose tissue may have some answers.

Now this post will be one of the more controversial ones because some people might interpret the message of this post to imply that I want to do some type of eugenic manipulation on human beings to create ‘super-humans’. I am not, since there is no evidence that we can even do that type of thing, from at least the research I have found.

Instead of using some type of stem cell like genetic manipulation on the embryo of an offspring to make sure that they are going to be much more than what they were genetically programmed to be, I suggest that we as parents, or as future parents consider that it might be smart to consider the idea of changing the environment of where our sons or daughters live to make sure that they get a much better chance of growing to their maximum level.

At this point, I am not sure how I feel about the application of genetic “gattaca like” manipulation to create children who probably would one day look down at us for being so ‘below average’ and having to settle with bodies that are so small and limited. I don’t want to be the cause of creating a generation of super-mutant humans who will think that just because their genetic parents decided to pay for them to have the best physical attributes, that would imply that by default of their existence they are better than all of their predecessors.

What I would suggest that we might consider of doing as parents or future parents who want the best for our children, and probably will implement are a series of steps to ensure that my child gets the best chance to be as vertically advantaged as possible.

I once stated that for most humans, the two most important qualities that are most prized by almost all cultures are…

1. Raw Intelligence in terms of High IQ
2. Having above average height, specifically being at least 2 standard deviation above the ‘average’ height of a large group 

I have always believed that if a person has extremely high IQ and is well endowed in stature, they would already have 95% of all the attributes that are needed to reach success to unlimited levels. Where others would have to struggle like crazy to get and achieve, it would come easier to them and they would be able to influences others just by their mere presence.

In terms of what I am saying, I am saying that beyond the emotional and mental qualities for success, we must always start with the biological anthropomorphic measurements and attributes first, and have all of the genetic and biological advantages.

Now these days the first quality is already being researched and trying to be implemented by many organizations and companies.

In one of my earliest posts of this website that had absolutely nothing to do with height or height increase, I had talked about how it might be possible to increase one’s cognitive function and focus from taking a nootropic, which is a type of pill that helps a person get more focus, and help them get things done quicker. The post was “How To Become Smarter By Using Provigil And Piracetam“. This post was the first of many posts where I talked about the importance of not just being bigger in stature, but also being smarter to be able to compete in this modern world.

The pill that is supposed to make a person ‘smarter’ was called Provigil. Another name for it is Modafinil. Other types of nootropics include Modalert, Piracetam, and more. I personally know at least a few people who are entrepreneurs and own large companies who have started to take Provigil/Modafinil to improve their concentration and working ability so that success will be more likely to occur. The desire to improve our brain function has already been implemented by the people who are willing to try to hack their own bodies to find out how to optimize and maximize for productively and efficiency.

Some companies in China are already trying to create smarter babies. I wrote about what these companies are doing in the post “China Is Most Likely Trying To Engineer Taller Humans Currently As Well As Geniuses (Important!)“. BGI Shenzhen has had a lot of press and stories written about their bold move in trying to sequence the genes of 2 thousand of the smartest humans in the world to find the alleles that would determine , and possibly lead, to humans that are just innately intelligent. The Huffington Post wrote a piece on this issue “Is China Really Engineering Baby Geniuses?“

So the main point with this first part is to show that beyond us trying to figure out a way to make our bodies bigger, in giving ourselves a competitive advantage over other people, there is also considerable amounts of effort to also increase our brains to make use as smart as possible.

So if the reader is willing to actually take the steps to make their children bigger, these are the ideas that I have thought of and proposed to help make our children taller.

Step #1: Relocation for Healthcare Benefits

Moving ourselves to countries & societies which have amazingly good healthcare systems. When we look at the average height of people in Canada compared to the USA, we see that Canadians are actually taller than Americans. Back in 2010 the website Phys.Org published a paper showing that Canadians are actually taller entitled Canadians lead longer, healthier lives than Americans. This phenomena where countries which have better health care seem to have taller adults seem to be true for also places like Northern Europe (In countries like the Netherlands, Norway, and Denmark) , where the people there have some of the best healthcare system.

Better healthcare often means that the mother after going through labor and giving birth have more time to stay at the hospital or at home to raise the baby during the critical few months after birth. They are given better quality of healthcare by nurses, doctors, and therapists all there to advise on how to best raise the baby during the period of life when the person is most vulnerable.

Since the human body grows the most during the 1st year, by as much as 1 feet on average, that first year of growth is the most important. Any type of infection can actually decrease the immunity in the baby’s body.

Course of action: Moving to Canada, Switzerland, Norway for the healthcare benefits.

Step #2: Relocation for more personal freedoms and expressions

There is also a small correlation seen between countries which give a lot of personal freedom to  the individual and their height. The best example would be in The Netherlands. The capital, Holland has been known for almost 30 years now for it’s extremely liberal policy on many topics which almost all other countries in the world forbade, like prostitution, marijuana usage, and drug usage. I may be completely wrong but I suspect that the relaxed, more liberal nature of the Dutch societies views on topics which are considered taboo in most conservative countries means that the individual does not have to repress their desires.

It seems that countries which have happier citizens on average tend to have taller people. (Of course there are some clear examples where this idea is challenged. I note that people in Thailand are very happy and always smiling but they are not the tallest ethnic group in the world, but the issue on body size is also heavily correlated with relative position of the country to the equator of the earth. )

Course of action: Moving to Netherlands, Belgium, or Norway for the higher quality of life.

Note: Anecdotal evidence ad stories suggest that children who are born and raised in suburbs, not the rural or urban communities end up the tallest of the three groups. This could be from a sort of goldilocks-zone idea, where they are not completely socially isolate from people, but also not in an environment where it is not so overly crowded like in a city.

Step #3: Breastfeeding the baby for a much longer duration

Most parenting books on babies say that one should start weaning the baby off of the mother’s breastmilk within 1 year, and then you start to transfer the move to formula. My personal research on the compounds Colostrum and Casein Phosphopeptide suggest that babies would get the anti-bacterial, anti-fungal, and anti-viral nutrition that these two compounds

Nature tends to have a good idea on what is the optimum food for humans, and the mother’s breast milk is probably the best type of food for the growing baby, and formula is something which I theorize not good for the baby.

Studies I have found showed that babies who started to use formula earlier did grow bigger, but only in terms of weight. Compared to babies who were still on breastmilk, the formula consuming baby was fatter but not taller. In fact, babies who consume formula earlier are probably more likely to start puberty earlier in life, resulting in a final adult height that is slightly lower.

Course of action: Continue to raise the baby on breast milk until age 2.

Step #4: Having A Diet Of Lean Meat and Vegetables with less emphasize on Simple Carbohydrates

I admit that I am a little biased on this issue since I have been a follower of the Paleo diet ideology. There are only a small collection of evidence in showing that paleolithic humans, who did only hunting and gathering,  who lived on before the advent of agriculture and farming, were actually much taller than their neolithic relatives. Dave Asprey from the Bulletproof Executive Podcast has stated that it seems that the onset of Cavities and Periodontal Disease seems to be caused by the overconsumption of simple carbohydrates. One can actually reverse cavities and heal them up using Fats and Vitamin K2 intake.

If the the development of agriculture, which meant that humans can finally settle down in one place, and grow the grains/carbohydrates which makes most of human kind’s diet today, like rice, wheat, corn, and rye, really did mean that there is a drop in the overall human race’s height, then by the reverse logic, humans should be able to increase the average height of a population their more consumption of proteins like meat and less on simple carbohydrates.

Course of action: Don’t allow your child to become vegetarians, for growth reasons. When they are adults, they can choose to not eat Betsy the cow, but while they are still growing, do allow that lifestyle choice.

Step #5: Getting more milk derivative products into the diet

I had looked at the relationship between milk consumption, calcium, growth, and final adult height in previous posts. The post The Real Correlation Between Milk, Calcium, Bone Growth, And Height forced me to analyze whether the correlation was real or not. There seems to be a weak correlation but it is there. People who get more consumption of milk derivative products like cheese and yogurt tend to be at least a fraction of an inch taller than the people who consume milk products at the average level. It is not much but it is there.

In addition, we do find that people who are Lactose Intolerant tend to be slightly shorter than people who don’t suffer from lactose intolerance.

Course of action: Drink more milk and start to develop a habit of enjoying the taste of cheese

Step #6: Getting accurate exercise, but more specifically aerobic and some bone loading

Exercise like a quick intense sprint of 100 meters does indeed cause a release of extra HGH into the child’s system right afterwards, mostly for tissue healing and anabolic processes. That is the aerobic part.

It turns out that children who get some exercise do end up slightly taller than their peers who don’t exercise. The extra amount of loading on the bones does seem to cause the ossification of the growth plates to occur much faster.

Studies looking at the bone density of swimmers and soccer players compared to their more lethargic peers suggest that children who are swimmers have lower bone density and soccer players have higher bone density.

However, the correlation between bone density and adult height for children who are still growing seem to be inverse, but it is a very weak correlation. I am theorizing that children who are swimmers do end slightly taller as adults than children who play soccer. The child soccer player does have higher bone density but as adults, they tend to be slightly shorter. (Note that this is a personal observation, but not based on scientific studies).

Reference: Bone geometry and strength adaptations to physical constraints inherent in different sports: comparison between elite female soccer players and swimmers

Course of action: Get your child into a sport, which has some potential for bone loading, to stimulate endochondral ossification to be faster, but you don’t want to load the bones too much. Football and Soccer are not recommended because the amount of loading is higher than optimum. Swimming is recommended.

Step #6: Always getting the adolescent to sleep around 9-10 PM, so they wake up in syne with the morning light

If we assume that the human species is derived from primates and apes, then we can logically reach the conclusion that millions of years ago our ape ancestors as day time creatures went to sleep when the sun went down and woke up when the sun rose back up around 8-10 hours later.

Our most instinctual natural sleeping patterns are supposed to be in sync with the rise and fall of the sun. There are enough studies which show that the time when children get the highest levels of HGH influx into their body system is during the night time, when they are in deep sleep. It is during deep sleep that the natural growth hormones go through their body the most.

To have the optimum sleep, I propose that we get our child to go to sleep early, and wake up early.

I personally know for a fact that the best sleeps I ever have had in my life was in the outdoors when camping where there was no artificial light available so I had to go to sleep when the sun went down and there was no more light. Waking up afterwards with the rising of the sun seems to refresh the brain to crystal clarity. I think this is what our brains have been naturally conditioned by millions of years to prefer. This is why I think that having a sleeping pattern that is in sync with the sunlight progression leads to better, deeper, longer sleeps which result in more GH being pumped into the body, resulting in slightly better growth.

In addition, it turns out that height increase almost exclusively happens when people are sleeping, not when they are standing up during the day when they are awake.

Note: Most of the growth spurts that are noted from anecdotal stories suggest that growth spurts happen most often during the summer time, not during the normal Sept – May American school year. This is why you get the phenomena where you notice that a previously short male from that past school year seemed to have sprouted up like a bamboo after you see them in the next school year on the first day of school in August or September, which was only a 2-3 month difference.

Course of action: Get your child to develop a good habit of having deep, non-troubling sleep. Get them to bed earlier around 9-10 PM so that they can get up with the sun, which usually rises up around 5-6 AM, since our reptilian brain has been evolutionarily evolved to rise and rest with the sunlight progression.

Step #7: Avoid Smoking

The stunted growth effects of smoking is not as bad as some people might make one think, but the effect is real. People who start to smoke a lot as children do end up on average a fraction of an inch shorter than their non-smoking peers. It is only a fraction of 1 inch but that is enough of a positive correlation in showing the stunted growth effects of habitual smoking as children.

So these are the 7 steps and ideas I currently have on how one can raise their child to make sure that their growth is optimized so they can grow to their maximum height.