While I was doing chemical research for something else today, specifically on the possibility of starting my own chemistry based cosmetic company (similar to what Jessica Alba did with her Honest company to become a billionaire) I found myself looking into at the active ingredients of many of the most common items in one’s bathroom.

It took maybe 3 hours of checking, scouring, and reading (on Wikipedia) to figure out what exactly were the compounds found in my mouthwash, soap, toothpaste, hand lotion, and sunscreen.

Eventually I came across something that was lying on my bathroom medicine cabinet, Benadryl.

I once remembered a friend of mine telling me that you can knock yourself out by drinking a lot of Vick’s Nyquill (aka cough syrup), which has the active chemical compounds of the following below… (source)

Active ingredients (in each 15 ml TBSP) – Purpose

• Acetaminophen 325 mg  – Pain reliever/fever reducer
• Dextromethorphan HBr 15 mg – Cough suppressant
• Doxylamine succinate 6.25 mg – Antihistamine

Antihistamines are a very common type of drug. So from Vick’s Nyquill, I wanted to know the active ingredient of Benadryl. Does Benadryl have a similar effect as Nyquill, where if you take too much, you will get knocked out?

(Side Fun Fact: Interestingly, people often mistake the idea of chloroform as a drug used to knock people out, but it is actually Ether. Chloroform is talked a lot about in Movies, and shown used in Kidnappings, but Ether would be more effective, since it is faster acting on the human system)

(Side Fun Fact #2: Similarly, there is more than one way to make truth serum, which really just lowers people’s inhibitions and acts as a sedative, making them groggy. The recent news about thieves who steal from tourists using the NIghtshade derived Scopolamine and Atropa belladonna. You can also use Sodium Pentothial (aka Sodium Pentathol.)

So what are the active ingredients in Benadryl, the Anti-Histamine Drug most often used to treat allergies like hay fever?

Well, Benadryl is actually a Brand Name for something else, called Diphenhydramine. In the UK, the active ingredient would be acrivastine and/or cetirizine.

While I was doing more research into the compound Diphenhydramine, It led me to an article on Meclizine, aka Meclozine. Medical professionals knew about the bad side effects of Diphenhydramine for a while, and wanted a type of anti-histamine which did not have that type of drowsiness which comes with it.

In my own searching, I remember writing about Meclozine as a one of the most biggest breakthroughs we have made on this website. Tyler back in 2014 wrote a post entitled Game Changing Breakthrough OTC Height Supplement-Meclozine. I myself also wrote about it entitled Achondroplasia Treatment and Increase Height Using Meclozine aka Meclizine – Great News For Parents!

The science behind it seems to be valid. However, there have been a few sources we found on the internet which suggests the exact opposite. Study of possible correlation between BODY HEIGHT DECREASED and MECLOZINE (MECLOZINE)

This one source however does not take away from the multiple sources which show that Meclizine has bone enhancing abilities.

Google patents – Therapeutic agent for systemic bone disease and use thereof – WO 2014141847 A1

This patent was based on an idea to treat achondroplasia by having as one of the active ingredients Meclizine, which they noted is OTC (Over-The-Counter). These same inventors from Japan, wrote a piece called “Meclozine, Motion Sickness Medicine, Has The Therapeutic Potential In Achondroplasia” – (Masaki Matsushita).

It is interesting that Meclozine (aka Dramamine) has sort of replaced the Benadryl/Diphenhydramine as the type of antihistamine to use now.

It seems that Meclozine is actually so common, and easy to get that you can buy it from Amazon. Before, Tyler Linked to the chemical. Here it is again, for sale from Amazon for around $35. (No affiliate link)

Someone asked Tyler whether taking the Meclozine would work with people with closed growth plates. Tyler said that you should take it with doing LSJL. I will let the readers decide on whether it will work for adults.

However, for young children, this chemical seems to have noticeable effects, especially if you get the compound into your blood, and not through your digestive system (aka orally).

Teriparatide Improves Trabecular Osteoporosis but Simultaneously Promotes Ankylosis of the Spine in the Twy Mouse Model for Diffuse Idiopathic Skeletal Hyperostosis.

Full study->teriparitadeboneformation

“Diffuse idiopathic skeletal hyperostosis (DISH) is a common skeletal disorder in the elderly, which can develop into periosteal hyperostosis and paradoxically into immobilization-associated trabecular osteoporosis. The bone anabolic agent, teriparatide (TPD), seems to be a rational treatment for the immobilization-associated osteoporosis. However, it can lead to development of hyperostosis lesions in DISH patients. Here, we demonstrate TPD effectively treats trabecular osteoporosis while simultaneously promoting ankylosis of the spine in DISH model tiptoe-walking Yoshimura (twy) mice, compared with the ICR mice. Eighteen male twy mice were divided into three groups, and ICR mice were used as a normal control. Subcutaneous injections of TPD or phosphate-buffered saline (PBS) were performed according to three dosing regimens; 40 µg/kg once daily (TPD × 1 group), 40 µg/kg three times daily (TPD × 3 group), and PBS (control; Ctl group). Treatment was commenced at the age of 7 weeks and continued for 5 weeks. Micro-computed tomography (µCT) and histological analysis were performed. Longitudinal µCT study revealed that trabecular bone volume in both the vertebral body and distal femur decreased with time in the Ctl group, but increased dramatically in the TPD × 3 group. The twy mice developed ankylosis of the spine, the progression of which was accelerated with TPD therapy. We also confirmed that TPD therapy promoted ossification of spinal ligaments. Histomorphometrical study revealed that TPD treatment increased bone formation at the vertebrae enthesis region{This is the key to where this has promise} and in the trabecular bone. TPD therapy effectively treats trabecular osteoporosis, but potentially promotes ankylosis of the spine in patients with DISH.”

“The twy mice are mutant mice showing multiple osteochondral lesions, and have been used as a model for DISH and ossification of the posterior longitudinal ligament”

Teriparatide increased ectopic calcification(Fig3C).

“both TPD × 1 and TPD × 3 treatments promoted ectopic calcification. Histologically, there were no cells inside the ectopic calcification but there were fibroblast- or osteoblast-like cells around the ectopic calcification.”<-Fibroblast cells could be precursors to chondrogenic cells.

Here you can see the effects of teraparatide, it can increase height of the spine but also can cause scoliosis:

TISSUE MODIFICATION OF THE LATERAL COMPARTMENT OF THE TIBIO-FEMORAL JOINT FOLLOWING IN VIVO VARUS LOADING IN THE RAT

“This study describes the first application of a varus loading device (VLD) to the rat hind limb to study the role of sustained altered compressive loading and its relationship to the initiation of degenerative changes to the tibio-femoral joint. The VLD applies decreased compressive load to the lateral compartment and increased compressive load to the medial compartment of the tibio-femoral joint in a controlled manner.

Mature rats were randomized into one of three groups: unoperated control, 0% (sham) or 80% body weight (BW). Devices were attached to animal’s leg to deliver altered loads of 0% and 80% BW to the experimental knee for 12 weeks. Compartment-specific material properties of the tibial cartilage and subchondral bone were determined using indentation tests. Articular cartilage, calcified cartilage and subchondral bone thicknesses, articular cartilage cellularity, and degeneration score were determined histologically.

Joint tissues were sensitive to 12 weeks of decreased compressive loading in the lateral compartment with articular cartilage thickness decreased in the peripheral region, subchondral bone thickness increased, and cellularity of the midline region decreased in the 80% BW group as compared to the 0% BW group. The medial compartment revealed trends for diminished cellularity and aggregate modulus with increased loading.

The rat-VLD model provides a new system to evaluate altered quantified levels of chronic in vivo loading without disruption of the joint capsule while maintaining full use of the knee. These results reveal a greater sensitivity of tissue parameters to decreased loading versus increased loading of 80% BW for 12 weeks in the rat. This model will allow future mechanistic studies that focus on the initiation and progression of degenerative changes with increased exposure in both magnitude and time to altered compressive loads.”

” The VLD applies altered loads in addition to the normal loads across the joint without disruption of the joint capsule while maintaining full use and range of motion of the joint.”

The mice were 9-month old sprague dawley.  The rats had the plates attached surgically so it’s not really an exact approximation of LSJL.  And the 0% BW results were drastically different from control so the apparatus definitely had an effect.

“Gross observation of the tibial plateau revealed minimal erosion or fibrillation of the articular cartilage in all experimental groups.”

“The thickness of the articular cartilage in the peripheral region of the lateral compartment decreased 19% in the 80% BW group as compared to the 0% BW group and 26% as compared to the control group. In contrst, the thickness of the subchondral bone increased 38% in the 80% BW group as compared to the 0% BW group”<-So loading increases subchondral bone “thickness” but does this thickness add to height?

Here’s a comparison between sham control(0% BW) and 80% BW.  Loading definitely decreased chondrocyte number but it didn’t seem to decrease articular cartilage height and subchondral bone height seemed to be higher.

Subchondral bone thickness is considered height.

Short and tall stature: a new paradigm emerges.
Full Study->jeffreybaron study

“In the past, the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis was often considered to be the main system that regulated childhood growth and, therefore, determined short stature and tall stature. However, findings have now revealed that the GH-IGF-1 axis is just one of many regulatory systems that control chondrogenesis in the growth plate, which is the biological process that drives height gain. Consequently, normal growth in children depends not only on GH and IGF-1 but also on multiple hormones, paracrine factors, extracellular matrix molecules and intracellular proteins that regulate the activity of growth plate chondrocytes. Mutations in the genes that encode many of these local proteins cause short stature or tall stature. Similarly, genome-wide association studies have revealed that the normal variation in height seems to be largely due to genes outside the GH-IGF-1 axis that affect growth at the growth plate through a wide variety of mechanisms. These findings point to a new conceptual framework for understanding short and tall stature that is centred not on two particular hormones but rather on the growth plate, which is the structure responsible for height gain.”

Note extracellular fluid is listed as a factor and extracellular fluid flow can be modified by LSJL.

This page lists genes that cause mutations to linear growth.  This page lists other mutations and their effects on stature.

“the vast majority of children with short stature do not have a well-substantiated defect in the GH–IGF-1 axis.”

“Many new genes have been identified that, when mutated, result in short stature or tall stature, the majority of which do not participate in the GH–IGF-1 system”

“Estrogen has complex effects on the growth plate, not only altering growth rate, but also accelerating the loss of progenitor cells in the resting zone and thereby speeding up the developmental program of growth plate senescence, which causes early cessation of growth”

“tumour necrosis factor, IL-1β and IL-6 act directly on growth plate cartilage to suppress bone growth”

“fairly low doses of ionizing radiation, such as a single dose of 10 Gy, can impair longitudinal growth. Mechanical compression across the growth plate also impairs the elongation of bones, which is partly due to decreased enlargement of hypertrophic chondrocytes.”<-Chondrocyte hypertrophy size increases due to lsjl.

“FGFR-3 signalling negatively regulates growth by decreasing proliferation in the proliferative zone, decreasing production of the extracellular matrix, accelerating the onset of hypertrophic differentiation and decreasing the size of the hypertrophic chondrocytes”

“~2% of children who present with idiopathic short stature have mutations in NPR2, Conversely, overexpression of CNP or activating mutations in NPR2 result in tall stature.”

” Binding of CNP to NPR2 stimulates the guanylyl cyclase activity of the receptor, thereby increasing synthesis of cGMP, which activates the type II cGMP-dependent protein kinase”

“Of individuals presenting with idiopathic short stature, 2–15% have mutations in SHOX, with the exact percentage depending on the study. Conversely, increased copies of SHOX are associated with tall stature in individuals with Klinefelter syndrome and other types of sex chromosome aneuploidy”

“Sotos syndrome (characterized by tall stature) is associated with decreased activity of the Ras–MAPK pathway.”

“Ras, a small GTPase, signals via MAPK cascades to phosphorylate numerous cytoplasmic and nuclear proteins, regulating cell proliferation and differentiation.”

“heterozygous mutations in DNA methyltransferase 3A (DNMT3A) cause tall stature, a distinctive facial appearance and intellectual disability.”

“heterozygous mutations in EZH2, which encodes an enzyme that specifically methylates lysine residue 27 of histone 3 (H3K27, which is associated with transcriptional repression), are associated with Weaver syndrome (characterized by prenatal and postnatal overgrowth and a markedly advanced bone age).”

There’s a lot more covered in the study than I mentioned here.  The full study is worthwhile to read.

It’s frustrating how much bodybuilding research there is in terms of sets, reps, and all sorts of factors to build up muscle and how little there is in terms of height.  Note that most of this research does not come from science it comes from tons of independent bodybuilders.

With muscle building we know that stressing the muscles in general increases their size.  Bodybuilders don’t wait for calf and pec implants to get bigger muscles.

We don’t know though how to lengthen bone?  We don’t know what stimulus to apply?  Actually we have a pretty good idea.

To induce chondrogenic differentiation(chondrocytes are the basis for the growth plate) one method is to induce a hydrostatic pressure of at least 0.1 MPa.  A blood pressure cuff during a heart beat generates about 120mmHg which is about 0.015MPa an order of magnitude of what we need.  To get 0.1MPa we’d need a blood pressure of about 750mmHg which would probably cause death.  There has to be a way for the body to safely induce hydrostatic pressure of 0.1MPa-10MPa’s to induce chondrogenic differentiation.  HP levels of the articular cartilage can vary between 1-5MPa in response to physiological(occurs normally) stress.  There are two possible ways to make up the difference in the hydrostatic pressure deficit(0.015MPa versus 0.1MPa or ideally higher) fluid flow and bone deformation.

Ultrasound levels of 30–200 mW/cm2, Frequency=1–1.5 MHz are one possibility(you’d target in the epiphysis).  Note I have not tested this so attempt at your own risk!  Muscular contraction can also increase marrow hydrostatic pressure.  You’d probably need to use external electrical stimuli to generate the muscular contraction needed to induce significant hydrostatic pressure.  Again I can not say whether or not this is safe or not!

An increase in hydrostatic pressure also results in an increase in fluid flow which may be the primary inducer of chondrogenic differentiation rather than the HP itself.  Thus you could find ways to induce fluid flow directly and in conjunction with an increase in hydrostatic pressure to get the needed stimulus to induce chondrogenic differentiation.

The growth plate is exposed to high hydrostatic pressure via the bone pressing down on it.  If we create a fibrous layer in a neo-growth plate region maybe the hydrostatic pressure to encourage a growth plate will occur naturally.  Note that LSJL does encourage fibrous tissue differentiation.  If we can create a fibrous tissue layer, the compression force of the bone itself will create the hydrostatic pressure and induce chondroinduction.

Fluid flow induces recruitment of integrins to focal adhesions.  This alteration in cell signaling by fluid flow directly could induce chondrogenic differentiation.

So we know the key to growing taller is to induce a new growth plate in the bone as bone tissue is not mechanically suited for interstitial growth.  We know that this can happen at around 0.1MPa hydrostatic pressure in the bone epiphysis.  It’s possible to make up for a deficit in hydrostatic pressure levels via other factors like fluid flow via dynamic lateral compression.  There’s also the possibility of using ultrasound and electrical muscle stimulation.  Such levels would have to be supranormal as no muscle stimulation of longitudinal bone growth has yet to be reported.  Since it is supranormal all the effects are not known so it would have to be tested somewhat for safety first.