What factors can cause lack of results in the LSJL height increase program?

Previously, we discussed possibilities of how to get over various stagnations in the LSJL height increase routine for those who started out gaining height but whose gains slowed down or ceased.  What if you never gained a single cm at all?  It may not be a failure of the routine but rather certain genetic and environmental factors that impair gains.  Some people have reported gains, some have stalled, and others have gotten no gains at all.

LSJL requires some factors to work:

Sufficient Telomere Length for chondrogenic differentiation(can potentially be rectified by Astragalus)
TGF-Beta1 release by the osteoblasts/osteocytes(and possibly the periosteum)
Hydrostatic Pressure on mesenchymal stem cells for chondrogenic differentiation

So there could be issues with the mechanotransduction pathway for TGF-Beta and there could be issues with mesenchymal stem cell proliferation and differentiation.

Too high or too low levels of Barium may affect these pathways.  Remember that Baryta Carb has been used to treat dwarfism in some cases.  Most height increase foods like milk already contain high barium.  So if you are drinking a lot of milk, eating a lot of cereal, hot dog, and nuts.  Your barium levels may be too high and that could be the reason of lack of gains due to closure of calcium voltage gate channels.  No way to know for sure without getting the blood work done.  Potassium supplementation may be able to help with too high barium levels.

Intoxication by large amounts of barium nitrate overcome by early massive K supplementation and oral administration of magnesium sulphate.

"Suicide by ingestion of barium is exceptionally rare. Adverse health effects depend on the solubility of the barium compound. Severe hypokalemia, which generally occurs within 2 hours after ingestion, is the predominating feature of acute barium toxicity, subsequently leading to adverse effects on muscular activity and cardiac automaticity. We report one case of acute poisoning with barium nitrate, a soluble barium compound. A 75-year-old woman was hospitalized after suicidal ingestion of a burrow mole fumigant containing 12.375 g of barium nitrate. About 1 hour post-ingestion, she was only complaining of abdominal pain. The ECG recording demonstrated polymorphic ventricular premature complexes (VPCs). Laboratory data revealed profound hypokalemia (2.1 mmol/L). She made a complete and uneventful recovery after early and massive potassium supplementation combined with oral magnesium sulphate to prevent barium nitrate absorption."

"Toxic effects can occur following ingestion of as little as 200 mg of soluble barium compound."<-So you want to keep barium levels below 200mg probably below 100mg so you have a cushion.  Brazil nuts for instance contain 4mg per gram of nut so you'd have to eat 25g to hit 100mg.

If you think you might be deficient in barium you might want to try a little bit of brazil nut oil: Raw Organic Brazil Nut Oil-250 ml.  Most foods have below 0.002mg/g of Barium so too high of barium is rare unless you eat a very specific diet of food or there's a lot of barium in the drinking water.

If your bone is not increasing in thickness then it means that the mechanotransduction pathways are not working and it could possibly be a problem with barium above or below the optimal range.  If your bone is increasing in thickness then it probably isn't a mechanotransduction problem. It could also be something else like a calcium deficiency   This study states that it's the actin cytoskeleton involved rather than proteins that affect the calcium voltage gate channels.

L-type calcium channel activity in osteoblast cells is regulated by the actin cytoskeleton independent of protein trafficking.

"Voltage-dependent L-type calcium channels (VDCC) play important roles in many cellular processes. The interaction of the actin cytoskeleton with the channel in nonexcitable cells is less well understood. We performed whole-cell patch-clamp surface biotinylation and calcium imaging on different osteoblast cells to determine channel kinetics, amplitude, surface abundance, and intracellular calcium, respectively. Patch-clamp studies showed that actin polymerization by phalloidin increased the peak current density of I (Ca), whereas actin depolymerization by cytochalasin D (CD) significantly decreased the current amplitude[actin polymerization affects the current of Ca]. This result is consistent with calcium imaging, which showed that CD significantly decreased Bay K8644-induced intracellular calcium increase. Surface biotinylation studies showed that CD is not able to affect the surface expression of the pore-forming subunit α(1C). Interestingly, application of CD caused a significantly negative shift in the steady-state inactivation kinetics of I (Ca). There were decreases in the voltage at half-maximal inactivation that changed in a dose-dependent manner. CD also reduced the effect of activated vitamin D(3) (1α,25-D3) on VDCC and intracellular calcium. We conclude that in osteoblasts the actin cytoskeleton affects α(1C) by altering the channel kinetic properties, instead of changing the surface expression, and it is able to regulate 1α,25-D3 signaling through VDCC. Our study provides a new insight into calcium regulation in osteoblasts, which are essential in many physiological functions of this cell."


So, the amount of actin polymerization is what affects Calcium release more than any compound.

"Physiological hormones, such as parathyroid hormone (PTH) and activated vitamin D₃, also modulate the calcium homeostasis of bone through voltage-dependent calcium channels[too high levels of calcium can lower PTH]. 1α,25 vitamin D increases the inward barium current through L-type calcium channels at low depolarizing potentials within seconds in a fashion similar to Bay K8644, an L-type calcium channel agonist"<-Barium, PTH, and Vitamin D3 affect the ability of L-type calcium channels

"Calcium channels can regulate mechanical load-induced bone formation. Application of cyclic strain to the substratum resulted in increased incorporation of calcium in Ros 17/2.8 cell cultures, and the response could be diminished in the presence of verapamil, a blocker of voltage-dependent calcium channels"<-If the voltage-dependent calcium channels don't work neither will LSJL or other mechanical stimulation.

Actin polymerisation is good for inducing TGF-Beta the problem is that we want mesenchymal stem cells to not have actin polymerisation as that results in cell movement and not stopping to condense and form new growth plates.

Now the next factor that may be preventing you from getting gains with LSJL is problems with cellular proliferation and differentiation.  Namely with Myostatin.  Muscle is the primary regulator of myostatin so if you have large muscles you probably don't have a problem with myostatin.  Conversely, if you have small muscles you likely do.  Weight lifting and creatine can inhibit myostatin.

If you have small muscles and didn't get results with LSJL try lifting weights and taking creatine.

As for chonrogenic differentiation, anything that inhibits adipogenic differentiation encourages chondrogenic differentiation.  If you're building up your muscles fine it probably isn't an issue with lack of differentiation but hypoxia may play a role.  Maybe your bone is overvascularized discouraging chondrogenic differentiation.  In that case increase the duration of clamping.

Checklist if you did not gain three months after LSJL:

1) Did my bone grow in thickness?  If not check barium levels and other factors related to the L-type Calcium Voltage Channels

If your bone did grow in thickness then:

2) Start working out and seeing if your muscles hypertrophy.  If not then take creatine and increase testosterone levels which inhibits myostatin.  See Lateral Synovial Joint Loading Supplement Guide for list.

3) Perform LSJL on the fingers to check for local factors or possible intensity issues.  If you can gain length in the fingers with the bar clamp then it is likely a local bone problem or possibly LSJL is not performed with optimal intensity.

4) For Vascularity/Hypoxia there is venous ligation which also increases hydrostatic pressure/fluid flow as well...  But realistically, you can increase duration of clamping.