Those who say that weightlifting stunts growth will have a field day with this one.  Small animals were used and if the loads mentioned in the study caused as much apoptosis then growth would be severly stunted by weight loading.  But if it indicated some cellular regeneration in regards to unplanned apoptosis due to mechanical that would be an amazing breakthrough.  We could trick the cells into thinking there was more apoptosis than there was and that would lead to overgrowth.

Secondary ossification centers evolved to make endochondral bone growth possible under the weight-bearing demands of a terrestrial environment

“The growth of long bones occurs in narrow discs of cartilage, called growth plates that provide a continuous supply of chondrocytes subsequently replaced by newly formed bone tissue. These growth plates are sandwiched between the bone shaft and a more distal bone structure called the secondary ossification center (SOC). We have recently shown that the SOC provides a stem cell niche that facilitates renewal of chondro-progenitrors and bone elongation. However, a number of vertebrate taxa, do not have SOCs, which poses intriguing questions about the evolution and primary function of this structure. Evolutionary analysis revealed that SOCs first appeared in amniotes[essentially egg laying reptiles, birds, and mammals] and we hypothesized that this might have been required to meet the novel mechanical demands placed on bones growing under weight-bearing conditions. Comparison of the limbs of mammals subjected to greater or lesser mechanical demands revealed that the presence of a SOC is associated with the extent of these demands. Mathematical modelling with experimental validation showed that the SOC reduces shear and normal stresses within the growth plate; while relevant biological tests revealed that the SOC allows growth plate chondrocytes to withstand a six-fold higher load before undergoing apoptosis{this provides evidence that too high a load could stunt growth}. Hypertrophic chondrocytes, the cells primarily responsible for bone elongation, were the most sensitive to loading, probably due to their low Young’s modulus (as determined by atomic force microscopy). Our present findings indicate that the primary function of the evolutionary delineation of epiphyseal cartilage into spatially separated growth plates was to protect hypertrophic chondrocytes from the pronounced mechanical stress associated with weight-bearing in a terrestrial environment.”

“hypertrophic chondrocytes undergo apoptosis or trans-differentiation, leaving their calcified extracellular matrix as a scaffold on which invading blood vessels and osteoblasts form new bone tissue.”<-interesting that the acknowledge the transdifferentiation theory.

“commonly to study bone growth (i.e., mice, rats and rabbits), the growth plate is separated from the articular cartilage by a bony fragment, the secondary ossification center (SOC). This skeletal element, formed during early postnatal development, splits the initially contiguous cartilaginous element into two independent structures, the growth plate and articular cartilage ”

“Growth plate chondrocytes appeared to be highly sensitive to load, with 40% dying upon application of a 1N load (as revealed by propidium iodide (PI) staining). At the same time, the SOC clearly protected these cells, allowing them to withstand a load an order of magnitude higher ”  An order of magnitude would be 10N

“directional compressive stress appears to be harmful to chondrocytes, especially hypertrophic chondrocytes”

Update:  I’m still working on a new non-LSJL method.

I don’t believe that chocolate can make you wildly taller but it tastes good.  I also think the optimal diet for longitudinal bone growth varies on developmental stage.

Chocolate and Chocolate Constituents Influence Bone Health and Osteoporosis Risk

“Bone loss resulting in increased risk of osteoporosis is a major health issue worldwide. Chocolate is a rich source of antioxidant/anti-inflammatory flavonoids as well as dietary minerals with the potential to benefit bone health. However, other chocolate constituents such as cocoa butter, sugar and methylxanthines may be detrimental to bone. Human studies investigating the role of chocolate consumption on serum bone markers and bone mineral density (BMD) have been inconsistent. A contributing factor is likely the different composition and thereby, nutrient and bioactive content amongst chocolate types. White, followed by milk chocolate, are high in sugar and low in flavonoids and most minerals. Dark chocolate (45-85% cocoa solids) is high in flavonoids, most minerals, and low in sugar with ≥70% cocoa solids resulting in higher fat and methylxanthine content. The aim of this review was to examine the relationship between consuming chocolate, its flavonoid content, and other chocolate constituents on bone health and osteoporosis risk. Studies showed postmenopausal women had no bone effects at moderate chocolate intakes; whereas, adolescents consuming chocolate had greater longitudinal bone growth{whether this fact can be used for any purpose though….}. Based on flavonoid and mineral content, unsweetened cocoa powder appeared to be the best option followed by dark chocolate with higher cocoa content in terms of supporting and preserving bone health. Determining dietary recommendations for chocolate consumption regarding bone health is important due to the growing popularity of chocolate, particularly dark chocolate, and an expected increase in consumption due to suggestions of health benefits against various degenerative diseases.”

“Diets that promote bone health have mainly focused on increasing Ca and
vitamin D consumption, but there is growing interest in phytochemicals[chemicals produced by plants]”

“Dietary polyphenols consist of a large group of plant-derived secondary metabolites
divided into four different classes, one of which is the flavonoids (diphenylpropanes C6-C3-C6).
Flavonoids contain several classes of bioactive compounds.  There is evidence
that intake of specific flavonoids may promote bone health including: soybean isoflavones (e.g.
genistein and daidzein), flavonols (e.g. aglycone quercetin) found in plums, and flavonones (e.g.
hesperidin) found in citrus pulp and juice.  Another food source noted for its flavonoid
content is chocolate.  Cocoa, a major constituent in chocolate, has the highest flavanol
content of all foods on a per-weight basis and contributes to greater total dietary intake of
flavonoids than tea, fruits, and vegetables ”

“Both animal models and human clinical trials have reported an inverse association
between reactive oxygen species (ROS) and bone health.  ROS can affect bone cells in
various ways including stimulation of osteoblast apoptosis and senescence and by upregulation
of receptor activator of nuclear factor kappa-B ligand (RANKL) to activate osteoclast
differentiation and bone resorption”<-I think though there is a role for ROS.  It’s just too many is a bad thing.  And bone can be inhibitory towards longitudinal bone growth but it’s degradation of bone(bone turnover) not degradation of bone building cells that would be beneficial.

“catechins preserved bone-forming osteoblasts by exerting anti-inflammatory actions”

” In a randomized, double-blinded placebo-controlled study, pre-pubertal (n=149, age 6.6-9.4 years) girls consumed two Ca-supplemented food products daily to achieve a Ca dose of 850 mg/d.  Results showed consuming Ca-supplemented chocolate bars, cakes or cocoa beverages for 48 weeks significantly increased height and bone mass acquisition in the radius and femur”

“Feeding murine dams chow diet supplemented with 400 mg unsweetened chocolate during pregnancy and lactation resulted in progeny with significantly shortened forefeet and hindlimbs.  Vascular endothelial growth factor (VEGF), which plays a role in ontogenesis and longitudinal bone growth related to angiogenesis in the epiphyseal growth plate, was significantly reduced in the femora of immature (age 4-weeks old) mice pups exposed perinatally to chocolate.  A follow-up study investigating the relationship of the chocolate constituent, catechins on angiogenesis and bone mineralization in the progeny of murine dams fed chocolate showed a negative correlation (r = -0.62, P<0.05) between embryo tissue epigallocatechin concentration and mean number of newly-formed blood
vessels.  Crystallinity of compact bone of diaphyses was 17% greater and femoral
epiphyseal cancellous bone was 30% greater in pups age 4-weeks old exposed perinatally to
chocolate compared to pups from control dams.  The authors suggested anti-angiogenic activity
of chocolate catechins disturbed the processes of bone elongation and mineralization “<-so chocolate may be better at different stages.

Here’s the study the chocolate study in girls:

Calcium–enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo–controlled trial.

“High calcium intake during childhood has been suggested to increase bone mass accrual, potentially resulting in a greater peak bone mass. Whether the effects of calcium supplementation on bone mass accrual vary from one skeletal region to another, and to what extent the level of spontaneous calcium intake may affect the magnitude of the response has, however, not yet been clearly established. In a double-blind, placebo–controlled study, 149 healthy prepubertal girls aged 7.9+/-0.1 yr (mean+/-SEM) were either allocated two food products containing 850 mg of calcium (Ca-suppl.) or not (placebo) on a daily basis for 1 yr. Areal bone mineral density (BMD), bone mineral content (BMC), and bone size were determined at six sites by dual-energy x-ray absorptiometry. The difference in BMD gain between calcium-supplemented (Ca-suppl.) and placebo was greater at radial (metaphysis and diaphysis) and femoral (neck, trochanter, and diaphyses) sites (7-12 mg/cm2 per yr) than in the lumbar spine (2 mg/cm2 per yr). The difference in BMD gains between Ca-suppl. and placebo was greatest in girls with a spontaneous calcium intake below the median of 880 mg/d. The increase in mean BMD of the 6 sites in the low-calcium consumers was accompanied by increased gains in mean BMC, bone size, and statural height. These results suggest a possible positive effect of calcium supplementation on skeletal growth at that age. In conclusion, calcium–enriched foods significantly increased bone mass accrual in prepubertal girls, with a preferential effect in the appendicular skeleton, and greater benefit at lower spontaneous calcium intake.”

“Both statural height and body weight, however, were significantly greater among the spontaneously high- versus low-calcium consumers (129.160.7 vs. 126.560.7 cm, P , 0.001; 27.560.5 vs. 25.760.5 kg, P , 0.001, respectively). ”

There were several non calcium enriched foods in the study and not just chocolate so it’s likely the calcium and not the chocolate making the girls taller.