It is well circulated throughout the height increase community that tennis can induce longitudinal bone growth of the hand. The below paper discusses this phenomenon.

Stimulation of Bone Growth Through Sports: A Radiologic Investigation of the Upper Extremities in Professional Tennis Players

“This contribution addresses the following questions: Does unilateral sports-specific strain affect the skeletal system of the athlete? Specifically, can any differences be found in longitudinal growth of the bones of the forearm and hand in professional tennis players between the stroke arm and the contralateral arm? An investigation was conducted involving 20 high-ranking professional tennis players (12 male and eight female players) between 13 and 26 years of age{we’d want older players to confirm that longitudinal bone growth can be increased as adults} as well as 12 controls of the same age range. The radiologic examinations of the bones of the forearm and hand yielded an increase in density of bone substance and bone diameter as well as length in the stroke arm as compared with the contralateral arm. Whereas the first results confirm previous findings, the stimulation of longitudinal growth has never been reported. This change in bone structure and size can be attributed to two factors: mechanical stimulation and hyperemia of the constantly strained extremity{hyperemia is enhanced blood flow}. It may thus be regarded as a biopositive adaptation process”

Note that tennis involves torsion of the arm/hands, vibration when the racket hits the ball, and alterations of the bone against gravity(inversion/eversion). All of these forces are likely stimulatory of longitudinal bone growth even past skeletal maturity.

“He found an increase of bone thickness, bigger bone ledges at the insertion of muscles and tendons, and a concentration of bone structure.”<-Is there any way we can mimic the stimulatory pulling and other forces of muscles and tendons?

“an increased vascularization results in an increase in longitudinal growth provided
it takes place during the phase of general growth. Reactive hyperemia is a well-known consequence of bone fractures.”

So there was a striking difference in the length of the ulna in professional tennis players and almost no different in control individuals.

So note that the metacarpal is what increased in length which is a part of the palm. In testing, the palm tends to be what lengthened in our testing.

“Any stroke will transmit mechanical stimuli (vibrations) from the racket to the hand. Because the absorption of these vibrations by the racket is very slow, most of them have to be absorbed by the hand”<-note that vibration is outright mentioned as a possible means behind the lengthening in this paper. We are currently testing vibration in combination with other methods to induce lengthening. I do not believe vibration alone can lengthen bone.

“The second factor seems to be a temporary hyperemia of the muscular system of the dominant arm in tennis players that is induced by sports-specific strain.”

You can see below the major difference in length between a tennis players arms

Below you can see that the metacarpal increase in length in the tennis group but not the control group:

So the key takeaways for the study are that tennis can increase bone length. However, this increase was all pre skeletal maturity but there are other studies that show increase past skeletal maturity. Including anecdotal cases. This still gives credence to the fact that the forces induced by tennis can induce lengthening. I believe that these forces are torsion, vibration, and inversion/eversion of the arm against gravity.

Here’s a statement from a paper that cites the above one called The bone remodelling cycle. “The majority of bone modelling is completed by skeletal maturity but modelling can still occur even in adulthood such as in an adaptive response to mechanical loading and exercise and in renal bone disease.”<-It is possible that this bone modeling could increase length if the stimulation is strong enough. The loads for the arms are superior for those in the legs which is why we tend to see anecdotal cases of lengthening in the arms and not the legs. Arms invert and evert all the time but this is much rarer in the legs for example. You only see inversion/eversion during for example hamstring curls or kicks. We move our arms in a much more dynamic fashion than legs in general. we also experience greater torsion on the arms than the legs. Think hammer curls for example. However, vibrational forces are about equal on the arms and legs.

I found a paper that has interesting insights on the height benefits of spinal traction and the duration that it lasts for.

Changes in stature during and after spinal traction in young male subjects

“Spinal traction is a relatively popular procedure for increasing the intervertebral space by applying separating forces. The parameters of time and magnitude of the traction forces may influence the outcomes from this procedure and need to be investigated. The duration of the benefits derived from traction is unknown and needs to be determined so that physiotherapists can provide better and more effective treatments. OBJECTIVE: This study analyzed the relationship between load magnitude and time during spinal traction in relation to stature variations. Traction effect duration was also analyzed. METHOD: Fifteen healthy male subjects (23.1 ± 5.77 years; 1.80 ± 0.17 m and 87.0 ± 9.6 kg) were assessed under three traction conditions (0, 30 and 60% of body weight, BW) of 42 minutes. Stature variation was used to determine intervertebral disc height variation. Stature was assessed every 7 minutes during traction of 42 minutes and every 5 minutes for 45 minutes after traction ceased. RESULTS: 0 and 30% BW traction produced similar gains (6.09 ± 1.89 mm, 5.70 ± 1.88 mm, respectively; p>0.05), while these were smaller (p<0.05) than at 60% BW (7.01 ± 1.98 mm){since 60% BW traction produced more benefits than 30% it begs the question of whether even more percent of bodyweight would have greater benefit and when the stopping point would. The additional 1mm increase due 60% BW traction is pretty significant}. Significant differences (p<0.05) between 60% BW and the other conditions occurred only after the 21st minute. Stature loss after traction showed that the traction effects were transient and lasted for approximately one hour{it is conceivable to do a traction style exercise every hour but not for 42 minutes}. This suggests that traction loads of 30% BW are insufficient to produce stature gains similar to those observed with 60% BW. CONCLUSION: Traction showed a short-duration transient effect. For this effect to be maintained, it must be repeated at one-hour intervals. Its use is questioned because of its transient nature.”

“The objective of traction is to produce a separating force over the intervertebral discs to counteract the shrinkage caused by compressive loading and restore its mechanical functioning, thereby relieving symptoms. “

HEre’s an image of the traction:

“The stature profile after traction indicated that all the participants lost stature, irrespective of their previous gains (p<0.05). On average, the participants shrank by 3.01 ± 1.09 mm (0% of body weight), 3.35 ± 1.35 mm (30% of body weight) and 4.56 ± 1.51 mm (60% of body weight).”<-the greater the height gain, the more shrinkage there was. “It was noticed that, during the period after the procedure, the participants lost 49.0%, 58.7% and 65.0% of the gains obtained during traction (for 0, 30 and 60%, respectively)”

“As traction was applied only over the lumbar area, whole body length measurements must be interpreted with caution. It is possible that other spinal regions that were not interfered with during the traction protocol may have experienced a certain degree of height variation due to the lying down and standing positions”

“greater stature gains are expected under clinical conditions in which traction is applied continuously (i.e. with no breaks for measurements).”

” The condition of 60% of body weight showed a profile similar to the other two experimental conditions, but only until the 21^st minute.”<-it would interesting to do more testing on this to see if even higher loads had greater benefit.

“gains in stature were still being observed at the end of the protocol”

“up to 70 mm in space flights”<-if this is the theoretical cap and they only gain 7 mm in the study then there is much more theoretical benefit to gain.

” During the first instants of traction, the disc height gains could have occurred by a slow fluid influx. Negative hydrostatic pressure increases with traction load, which causes greater fluid absorption by the nucleus pulposus. Because the fluid cannot migrate very rapidly to the center of the intervertebral disc, tension is applied to the fibers of the annulus fibrosus, causing them to deform towards the center of the disc. Therefore, the first gains in intervertebral disc height may be much more related to pressure variations than elastic deformation of the annulus fibrosus and ligaments. After some fluid has been absorbed, the elastic elements of the intervertebral disc are deformed more intensively. “

70 mm is a lot of potential height gain from spinal traction. That is 7 cm or almost 3 inches. If we could find a way to keep and maintain that height. That would be pretty significant height gain!

According to this paper possibly. Toxoplasma is in food, cat feces, and can be transmitted from mother to child.

Are Toxoplasma-infected subjects more attractive, symmetrical, or healthier than non-infected ones? Evidence from subjective and objective measurements

The informal title and text of the article suggests doubt in the validity of the claims so will have to judge carefully. there’s also possibly selection bias, perhaps taller individuals are more likely to get infected. Especially since the parasite is sexually transmitted. It’s also possible that people who are more likely to be infected with taxoplasma also do other things that are beneficial to height like perhaps having a more diverse microbiome.

“Parasites are among the main factors that negatively impact the health and reproductive success of organisms. However, if parasites diminish a host’s health and attractiveness to such an extent that finding a mate becomes almost impossible, the parasite would decrease its odds of reproducing and passing to the next generation. There is evidence that Toxoplasma gondii (T. gondii) manipulates phenotypic characteristics of its intermediate hosts to increase its spread.”<-A beneficial parasite would be amazing. According to Wikipedia, “Up to half of the world’s population is infected by T. gondii, but have no symptoms” There are potentially negative effects though. Since half the population has it, it’s likely very easy to get so it’s not really worth it to go out to go it even if it did have beneficial effects.

“previous research has shown that Toxoplasma-infected men are, in average, 3-cm taller”

“Toxoplasma-infected men have higher testosterone levels than non-infected ones”

“Toxoplasma-infected (n = 35) and non-infected subjects (n = 178) were compared”

“Some sexually transmitted parasites, such as T. gondii, may produce changes in the appearance and behavior of the human host, either as a by-product of the infection or as the result of the manipulation of the parasite to increase its spread to new hosts.”

HEre are the studies cited in terms of toxoplasma and height:

Body height, body mass index, waist-hip ratio, fluctuating asymmetry and second to fourth digit ratio in subjects with latent toxoplasmosis

“Toxoplasma-infected men to be taller and Toxoplasma-infected men and women to have lower 2D : 4D ratios previously reported to be associated with higher pre-natal testosterone levels. The 2D : 4D ratio negatively correlated with the level of specific anti-Toxoplasma antibodies in Toxoplasma-free subjects. “

Higher perceived dominance in Toxoplasma infected men–a new evidence for role of increased level of testosterone in toxoplasmosis-associated changes in human behavior

“Toxoplasma is parasite of cats that uses any warm-blooded animals as intermediate hosts. It is known to induce shifts in behavior, physiology and even morphology of its intermediate hosts, including humans. The lower second to fourth digit ratio (2D:4D ratio) in infected man and women, and higher height in infected man suggest that sex steroid hormones like testosterone could play a role in these shifts.”

There are multiple papers that suggest that toxoplasma infected men are taller but given that height plays such a great role in mating success it is very likely that the taller height lends you to activities that increase the likelihood of getting it. We would have to understand better exactly how toxoplasma can make an individual taller.

There are some some studies that suggest toxoplasma can impact bone which could mean that it could impact height.

Seroprevalence and Association of Toxoplasma gondii with Bone Health in a Cohort of Osteopenia and Osteoporosis Patients

“an improvement in osteopenia and osteoporosis was observed in Toxoplasma-infected patients”

” we found higher mean T scores and bone mineral density of the spine and femur in the individuals infected with Toxoplasma, suggesting a protective role of toxoplasmosis in subjects with osteoporosis and osteopenia”

The below paper has some insight into supplemental and genetic factors that influence height that I have not seen before.

Nutrition, Other Environmental Influences, and Genetics in the Determination of Human Stature.

“It has been proposed that human linear growth goes through phases of saltation and stasis, with short bursts of rapid growth (up to 1.65 cm within a single day) between long periods (7–62 days) of no growth at all. However, saltatory growth was not observed in human studies by other groups or in other mammals using highly precise radiological measurements. From the perspective of growth plate biology, the continuous nature of chondrocyte recruitment, proliferation, and hypertrophy is inconsistent with long periods of inactivity punctuated by acutely robust proliferation and hypertrophy. Therefore, the hypothesized model of human saltatory growth remains somewhat controversial.”<-If it is possible to grow 1.65 cm in a single day then that means that there must be a way to get around soft tissue limitations in limb lengthening surgery.

“senescence is dependent on growth itself rather than on chronological age. To put it another way, chondrocytes in the growth plate might have a finite amount of growth potential, which is gradually exhausted, leading to the decline in growth rate and associated senescent changes.”<-but that does not mean that we can not alter growth plate senescence.

“On the basis of the assumption that growth itself drives growth plate senescence, growth-suppressing conditions such as nutritional deprivation or inflammation may preserve growth potential and delay senescence”<-there may be ways to trick the growth plate to think that it needs to delay senescence even while it is still growing normally. Possible mechanisms to do this may be via SIRT1.

“Childhood stunting in the first 2 years of age is associated with reduced stature in adulthood, suggesting some permanent loss of growth potential to some degree, despite catch-up growth.”

“Endocrine factors controlling embryonic and somatotrophic fetal growth are of placental and fetal origins and include insulin-like growth factors I and II (IGF-I and IGF-II), growth hormone 2 (GH-2), and human placental lactogen (hPL). In addition, the thyroid hormones thyroxine (T4) and triiodothyronine (T3) play a central role and impact tissue accretion and differentiation as well as having an indirect role in controlling the effectiveness of other hormones including IGFs. GH-2 or placental growth hormone directly affects placental development but is also correlated with IGF-I. While IGF-II is involved in early pregnancy, in late gestation, IGF-I, synthesized in the fetal liver in response to insulin levels determined by glucose availability, controls fetal growth. hPL is secreted by the placenta and is a somatogenic hormone. Glucocorticoids can impact fetal growth, although the presence of a barrier enzyme (11-β hydroxysteroid type 2) converts maternal cortisol, which may inhibit fetal growth, to cortisone”<-what would happen if things like GH-2 and IGF-2 were upregulated in adults?

“GH excess caused by pituitary adenomas leads to elevated IGF-I and gigantism, while GH deficiency in children leads to decreased IGF-I and stunted growth. Like many other hormonal axes, IGF-I provides negative feedback to limit GH secretion in the pituitary. Therefore, children with GH receptor mutations develop a condition called GH insensitivity, where target tissues produce a muted response to circulating GH, leading to increased GH but decreased IGF-I in the circulation and poor linear growth.”<-the GH receptor may be why gigantism is so rare and HGH does not always increase height drastically. The GH receptor may adapt to excess GH.

“Because FGF21 can signal via FGFR3, it is expected to suppress bone growth in rodents via activation of FGF signaling. What is unexpected, however, is that FGF21 can also suppress bone growth in part by inducing GH resistance both in the liver and at the growth plate. A transgenic mouse model with overexpression of FGF21 showed decreased GH-induced STAT5 (signal transducer and activator of transcription 5) signaling and, consequently, diminished hepatic and local expression of IGF-I”<-reducing FGF21 levels may be a way to increase height pre skeletal maturity.

“In both humans and mice, prolonged fasting increases circulating FGF21″<-This would suggest that fasting would reduce height. It may be possible to trick the body if you block FGF21 and fast, you may boost SIRT1 levels or some other mechanism that makes the body preserve catch up growth. So you may grow normally during fasting and then get the catchup period post fasting. You could also potentially block FGFR3 via some mechanism.

“nutrient deprivation may result in decreased local IGF-I signaling at the growth plate (due to GH resistance), followed by a reduction of AKT phosphorylation and decreased recruitment of the resting zone stem cell pool into the proliferative columns. Evidently, administration of exogenous IGF-I in the system was able to restore both AKT phosphorylation and recruitment of resting chondrocytes”

“Androgen itself may have an estrogen-independent effect on stimulating bone growth, because administration of a nonaromatizable androgen in boys has been shown to accelerate linear growth. Unlike that of estrogen, this effect does not appear to be driven by an increase in the GH–IGF-I axis, but rather by a direct, local effect on chondrocyte proliferation”

“[The] effect of estrogen on bone growth is the acceleration of skeletal maturation and induction of growth plate closure. In precocious puberty, premature estrogen exposure leads to advanced bone age, premature epiphyseal fusion, and decreased adult height. Conversely, in hypogonadism, the lack of estrogen leads to delayed fusion and tall stature. Much of this effect of estrogen on skeletal maturation is mediated locally at the growth plate, by accelerating the depletion of stem cells in the resting zone”<-the reduction of estrogen to increase height pre-skeletal maturity has been studied.

“leptin has a direct effect on growth plate chondrocytes that negatively impacts catch-up growth. Refeeding after undernutrition increased leptin levels, which stimulated local aromatase activity at the growth plate and in turn accelerated estrogen-driven skeletal maturation, limiting the amount of catch-up growth. These findings provided important mechanistic insights into why undernutrition often leads to incomplete catch-up growth and permanent growth deficit.”<-So leptin may increase growth rate but result in lower final height due to enhancing estrogens negative effects,

The image above suggests that we can alter genetics somewhat via epigenetics.

“Individual nutrients have been linked to growth and described as growth promoting, such as zinc, magnesium, phosphorus, and essential amino acids. Iron deficiency, common among children and a primary cause of anemia, will result in poor growth and development, and during pregnancy it causes fetal growth restriction due to hypoxia and increased maternal stress”<-We need to know how much of these nutrients are optimal and where more would have no additional beneficial effect.

“The importance of animal source protein and essential amino acids in promoting linear growth in children”

“gut microbiota dysbiosis leads to reduced plasma amino acids”<-this may be one of the ways in which the gut microbiome influences height.

“environment-driven changes in the gut microbiota can similarly affect linear growth via this pathway, animal research suggests that microbial metabolites may also directly stimulate IGF1 gene expression”

Aripiprazole is an antipsychotic but could have beneficial effects on cartilage since the growth plate is made of cartilage this makes this medication intriguing.

Aripiprazole has been used on children for ADHD but I could not find studies on its impact on height.

Drug Repurposing: Therapeutic Role of Aripiprazole in the Cartilage Defect

“The effect of aripiprazole on cartilage was evaluated in aripiprazole-treated adipose-derived mesenchymal stem cells (ADMSCs) and chondrocyte using qRT-PCR and 3D pellet culture. The cartilage restoring efficacy was verified in vivo by mixing it with a scaffold and introducing it into the artificially damaged cartilage of Sprague-Dawley rats.
Next, mRNA was sequenced for mechanistic analysis. As a result, aripiprazole significantly increased the mRNA expression of COL2A1 and SOX9, two cartilage differentiation-related genes, and chondrogenic condensation in vitro. Moreover, it effectively promoted cartilage regeneration in the cartilage defect rat
model. Analysis of mRNA sequencing data from chondrocyte treated with aripiprazole, using KEGG and GOBP , indicated that aripiprazole significantly upregulates genes associated with ribosomes and cytoplasmic translation, thus promoting chondrogenesis. In conclusion, we discovered that aripiprazole can effectively improve damaged cartilage, providing a promising approach for cartilage regeneration.”

The question is can this be used to generation growth plates or increase articular catilage height.

“treatments with aripiprazole and irinotecan were found to elevate the expression of COL2A1, SOX9, and ACAN, genes known to promote cartilage differentiation”

“Analysis of gene expression changes in chondrocytes treated with aripiprazole revealed a significant impact on genes associated with the ribosomal pathway and translation.”

“Metformin treatment (1 mM) inhibits micro RNA-34a while promoting SIRT 1 expression in osteoarthritic chondrocytes, regulating senescence and proliferation in human chondrocytes” SIRT1 could potentially keep growth plates open for longer.

“Statin medications, such as simvastatin, have also been investigated for their potential effects on cartilage regeneration. Statins are commonly used to lower cholesterol levels by inhibiting 3-hydroxy-3-methylglutaryl-CoA. However, they also have anti-inflammatory and antioxidant properties, which may benefit cartilage repair and regeneration. This mechanism is beneficial in preventing cartilage degradation. In a
simvastatin-treated model, type II collagen loss was inhibited, and the ERK-1/2 and p38 kinase pathways regulated the simvastatin-induced differentiation of chondrocytes.”

“several repurposed drugs have been used for cartilage regeneration, including apremilast
(primarily used for psoriatic arthritis), bevacizumab (antiangiogenic drug), and suramin (medication for African sleeping sickness)”. Drugs to investigate for height increase

It seems that this medication is one to watch but more testing will have to be done to see if it can impact height. The authors primarily mention that it helps damaged cartilage which could prevent growth plate height loss and prevent articular cartilage height loss but would not give additional height.