Saturday, June 9, 2012

Reach taller with prolactin?

Men do produce prolactin but not quite as much as women.  Neither group produce as much prolactin as lactating women during their second trimester.  This may be unfortunate as prolactin may have height increasing effects.  The study "Alcohol, height, and adiposity in relation to estrogen and prolactin levels in postmenopausal women.", found no relation between height and prolactin levels of course that study did not measure prolactin levels during development when prolactin could increase height.

There have been no studies to my knowledge of teenage pregnancy increasing height.  Fathers also experience an increase in prolactin.  There have been no studies either of young fathers and height growth.

Possible chondroregulatory role of prolactin on the tibial growth plate of lactating rats

"Besides calcium accretion in the cortical envelope, a marked increase in the length of long bone was observed in pregnant and lactating rats, and thus the growth plate change was anticipated. Since several bone changes, such as massive trabecular bone resorption in late lactation, were found to be prolactin (PRL)-dependent, PRL may also be responsible for the maternal bone elongation[Thus prolactin may increase height in developing humans]. Herein, we investigated the growth plate change and possible chondroregulatory roles of PRL in the tibiae of rats at mid-pregnancy until 15 days postweaning. We found that the tibial length of lactating rats was increased and was inversely correlated with the total growth plate height, as well as the heights of proliferating zone (PZ) and hypertrophic zone (HZ), but not the resting zone (RZ)[so it's unclear whether this is a growth rate increase or if prolactin can increase adult height]. Chondrocytes in all zones expressed PRL receptors as visualized by immunohistochemistry, suggesting that the growth plate cartilage was a target of PRL action. Further investigations in lactating rats treated with an inhibitor of pituitary PRL release, bromocriptine, with or without PRL supplement, revealed the PRL-induced decreases in total growth plate height and HZ height from early to late lactation. However, decreases in RZ and PZ heights were observed only in late and mid-lactation, respectively. \\"

"the tibial and femoral lengths of maternal rats were significantly increased by 2 and 3%, respectively, at late lactation"<-No mention is made of other bone lengths, but 2 to 3% is a pretty significant increase in height.

"In primiparous mole rats, the lumbar vertebral length was markedly increased during pregnancy, and this lengthening was dampened after delivery"<-increase in lumbar height + tibial and femoral height could lead to a significant increase in overall body height.

"This increase in bone length in lactating rats was previously shown to be dependent on PRL"

Now lactacting rats are losing calcium and PRL may counteract this loss. In turn, calcium may be the factor causing the bone length increase. However, the scientists who wrote this study suggest a direct effect of PRL on bone length.  "PRLR was widely expressed in the growth plate chondrocytes in the digits of neonatal rats.
Besides the growth plate chondrocytes, PRLR expression has been reported in articular chondrocytes from both humans and rats." <-Although we don't know if Prolactin receptors are present in human growth plate chondrocytes but they likely are as articular chondrocytes and growth plate chondrocytes are very similar.

"In the articular chondrocytes in vitro, PRL has been found to inhibit apoptosis induced by serum starvation  and to increase type II collagen expression. Moreover, PRL could directly induce proliferation and chondrogenic differentiation of the human marrow-derived mesenchymal stem cells to mature chondrocytes"<-So prolactin could help with LSJL by encouraging chondrogenic differentiation and thus growth plate generation.

Chondroregulatory action of prolactin on proliferation and differentiation of mouse chondrogenic ATDC5 cells in 3-dimensional micromass cultures.

"Lactogenic hormone prolactin (PRL) increases endochondral bone growth and bone elongation, presumably by accelerating apoptosis of hypertrophic chondrocytes in the growth plate and/or subsequent chondrogenic matrix mineralization. Herein, we demonstrated the direct chondroregulatory action of PRL on proliferation, differentiation and apoptosis of chondrocytes in 3-dimensional micromass culture of mouse chondrogenic ATDC5 cell line. The results showed that ATDC5 cells expressed PRL receptor (PRLR) transcripts, and responded typically to PRL by downregulating PRLR expression. Exposure to a low PRL concentration of 10 ng/mL, comparable to the normal levels in male and non-pregnant female rats, increased chondrocyte viability, differentiation, proteoglycan accumulation, and mRNA expression of several chondrogenic differentiation markers, such as Sox9, ALP and Hspg2. In contrast, high PRL concentrations of ≥ 100 ng/mL, comparable to the levels in pregnancy or lactation, decreased chondrocyte viability by inducing apoptosis, with no effect on chondrogenic marker expression. It could be concluded that chondrocytes directly but differentially responded to non-pregnant and pregnant/lactating levels of PRL, thus suggesting the stimulatory effect of PRL on chondrogenesis in young growing individuals, and supporting the hypothesis of hypertrophic chondrocyte apoptosis in the growth plate of lactating rats."

So PRL does stimulate chondrogenesis in males and PRL in pregnant females may have only increased growth rate but not height.  Thus prolactin may work like other estrogen-like compounds where you need an optimal dosage and that optimal dosage is unclear.

How is HSPG2 involved in height?

Perlecan modulates VEGF signaling and is essential for vascularization in endochondral bone formation.

"Perlecan (Hspg2) is a heparan sulfate proteoglycan expressed in basement membranes and cartilage. Perlecan deficiency (Hspg2(-/-)) in mice and humans causes lethal chondrodysplasia, which indicates that perlecan is essential for cartilage development. However, the function of perlecan in endochondral ossification is not clear. Here, we report the critical role of perlecan in VEGF signaling and angiogenesis in growth plate formation. The Hspg2(-/-) growth plate was significantly wider but shorter due to severely impaired endochondral bone formation. Hypertrophic chondrocytes were differentiated in Hspg2(-/-) growth plates; however, removal of the hypertrophic matrix and calcified cartilage was inhibited. Although the expression of MMP-13, CTGF, and VEGFA was significantly upregulated in Hspg2(-/-) growth plates, vascular invasion into the hypertrophic zone was impaired, which resulted in an almost complete lack of bone marrow and trabecular bone. We demonstrated that cartilage perlecan promoted activation of VEGF/VEGFR by binding to the VEGFR of endothelial cells. Expression of the perlecan transgene specific to the cartilage of Hspg2(-/-) mice rescued their perinatal lethality and growth plate abnormalities, and vascularization into the growth plate was restored, indicating that perlecan in the growth plate, not in endothelial cells, is critical in this process. These results suggest that perlecan in cartilage is required for activating VEGFR signaling of endothelial cells for vascular invasion and for osteoblast migration into the growth plate."

"Perlecan binds basement membrane components, such as laminins[lama4, lamc2, and lamc3 are upregulated by LSJL] and collagen IV[Col4A1 and Col4A2 are upregulated by LSJL], providing scaffolding for cells"

"perlecan promoted VEGFR2 phosphorylation"

"perlecan provides the strength and rigidity of the hypertrophic matrix structure by interacting with matrix molecules for proper growth plate development"

"Conditional VEGFA knockout in mice specific in chondrocytes using Col2a1Cre displayed an expansion of the hypertrophic zone, delayed vascular invasion, and impaired endochondral ossification "

"Forced expression of Runx2 in hypertrophic chondrocytes using the Col10a1 promoter reduced VEGFA expression and resulted in impaired cartilage matrix remodeling and an almost complete lack of bone marrow due to the inhibition of vascular invasion into hypertrophic cartilage"

It may be worth testing your prolactin levels and seeing if they're low or high.  If they are it may affect your ability to gain height.

There are prolactin boosters: Gozombas, Maximum International, 60 Tablets, 12 bottles, NEW PACKAGING!!!.  Although side effects for men are unclear and optimal dosing of prolactin for height gain/stimulating chondrogenesis is unclear as well.  Also the compound can contain other supplements that may have unclear effects on height.

Growing out of a caste - reproduction and the making of the queen mole-rat

"Naked mole-rats have a eusocial colony structure consisting of non-reproductive workers and a reproductively active caste where a single, dominant queen and 1-3 males produce all of the offspring. Well-established queens have elongated bodies that characterize their caste. Worker females retain the ability to transform into queens, however the trigger and time course for this physical transformation remain a mystery. Here, we show a direct link between periods of pregnancy and vertebral lengthening in nascent queens. Adult female mole-rats were paired with a male and radiographed weekly for two and a half years to track the growth of the lumbar vertebrae as the mole-rats became sexually mature and experienced pregnancies. The lumbar vertebrae of breeding females grew at an increased rate during each pregnancy but growth rates returned to normal between pregnancies and during extended periods without reproduction. The rate of lumbar lengthening was reduced to normal rates in older, established queens experiencing pregnancies. Our results imply that the length of a new queen mole-rat is proportional to the number of pregnancies experienced and suggest that hormones related to pregnancy may play the critical role in bone growth associated with caste transformation."

"growth is not uniform during the course of each pregnancy but instead appears to reach a maximum in the last few weeks of the 70-day gestation period."

"There is a 10-fold increase in growth rate during the pregnancy periods."

"lumbar expansion accommodates a larger reproductive tract"

What hormones produced are unique to mole rat?

Bromocriptine modulates the expression of PTHrP receptor, Indian hedgehog, and Runx2 proteins in the growth plate of lactating rats.

"In lactating rats, the endochondral bone growth is markedly enhanced, leading to the lengthening of long bone. This lactation-induced bone elongation could be abolished by a dopaminergic D2 receptor agonist{an agonist is an enhancer, so activation of the D2 receptor might reduce height} bromocriptine{So whatever bromocriptine does, the opposite may induce height growth unless the hormones have an equilibrium peak}, but how bromocriptine altered the expression of major chondroregulatory proteins in the growth plate cartilage was elusive. Here, we performed a quantitative immunohistochemical analysis to determine the expression of various peptides and transcription factors known to control the growth plate chondrocyte proliferation and differentiation [i.e., parathyroid hormone-related protein (PTHrP), PTHrP receptor, Indian hedgehog (Ihh), and runt-related transcription factor 2 (Runx2)], in bromocriptine-treated lactating rats. Bromocriptine markedly increased Ihh expression in hypertrophic chondrocytes during early and mid-lactation, while the expression of PTHrP receptor, but not its ligand PTHrP, was upregulated in the proliferative and hypertrophic zones during mid and late lactation. In contrast, the expression of Runx2, an important transcription factor for chondrocyte differentiation, was suppressed in the hypertrophic chondrocytes of bromocriptine-treated rats{the surpression of Runx2 is most likely to play a role in repression of longitudinal bone growth}. In conclusion, bromocriptine increased Ihh and PTHrP receptor expressions and decreased Runx2 expression, which might, in turn, enhance chondrocyte proliferation and delay chondrocyte hypertrophy, thereby slowing down endochondral bone growth."

Bromocriptine surpresses prolactin release.

"an increase in PTHrP receptor was correlated with an increased cell proliferation marker, cyclin D1, in the tibial growth plate of calcitriol-treated renal failure rats"

"The protein kinase A (PKA) pathway might mediate the downregulation of Runx2"


  1. nuff said, keep it normal.

  2. you talk of estrogen increasing height thats bshit estrogen does more harm than good in my opinion testostorone is the dominant sex hormone anabolically and androgenically and these two compete against each other estrogen induces cortisol which is the enemy for all development in the human body estrogen best left alone really controlled and minimised with chrysin now that is something that could have serious potential for increasing height .

  3. yes on 1 hand estrogen may have some height increase potential but if you promote this against testostorone you will always end up smaller and weaker than the super strong athlete with the sky high testostorone levels.Chrysin might not be effective as first thought but the theory of inhibiting aromatose is on the right tracks.

  4. my final point equilibrium is this really superior to high testostorone for height increase i am dubious about that equilibrium is average my opinion ask yourself who is the stronger taller who is the more muscular developed low test/high estrogen , equilibrium est/test levels or is it the athlete with the high testostorone low estrogen my money is on the latter there is also a very significant direct relationship between size and strength.

  5. I strongly advise any male NOT to even consider taking prolatin boosters unless you want breasts. I don't know if those over-the-counter products actually increase prolactin levels but you will not get taller by using them anyway.