Tuesday, February 21, 2012

Grow Taller with xenoestrogens?

Diethylstilbestrol is a synthetic xenoestrogen that has been reported to be available in the human diet indirectly through diary products. It has been known to cause neurological and sexuality issues. However, it's possible that these side affects could potentially be avoided by keeping the dosage low so as only to get the length gaining effects.

Developmental Exposure to Low Dose Xenoestrogens Alters Femur Length and Tensile Strength in Adult Mice.

"Developmental exposure to high doses of the synthetic xenoestrogen diethylstilbestrol (DES) has been reported to alter femur length and strength in adult mice. In this study we investigated the effects of developmental exposure to low doses of DES, bisphenol A (BPA)[bisphenol A is used in plastics like water bottles so you may already be getting low doses of bisphenol A], or ethinyl estradiol[this is present in oral contraceptive pills and it is also present in the urine of those who take oral contraceptive pills] (EE(2)) on bone geometry and torsional strength. C57BL/6 mice were exposed to 0.1 µg/kg/day DES, 10 µg/kg/day BPA, 0.01, 0.1, or 1.0 µg/kg/day EE(2) or vehicle from Gestation Day 11 to Postnatal Day 12 via a mini-osmotic pump in the dam[so they were exposed at a very young age for a very short period of time]. Developmental xenoestrogen exposure altered femoral geometry and strength assessed in adulthood by µCT and torsional strength analysis, respectively. Low dose EE(2), DES or BPA increased adult femur length. Exposure to the highest dose of EE(2) did not alter femur length, resulting in a non-monotonic dose response. Exposure to EE(2) and DES, but not BPA, decreased tensile strength. The combined effect of increased femur length and decreased tensile strength resulted in a trend toward decreased torsional ultimate strength and energy to failure. Taken together, these results suggest that exposure to developmental exposure to environmentally-relevant levels of xenoestrogens may negatively impact bone length and strength in adulthood."

All three of these compounds are present in common place sources like drinking water.  Thus, it may be possible to alter adult bone length by manipulating the consumption of potential sources of these compounds.  Estrogen operates best on height growth at an equilibrium quantity so we want to make sure that our estrogen is at just the right amount.

"Developmental exposure to 0.01 and 0.1 EE2 increased femur length 2.6% and 2.4% (t30 = -2.8, p = 0.008 and t25 = -2.17, p = 0.040, respectively)"

"Developmental DES exposure increased femur length 2.0% (t12 = -2.06, p = 0.031) in females and tended to increase femur length 1.3% (t9 = -1.03, p = 0.166) in males. Developmental BPA exposure, on the other hand, increased femur length 2.3% (t13 = -1.96, p = 0.036) in males and tended to increase femur length 1.0% in females (t14 = -0.84, p = 0.208) (Figure 2)."<-DES and BPA did not fail to increase femur length at the highest dose like EE2 so EE2 is the one you want to watch out for[EE2 is present in adult contraceptives]

However, "developmental exposure to 100 µg/kg DES, which is 1000 times greater than the dose used in the current study, resulted in shorter femurs that had increased total bone area and calcium content. These changes were the result of increased osteoblast activity as determined by an increased mineral apposition rate  and decreased resorption rate due to a decrease in the number of osteoclast cells"<-Extremely high levels of DES does reduce height growth.

Multigenerational exposure to ethinyl estradiol affects bone geometry, but not bone mineraldensity in rats.

"In F3 males, treatment with 10 ppb EE increased femur length compared with control, 2 ppb, or 50 ppb EE as a main effect."

"Sprague–Dawley rats for the parental (F0) generation were obtained from the NCTR breeding colony at weaning and housed two per cage until allocated to dose groups, after which time they were singly housed in polycarbonate cages with hardwood chip bedding. Ethinyl estradiol (EE, > 99% pure, Sigma, St. Louis, MO) was administered at doses of 0, 2, 10, and 50 ppb in Purina 5K96 chow (PMI Nutrition International, Richmond, IN), which is a modified NIH-31 diet that meets the nutritional specifications of NIH-31 but has had soy and alfalfa, major sources of phytoestrogens, removed and replaced by casein. These doses provided approximately 0, 0.1, 0.7, and 4 μg EE per kg body weight per day in males and 0, 0.2, 1, and 6 μg EE per kg body weight per day in females, and were selected such that the lower doses would approximate human oral contraceptive exposures, and the high dose would produce effects without overt toxicity"

"For the multigeneration reproductive study, males and females of the original parental generation (F0) were placed on a 5K96 diet at weaning and dosed feed was administered starting on postnatal day (PND) 42, approximately 1 month before breeding, and were maintained on dosed feed until termination at PND 140. For breeding, one male was cohabited with one female of the same treatment group for 14 days or until a vaginal plug was detected. Subsequent generations (F1–F4) were similarly bred. The F1 and F2 generations were exposed to the test compound administered in the diet continuously from conception through termination at PND 140. The F3 generation was removed from dose at weaning (PND 21)"<-So, estrogen increased height as long as it was below post natal day 21.  Perhaps, after day 21, the natural levels of estrogen increase so additional estrogen just puts it above equilibrium quantities of estrogen.

So what we can take from this is that when you're really young your levels of estrogen are too low to maximize height growth.  Then when development occurs estrogen levels become too high thus you likely want to lower these levels.

So to maximize height growth:

Baby/Toddler->Raise Estrogen to reach Equilibrium.
After->Lower Estrogen Levels.

The problem is finding the right levels.  Babies may not get the xenoestrogens they need to be tall from drinking water so other sources may be needed.

At some point, estrogen levels get too high for height growth so they have to be knocked down a little.


  1. for me the largest athletes like strongmen have next to no estrogen and testostorone is the dominating hormone which might partly explain their size men are much bigger generally and women are much smaller a good male is generally bigger from birth and the difference only becomes greater when testostorone kicks in

  2. doesnt estrogen causes apoptosis?
    the estrogen sub receptors?

  3. i have been consistently trying to gain height various methods for years and nothing finally today my measurements are 0.6 cm taller so im confident i have made a significant breakthrough through my studies progress and methodology time will tell if this is proof that adult height gain is a practical possibility .dav82

  4. my total gain adult height is 1cm increase overall

  5. If you want to grow taller, just knock testosterone and oestrogen back into place. That's it. Chondrogenesis will ensue with the slightest GH stimulation. But NOOOO! You guys want to do things differently. Good luck. Btw, letrozole and Anti-androgens are very cheap. As for GH, GHRP2 + MOD grf for a few weeks will be enough.

  6. dont androgens cause cell proliferation?
    estrogen needed for fgfs for stem cell proliferation