Estrogen Insensitivity Syndrome And The Use Of Gene Therapy To Increase Height

Me: When I was reading through the PubMed articles yesterday there was a passage in one of the papers that seemed to provide an insight on an idea which I had for a long time. It deals with the possibility of decreasing either the number of function of the estrogen receptors one has in one’s growth plates.

The idea is that there have been three documented cases written up in articles which have been submitted to PubMed looking at males who have one specific gene mutation which have caused them to be insensitive to the effects of estrogen. They would go on to have unclosed epiphyseal plates even past into their 30s. two of them was recorded around the 6′ 8″ mark and they seemed to have normal body functions except one big issue, which is infertility. The medical experts even got them to use a type of estrogen/ cortisol mixture to help seal their growth plates and remove most of the other side effects from the gene mutation.

The idea that I had was that it might be possible to use vectors to target that specific cell area when the child still has their growth plates open, right after they have just started to hit the puberty growth spurt but also start developing their body into adult maturity. The sperm of the child (assuming the subject is male) can be collected for later while the treatment causes their growth plates to be open and make them as tall as desired. ONce they reach adulthood and have decided to stop growing, they can go back to the doctor for estrogen treatment to close the growth plates. Their problem on infertility can be solved by using the old sperm samples they have stored up for in vitro fertilization. This can also help people avoid unplanned pregnancies. 

It will be a good idea to read up on the wikipedia article on what exactly is estrogen insensitivity syndrome.

Estrogen insensitivity syndrome

From Wikipedia, (HERE)

The estrogen insensitivity syndrome (EIS) or estrogen resistance is a form of congenital estrogen deficiency[1] caused by a defective estrogen receptor(ER). Thus, estrogens cannot be recognized and initiate their biological action.[2]

In humans, the condition is very rare and only one case has been described. A reported male with EIS was tall as estrogens were unable to act to close theepiphyseal line, at risk for osteoporosis, and sterile (suggesting that in humans estrogens are necessary for reproduction).[3]

ERKO mice

Estrogen insensitivity syndrome of can be experimentally induced in animals, typically mice, by knocking out the estrogen receptor. In so-called ERKO mice different estrogens receptors can be disabled allowing to study the role of such receptors.[4] ERKO mice show development of the respective female or male reproductive systems, and male and female alpha ERKO mice are infertile, beta ERKO males are fertile while females are subfertile, male and female double alpha and beta ERKO mice are sterile. The hypoplastic uterus does not respond to exogenous stimulation by estrogens. Males are infertile with atrophy in the testes. Bones age is delayed and bones are more brittle. Variations in these patterns can be achieved by selectively disabling the alpha or beta ERs.

AIS

In contrast to EIS, the androgen insensitivity syndrome (AIS) where the androgen receptor is defective is relatively common. This can be explained by the genetics of each syndrome. AIS is a X-linked recessive condition and thus carried over into future generations. EIS is not compatible with reproduction, thus each occurrence in humans would have to be a de-novo mutation and is not transmitted to offspring.

Congenital estrogen deficiency can also be caused by a defect in the aromatizing enzyme.

Tyler: Here’s a study I found that might be related.

The estrogen receptor antagonist ICI 182,780 can act both as an agonist and an inverse agonist when estrogen receptor α AF-2 is modified

“Estrogen exerts important effects in the skeleton, which are primarily mediated via estrogen receptor (ER)α, which stimulates target gene transcription through two activation functions (AFs), AF-1 in the N-terminal and AF-2 in the ligand-binding domain. Previous studies demonstrate that ERα ligands might act as agonists, partial agonists, or antagonists. ERα antagonist ICI 182,780 (ICI) acts in a tissue-dependent manner in mice lacking ERαAF-2, resulting in no effect, agonistic activity, or inverse agonistic activity. Importantly, ICI exerted a pronounced inverse agonistic activity in the growth plate of mice lacking ERαAF-2. We propose that ERα lacking AF-2 is constitutively active in the absence of ligand in the growth plate, enabling ICI to act as an inverse agonist. ”

So can ICI increase height?

“The bone-sparing effect of estrogen is primarily mediated via estrogen receptor (ER) α, which stimulates target gene transcription through two activation functions (AFs), AF-1 in the N-terminal and AF-2 in the ligand-binding domain. Ovariectomized wild-type mice and mice with mutations in the ERα AF-2 (ERαAF-20) were treated with ICI, estradiol, or vehicle for 3 wk. Estradiol increased the trabecular and cortical bone mass as well as the uterine weight, whereas it reduced fat mass, thymus weight, and the growth plate height in wild-type but not in ERαAF-20 mice. Although ICI had no effect in wild-type mice, it exerted tissue-specific effects in ERαAF-20 mice. It acted as an ERα agonist on trabecular bone mass and uterine weight, whereas no effect was seen on cortical bone mass, fat mass, or thymus weight. Surprisingly, a pronounced inverse agonistic activity was seen on the growth plate height, resulting in enhanced longitudinal bone growth. ERα lacking AF-2 is constitutively active in the absence of ligand in the growth plate, enabling ICI to act as an inverse agonist. ”

So if you’re estrogen insensitive such that you lack AF-2 ICI(an ERalpha agonsit) can help you grow taller.

“the ICI–ERα complex is unstable, resulting in accelerated degradation of the ERα protein”

“ICI is used as an adjuvant endocrine therapy to treat ER-positive metastatic breast cancers in postmenopausal women with disease progression following the first line of antiestrogen therapy, as tamoxifen-as well as aromatase-resistant tumors might remain sensitive to ICI treatment”

“E2 reduced both the thymus weight (–73%) and the bone-marrow cellularity (–52%) in WT mice,whereas no effect of ICI was observed on these two parameters in WT or ERαAF-20 mice”

“The increase in growth plate height by ICI in the ovx ERαAF-20 mice resulted in an increased tibia and femur length (+4.2% and +2.8%, respectively) and was specific to the appendicular
skeleton, as neither the crown-rump length (axial skeleton) nor the total body weight was altered”

The increase in height by ICI was not due to altered IGF-1 levels.

ICI resulted in a slight, not statistically significant increase in femur and tibia length in wild type mice.

But some Estrogen receptors are constitutively active even when not binding so even if you don’t have estrogen, the estrogen receptors still decrease your height thus highlighting the purpose of inhibiting the estrogen receptors themselves with something like ICI.

Increase Height And Grow Taller Using Vertebroplasty And Percutaneous Vertebroplasty

There is another surgical type called Vertebroplasty which I just discovered done by orthopedic surgeons which seems to lead to increased height. It seems that the Vertebroplasty method has been compared already to the kyphoplasty method and the height increases have been compared with the results showing that kyphoplasty results in more height increase of 5 mm as compare to the 2-3 mm increase shown by people who go through vertebroplasty. Overall, this is a completely new development for this website and I will need to do further research to see what are the clinical and current possibilities of using vertebroplasty and/or kyphoplasty for possible future cosmetic reasons to increase in height.
The issue with vertebroplasty and kyphoplasty is that the two are similar in principle, with a type of cement block placed in the vertebrate at an angle to realign the vertebrate to be straighter.

Increase in Vertebral Body Height after Vertebroplasty

Akio Hiwatashia, Toshio Moritania, Yuji Numaguchia and Per-Lennart Westessona+Author Affiliations

  • aFrom the Department of Diagnostic Radiology, University of Rochester Medical Center, Rochester, NY
  • Address reprint requests to Akio Hiwatashi, M.D., Department of Diagnostic Radiology, University of Rochester Medical Center, 601 Elmwood Ave, Box 648, Rochester, NY 14642-8648

Abstract

BACKGROUND AND PURPOSE: 

During clinical work, we have seen increases in vertebral body height associated with vertebroplasty, but our literature search revealed no reports as to how often and to what degree those increases occur. The purpose of this study was to document the frequency and degree of changes in vertebral body height after vertebroplasty.

METHODS: 

The heights of 85 vertebral bodies in 37 patients were measured before and after vertebroplasty. In addition, one adjacent vertebral body was measured in each patient as a control. Twenty-six patients had compression fractures in the thoracic spine, and 24 patients had compression fractures in the lumbar spine. Vertebroplasty was performed with a bilateral transpedicular approach by injecting polymethylmethacrylate, under biplane fluoroscopic control. Measurements were performed on preoperative MR images and on postoperative CT sagittal reformations. Anterior, central, and posterior vertebral body height measurements were obtained in the midsagittal plane.

RESULTS: 

The average increase in vertebral body height was 2.5 mm anteriorly, 2.7 mm centrally, and 1.4 mm posteriorly. Thirteen of 85 treated vertebrae remained unchanged. All control vertebral bodies also remained unchanged.

CONCLUSION: 

Vertebral body height often increases during vertebroplasty. The clinical significance of increasing vertebral body height is unknown.

Copyright © American Society of Neuroradiology

Significance of Dynamic Mobility in Restoring Vertebral Body Height in Vertebroplasty
  • Y.-J. Chena,c, H.-Y. Chenb, P.-P. Tsaib, D.-F. Loa, H.-T. Chena and H.-C. Hsua,c  – Author Affiliations
  • aDepartments of Orthopedic Surgery (Y.-J.C., D.-F.L., H.-T.C., H.-C.H.)
  • bRadiology (H.-Y.C., P.-P.T.), China Medical University Hospital, Taichung, Taiwan
  • cDepartment of Orthopedic Surgery, School of Medicine (Y.-J.C., H.-C.H.), China Medical University, Taichung, Taiwan.
  • Please address correspondence to Yen-Jen Chen, MD, Department of Orthopedic Surgery, China Medical University Hospital, No 2, Yuh-Der Rd, Taichung 404, Taiwan; e-mail: yenjenc.tw@yahoo.com.tw

Abstract

BACKGROUND AND PURPOSE:

Many authors have reported the increase in vertebral body height after vertebroplasty. However, McKiernan et al demonstrated dynamic mobility in patients who underwent vertebroplasty and concluded that any article that claims vertebral height restoration must control for the dynamic mobility of fractured vertebrae. The purpose of this study was to compare prevertebroplasty (supine cross-table with a bolster beneath) with postvertebroplasty vertebral body height to find out whether vertebroplasty itself really increases the vertebral height.

MATERIALS AND METHODS:

From July 2005 to July 2010, 102 consecutive patients with 132 VCFs underwent vertebroplasty at our institution. The indications for vertebroplasty were severe pain that was not responsive to medical treatment, and MR imaging−confirmed edematous lesions. Prevertebroplasty (supine cross-table with bolster beneath) lateral radiographs were compared with postvertebroplasty radiographs to evaluate the height change in vertebroplasty. Kyphotic angle and anterior vertebral body height were measured.

RESULTS:

The patients ranged in age from 62 to 90 years. There were 16 men and 86 women. The difference in the kyphotic angle between supine cross-table with bolster and postvertebroplasty was −0.49 ± 3.59° (range, −9°–16°), which was not statistically significant (P = 0.124). The difference in the anterior vertebral body height between supine cross-table with bolster and postvertebroplasty was 0.84 ± 3.01 mm (range, −7.91–8.81 mm), which was statistically significant (P = .002).

CONCLUSIONS:

The restoration of vertebral body height in vertebroplasty seems to be mostly due to the dynamic mobility of fractured vertebrae; vertebroplasty itself does not contribute much to the restoration of vertebral height.

SPINE

Kyphoplasty and Vertebroplasty Produce the Same Degree of Height Restoration

  • A. Hiwatashia,b, P.-L.A. Westessona, T. Yoshiurab, T. Noguchib, O. Togaob, K. Yamashitab, H. Kamanob and H. Hondab – Author Affiliations
  • aDivision of Diagnostic and Interventional Neuroradiology, Department of Imaging Sciences, University of Rochester Medical Center, Rochester, NY
  • bDepartment of Clinical Radiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
  • Please address correspondence to Akio Hiwatashi, MD, Department of Clinical Radiology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; e-mail: hiwatasi@radiol.med.kyushu-u.ac.jp

Abstract

BACKGROUND AND PURPOSE:

There are few comparative studies regarding morphologic changes after kyphoplasty and vertebroplasty. The purpose of this study was to compare restoration of vertebral body height and wedge angle and cement leakage with kyphoplasty and vertebroplasty in osteoporotic compression fractures.

MATERIALS AND METHODS:

Forty patients (57 vertebrae) were treated with kyphoplasty, and 66 patients (124 vertebrae) were treated with vertebroplasty. Cement leakage into the disk space and paravertebral soft tissues or veins was analyzed on immediate postoperative CT scans. The height and wedge angle were measured before and after treatment and analyzed with the Mann-Whitney U test and χ2 test.

RESULTS:

Kyphoplasty and vertebroplasty both improved vertebral body height and the wedge angles (P < .05). However, these differences were not statistically significant when the 2 techniques were compared (P > .05). There were 18% of the kyphoplasty group and 49% of the vertebroplasty group that showed cement leakage into the paravertebral soft tissues or veins (P < .01). Cement leakage into the disk space occurred in 12% of the kyphoplasty group and in 25% of the vertebroplasty group (P < .01). However, no complications related to cement leakage were noted.

CONCLUSIONS:

Both kyphoplasty and vertebroplasty achieved the same degree of height restoration and improvement of the wedge angle. Kyphoplasty resulted in less cement leakage into the disk space and paravertebral soft tissues or veins than vertebroplasty.

Copyright © American Society of Neuroradiology

Kyphoplasty versus Vertebroplasty to Increase Vertebral Body Height: A Cadaveric Study

  • Akio Hiwatashi, MD, Ravinder Sidhu, MD, Ryan K. Lee, MD, Ramon R. deGuzman, MD, Diane T. Piekut, PhD and Per-Lennart A. Westesson, MD, PhD, DDS
  • 1From the Departments of Radiology (A.H., R.S., R.K.L., R.R.d., P.L.A.W.) and Neurobiology and Anatomy (D.T.P.), University of Rochester Medical Center, 601 Elmwood Ave, Box 648, Rochester, NY 14642-8648. Received September 26, 2004; revision requested December 2; revision received December 21; accepted January 21, 2005.
  • Address correspondence to A.H. (e-mail: Akio_Hiwatashi@urmc.rochester.edu).

Abstract

PURPOSE:

To prospectively compare the vertebral height restoration achieved with kyphoplasty and vertebroplasty in fresh cadavers by using multi–detector row computed tomography (CT).

MATERIALS AND METHODS:

Institutional review board approval was not required because the donors had registered in and consented to an anatomic gift program prior to their death. Thirty-seven vertebrae were harvested from four donated cadavers of elderly female individuals (mean age, 82 years; age range at death, 73–87 years). The vertebrae were dissected free of the surrounding muscles and imaged with multi–detector row CT. Compression fractures were induced, and the vertebrae were again imaged. The vertebrae were randomized to be treated with kyphoplasty (n = 19) or vertebroplasty (n = 18) and were then imaged at multi–detector row CT. The anterior, central, and posterior vertebral body heights and wedge angles were measured in the midsagittal plane of the reformatted images. The amount of cement injected was determined by weighing the vertebrae before and after treatment. The statistical significance of changes in vertebral body height, wedge angle, and weight with the two treatment techniques was evaluated with the independent t test or Mann-Whitney U test.

RESULTS:

The increase in vertebral height was greater with kyphoplasty than with vertebroplasty (5.1 mm vs 2.3 mm, respectively; P < .05). The original vertebral height was restored in 93% of vertebrae with kyphoplasty and in 82% with vertebroplasty (P < .05). There was a greater decrease in wedge angle with kyphoplasty than with vertebroplasty (3.1° vs 1.6°, respectively); however, this difference was not significant (P > .05). There was no significant difference in the amount of cement injected with kyphoplasty and vertebroplasty (P > .05).

CONCLUSION:

Kyphoplasty increased vertebral body height more than vertebroplasty in this model of acutely created fractures in fresh cadaver specimens.

© RSNA, 2005

SPINE

Kyphosis Correction and Height Restoration Effects of Percutaneous Vertebroplasty

  • Michael Mu Huo Tenga, Chao-Jung Weia, Liang-Chen Weia, Chao-Bao Luoa, Jiing-Feng Lirnga, Feng-Chi Changa, Chien-Lin Liub and Cheng-Yen Changa – Author Affiliations
  • aDepartment of Radiology, Taipei Veterans General Hospital and National Yang-Ming University, Taiwan
  • bDepartment of Surgery, Taipei Veterans General Hospital and National Yang-Ming University, Taiwan
  • Address reprint requests to Dr Michael Mu Huo Teng, Department of Radiology, Taipei Veterans General Hospital, 201, Sec 2, Shih-Pai Road, Peitou District, Taipei 11217, Taiwan

Abstract

BACKGROUND AND PURPOSE: 

Percutaneous vertebroplasty is known for its pain-relieving effect. Our purpose was to evaluate its effect on the kyphosis angle, wedge angle, and height of the fractured vertebral body.

METHODS: 

We reviewed digital radiographs of 73 vertebral bodies in 53 patients before and after vertebroplasty. We measured the spinal kyphosis angle and the wedge angle of the fractured vertebral body. Ratios of the height of the anterior border, center, and posterior borders of the collapsed vertebra to the height at the posterior border of an adjacent normal vertebral body were measured. Gain from vertebroplasty and the restoration percentage (gain divided by loss) were calculated for each parameter.

RESULTS:

The kyphosis angle, wedge angle, anterior height, center height, and posterior height significantly improved after vertebroplasty. The mean reduction in the kyphosis angle was 4.3°, and the wedge-angle reduction was 7.4°. The mean wedge-angle reduction in fractured vertebral bodies containing gas was 10.2°. Restoration percentages for the kyphosis angle and wedge angle were 19% and 44%, respectively. Gain in the height of the fractured vertebral bodies was 16.7% for the anterior border, 14% for the center, and 7% for the posterior border. Restoration percentages for the height of the vertebral body were 29% for the anterior border and 27% for the center.

CONCLUSION: 

Vertebroplasty increases the height of the fractured vertebra and reduces the wedge and kyphosis angles. These effects are most remarkable in fractured vertebra containing gas.

Copyright © American Society of Neuroradiology

Increase Height By Using Balloon Kyphoplasty

It seems that there are now even more ways and possibilities to increase height, and this way is through surgical implantations into the vertebrate bones which has been traditionally been used to heal vertebrate and disk ruptures which cause chronic back pain. So far this type of surgery is only done for people who are old and need the surgery for medical reasons to elevate pain. The amount of extra height they seem to get is what would be called lost height from age degeneration and it is only about a few millimeters.

Journal of Neurosurgery: Spine, January 2003 / Vol. 98 / No. 1 / Pages 36-42

CLINICAL ARTICLES

Balloon kyphoplasty: one-year outcomes in vertebral body height restoration, chronic pain, and activity levels

      Jon T. Ledlie, M.D., and Mark Renfro, M.D.Tyler Neurosurgical Associates, Tyler, Texas

Abbreviations used in this paper:  AP = anteroposterior; VAS = Visual Analog Scale; VB = vertebral body; VCF = vertebral compression fracture.

Address reprint requests to: Jon T. Ledlie, M.D., Tyler Neurosurgical Associates, P.A., 700 Olympic Plaza, Suite 850, Tyler, TX 75701. email: jledlie@tylerneuro.com.

Abstract

Object. The authors assessed the safety of balloon kyphoplasty in the reduction and repair of osteopenic vertebral compression fractures and report functional outcomes (back pain and activity levels) in the first 96 patients (with 133 fractures) at their institution. Additionally they provide radiographic outcomes in the first 26 patients (41 fractures) treated and followed for 1 year.

Methods. The authors conducted a retrospective chart review of functional outcomes and evaluated radiographs obtained at 1 week, 1 month, 3 months, 6 months, and 1 year postoperatively.

Conclusions. Balloon kyphoplasty safely increases vertebral body height, decreases chronic back pain, and quickly returns geriatric patients to higher activity levels, leading to increased independence and quality of life.

Effects of Pulsed Electromagnetic Fields on Human Articular Chondrocyte Proliferation

Me: The study that was done and written down below seem to suggest that the PEMF technology seem to be able to work only on chondrocyte cultures that are of low density for a long time, not high density which is shorter. This suggest that the proliferation of chondrocytes and the ability of using some form of external stimuli to make it divide and multiply more is more dependent on the availability of growth factors and the environmental constrictions. The implications means that if we ever plan to use electrical and ultrasonic technology to increase chondrocytes it would be a good idea to first add the needed extra growth factors, whatever they may be, into the extracellular cartilage matrix before we start using the PEMF and/or LIPUS devices. 
Effects of Pulsed Electromagnetic Fields on Human Articular Chondrocyte Proliferation
2001, Vol. 42, No. 4 , Pages 269-279

Monica De Mattei1, Angelo Caruso1†, Furio Pezzetti1, Agnese Pellati1, Giordano Stabellini3, Vincenzo Sollazzo2 and Gian Carlo Traina2

1Dipartimento di Morfologia ed Embriologia, Università Statute, 44100, Ferrara, Italy
2Dipartimento di Scienze Biomediche e Terapie Avanzate, Università di Ferrara, 44100, Ferrara, Italy
3Istituto di Anatomic Umana Normale, Università Statute, 20133, Milano, Italy
†Correspondence: Angelo Caruso, Dipartimento di Morfologia ed Embriologia, University di Ferrara, via Fossato di Mortara 64, 44100, Ferrara, Italy+39+532-29153939-0532-291533 g4f@dns.unife.it 

Low-energy, low-frequency pulsed electromagnetic fields (PEMFs) can induce cell proliferation in several cell culture models. In this work we analysed the proliferative response of human articular chondrocytes, cultured in medium containing 10% FBS, following prolonged exposure to PEMFs (75 Hz, 2.3 mT), currently used in the treatment of some orthopaedic pathologies. In particular, we investigated the dependence of the proliferative effects on the cell density, the availability of growth factors and the exposure lengths. We observed that PEMFs can induce cell proliferation of low density chondrocyte cultures for a long time (6 days), when fresh serum is added again in the culture medium. In the same conditions, in high density cultures, the PEMF-induced increase in cell proliferation was observed only in the first three days of exposure. The data presented in this study show that the availability of growth factors and the environmental constrictions strongly condition the cellular proliferative response to PEMFs.

The effects of pulsed low-intensity ultrasound on chondrocyte viability, proliferation, gene expression and matrix production

Me: This shows one of the studies done testing the possibility of using the LIPUS technology to increase the chondrocyte proliferation. In this study though it is called PLIUS, not LIPUS as we have called it but they are the same thing. Again I note that this study is critical in showing whether using LIPUS is even worth looking deeper into. From only being able to get to the abstract, my opinion on the technology is mixed. PLIUS was shown to inhibit the expression of type X collagen. It seems that using the lower level of PLIUS intensity of 2 mW/cm^2 seem to inhibit chondrocyte hypertrophy which is something that we desire since chondrocyte hypertrophy means that they are no longer in the zone to proliferate which is something we don’t want. We want to hold off on any type of Collagen Type X production as much as possible to increase the number of chondrocytes available to be in the hypertrophy zone to increase in size. 
Original contribution

The effects of pulsed low-intensity ultrasound on chondrocyteviability, proliferation, gene expression and matrix production

  • Zi-Jun Zhang*, James Huckle†, Clair A Francomano*, Richard G.S Spencer*,
  • * National Institutes of Health, National Institute on Aging, Baltimore, MD, USA
  • † Smith and Nephew Group Research Centre, York Science Park, Heslington, York, UK
  • http://dx.doi.org/10.1016/j.ultrasmedbio.2003.08.011, How to Cite or Link Using DOI
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Abstract

This study was designed to examine the effects of pulsed low-intensity ultrasound (PLIUS) on chondrocyteviability, proliferation, matrix production and gene expression. Chondrocytes were isolated from the distal part of the sternum of 16-day-old chick embryos and cultured in alginate beads. PLIUS at 2 mW/cm2 (group PLIUS2) and 30 mW/cm2 (group PLIUS30) was applied to chondrocytes for a single 20-min treatment. A control group was treated without PLIUS. The viability of chondrocytes was not affected by exposure to PLIUS. PLIUS influenced chondrocyte proliferation in an intensity-dependent manner. By day 7 after application of PLIUS, the gene expression and synthesis of aggrecan was the same as in the controls. At this same time point, the expression and synthesis of type II collagen was not different between the controls and PLIUS30, but was increased in PLIUS2. PLIUS was shown to inhibit the expression of type X collagen. This inhibition of chondrocyte hypertrophy may prove to be significant in the management of cartilage degeneration. (E-mail: spencer@helix.nih.gov)

Dietary Lactose Improves Endochondral Growth and Bone Development And Mineralization

Me: It would seem that from just reading this neat little abstract that the common food product of milk may actually be causing kids to grow taller from not just increased Vitamin D and Calcium intake and density. It seems that the Lactose sugar themselves also help with endochondral growth. I am even willing to make the daring hypothesis that it could be possible that lactose could be the real ingredient in milk that causes kids to grow and maybe it is not from the Vitamin D and Calcium, since there have been many studies done that refuted and confirmed the age old thinking that Milk will increase a kids growing rate and height from the Calcium and Vitamin D intake. However, it is important to know that there is more in milk that can cause growth and height increase than what was previously believed to be in it.
J Nutr. 1988 Jan;118(1):72-7.

Dietary lactose improves endochondral growth and bone development and mineralization in rats fed a vitamin D-deficient diet.

Miller SC, Miller MA, Omura TH.

Source

Division of Radiobiology, School of Medicine, University of Utah, Salt Lake City 84112.

Abstract

Lactose promotes the intestinal absorption of calcium independent of the vitamin D endocrine system. The purpose of this study was to determine the effect of lactose supplementation on endochondral bone growth, bone development and mineralization in weanling rats fed a vitamin D-deficient diet. Rat pups were weaned from vitamin D-deficient dams and fed a vitamin D-deficient diet containing sucrose as the primary carbohydrate source or a similar diet but containing 20% lactose. After 4 wk, body weights, serum calcium levels and endochondral bone elongation rates in the lactose-fed animals were higher than in rats fed the sucrose diet. In addition, bone weights, bone calcium content, percent bone ash of bone dry weight, percent metaphyseal osseous tissues and bone osteoid content in the lactose-fed rats were different from those in the rats fed the sucrose diet. In all cases the changes in osseous tissues that were observed in the animals fed the lactose-supplemented diet were toward normal values as observed in age-matched animals fed a vitamin D-replete diet. The improvements in bone growth and development due to lactose supplementation occurred independent of the vitamin D endocrine system and are likely the result of improved calcium absorption in the intestine.

PMID: 3335941      [PubMed – indexed for MEDLINE]