Tuesday, February 28, 2012

Does Bone Mineral Density affect Height?

Previously, it was though that bone density did not affect height and could only lower height by bone deformities.  However, this study suggests otherwise:

Usefulness of estimated height loss for detection of osteoporosis in women.

"Most of us are the tallest at around 30-35 years old because of the peak bone mass at that time"<-This suggests that higher bone density increases height.  If the authors of the study didn't believe that then they would have suggested that peak height is at age 25 or so.

"A lower bone mineral density had a greater influence on height loss in the femur than in the lumbar vertebrae"<-this is surprising as you'd expect it to have more of an impact in the vertebrae as weak vertebrae would result in poorer posture and thus lower height.  This leads credence to the theory that bone density has more impact on height than just bone strength influencing posture.  Bone Density may have a direct affect on the length of the bones.

The scientist who made these assertations is Yeoum SG.

Longitudinal change in height of men and women: implications for interpretation of the body mass index: the Baltimore Longitudinal Study of Aging.

"Among both men and women, cross-sectional height decreased with age"<-Including between 20 and 35.  However, the change in height between 20 and 40 is very small so it could be related to measurement or study error.  Other data in the study suggest an increasing slope in height between the ages of 17-30(Figure 2).

Increased physical activity is associated with enhanced development of peak bone mass in men: A five year longitudinal study.

"Peak bone mass is believed to be achieved before the end of the third decade in life, depending on 
bone site"<-So before age 39.

"Previous intervention studies in children, adolescents and young adults have reported that physical activity interventions result in increased bone mineral content (BMC), areal bone mineral density (BMD) and cortical bone size."<-So if exercise increases BMC and BMC increases height then exercise will increase height.

"For each hour of increased physical activity, aBMD of the lumbar spine and BMC of 
the total body increased with 0.005 g/cm-squared and 5.4 g, respectively, while cortical cross sectional 
area and total cross sectional area of the tibia increased with 0.36 mm-squared and 0.49 mm-squared,
respectively, between the baseline and follow-up visits"

In the study, the individuals who exercised 4 or more hours per week but hardly exercised at all went from an average of 182.4 height to 183 height.  With the mean age being about 18.9 at the start so natural growth cannot be excluded.  Those individuals who exercised before the study and stopped still increased average height from 181.3 to 181.8.  The individuals who exercised before the study and continued throughout the study had the exact same height growth of 181.3 to 181.8.

So perhaps the people who stopped the exercise maintained the benefits of 0.1cm in height.  The sedentary individuals who stayed sedentary went from 181.7 to 182.2.

Thus, exercise may add at least 0.1cm as individuals who added exercise grew 0.6cm over individuals in all other groups who only grew 0.5 cm.  Additional exercise may add additional height.  A confounding variable however is that the sedentary individuals who added exercise were taking 100mg more calcium then everyone else.  But Calcium relates to Bone Mineral Content so it still shows a trend of Bone Mineral Content being able to increase height.

The BMC increased by 5.4g for each hour of exercise between baseline and follow up visits.  The grew that grew the most exercised for 6.2 hours.  However, the group that started exercising for over four hours a week and ended exercising over four hours exercised for 7.9 hours and gained less height.

Here's another study that shows height loss in adults, unfortunately I could not find the full study for this:

Longitudinal shrinkage in lower legs: "negative growth" in healthy late-adolescent males.

"Forty-one healthy male subjects, aged 15.7 to 19.8 years participated in a study on lower leg length (LLL) growth, body height and weight increments. All subjects were measured and weighed at weekly intervals over a period of one year. Body height was determined by an anthropometer, body weight by conventional scales, and LLL was measured by a hand-held knemometer. The state of maturity of the proximal tibial epiphyses was determined by magnetic resonance imaging (MRI). Skeletal maturity was independently assessed by two radiologists. The growth plates were categorized as being open (category I), centrally but not completely fused (category II), or completely fused (category III).
Our findings demonstrate that in these adolescents, final tibial growth is characterized by longitudinal shrinkage. As shown in the MRI, when the proximal tibial growth plates have fused (i.e., at an age when lower leg growth is commonly believed to have completed), the lower leg of healthy adolescent males begins to shrink with a negative growth rate of -2.4 (SD 2.1) mm/year.
We assume that the final period of growth includes small reductions in bone length, possibly due to stabilization and rearrangements in the formerly growing cartilaginous tissues[so essentially bone modeling reduces height?]."

The height reduction with age is not likely related to something that varies like bone modeling but rather something like bone mineral content which decreases linearly with age.

There is not likely a linear relationship between BMC and height but rather a threshold value of BMC to maximize height.  Supramaximal values of BMC will not increase height past a further point.


  1. how could bone mineral content not effect height? thats a bit of a unscientific assumption to make, i would hazard a guess to think increases in mineral content would increase ossification faster/make it harder for stem cells to thrive in the growthplate. more minerals = mineral overflow, the minerals got to go somehwere, it might speed up mineraliztion of the cartilage matrix , growth plates/ well im just putting this out for some thoughts.

  2. well two scenarios i see with more minerals: more mineralization = it stops
    height in growth plates or it increases height like cnp without growthplates, using osteoblast

  3. hey tyler, ive been thinking a lot about things, so much that i couldn't sleep from a restless mind, so i was wanting to ask if you could (let this be a reminder at least) that when you have the time-hours/days for some paper searching and reading, could focus onto bone mineralization and demineralization and in particular epiphyseal plate bone demineralization? the time you mentioned that stem cells cant get get through/ or proliferate/expand, because of the mineral environment, really bothered me or at least made me really want to focus on this area especially. i know that you look into every aspect of height increase, but im more concerned in the one way that holds the most promise, i think stem cells arent really a problem if we can use lsjl, and increase hormones, which should help generate and maximize cells, i think the mineralization (or ossification) is the key "enemy" here.
    sincerely -reader

    oh' and there probably is a way for us to safely and cheaply demineralize bone right? i have my hunches that there has to be something out there, something like a mineral chelator or acid or something like lipus, or magnetic waves for more exotic ideas. but i know that we want to make sure that this is something that is safe and is looked over before recommended to anyone, so i do understand that, i think though that the real height increasing techniques likely will be this. regardless of some difficulties in the way.

  4. well, to be precise i am referring to localized bone demineralization, just for ossification zones. just unossify the ossified zones..safely, i think it would work.

  5. id remind to continue on for looking into dentin and hydrostatic pressures, thnx for all the work,

  6. Hey Tyler, just wondering what happened to the forums. Have been checking this site for the last 3 months and the forums still are not there.

    Also wondering how your progress is going. We haven't had an update in a while. I guess I've found this site I bit late, but to me it sounds like lsjl works for at max an inch or so, and then stops working. Would love to hear from you man.


  7. i am continuing to see results i am now 1.5 cm taller by my measuring system which is as accurate as possible with heel to floor and card straight as possible my advice is you have to perservere and keep improving lsjl it took me years of work and only now recently have i seen any reward you know when you are taller because you feel its hard to explain

  8. the biggest factors for lsjl failure are 1)people give up after seeing weeks and months off effort with no reward which then damages motivation2)their routine is poor 3)their nutrition levels are poor 4)lack of knowledge and some people are genetically unresponsive to lsjl i have made 1.5 cm which dont sound a lot but it is over half an inch and it looks and feels massive gap between my old and new marks 69.5 inches on my wadrobe and it does and should work eventually for me it took over 2 years before i see any results whatsoever of lsjl and nutrition is also of huge importance

    1. Hi, mind if you post me the method and nutrition i will like to proof it myself contact me at this email please smmtmm@hotmail.com I am willing to be a candidate for this and help speed up the truth and discovery of this method. God bles.

  9. good site

  10. know your busy tyler but in the future can you look into whether increasing thyroid hormones levels would increase osteoclast and therefore reduce ossification/bone mineralization?

  11. http://jcb.rupress.org/content/149/6/1297.abstract
    "FGF signaling inhibits expression of alkaline phosphatase, and blocks mineralization. Furthermore, we could also show that overexpression of FGF2 in transgenic mice leads to increased apoptosis in their calvaria. These data provide the first biochemical analysis of FGF signaling in osteoblasts, and show that FGF can act as a cell death inducer with distinct effects in proliferating and differentiating osteoblasts.

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