Author Archives: Senior Researcher

The Connection Between Bone Loss From Osteoporosis And Decreases In Height In East Asian Females

Usefulness of Estimated Height Loss for Detection of Osteoporosis in Women

J Korean Acad Nurs. 2011 Dec;41(6):758-767. English.
Published online 2011 December 31.  http://dx.doi.org/10.4040/jkan.2011.41.6.758

© 2011 Korean Society of Nursing Science

Usefulness of Estimated Height Loss for Detection of Osteoporosis in Women

Soon Gyo Yeoum,1 and Jong Hwa Lee2

1Associate Professor, Department of Nursing, Seoil University, Seoul, Korea.

2Full-time Lecturer, Department of Nursing, Kunsan College of Nursing, Gunsan, Korea.

Address reprint requests to: Yeoum, Soon Gyo. Department of Nursing, Seoil University, Seoildaehak-gill 22, Jungrang-gu, Seoul 131-702, Korea. Tel: +82-2-490-7580, FAX: +82-2-490-7555, Email:yeoumsg@seoil.ac.kr

Received May 30, 2011; Revised June 04, 2011; Accepted December 09, 2011.

Abstract

Purpose

This study was done to examine the threshold value of estimated height loss at which the risk of osteoporosis increases and to verify its discriminative ability in the detection of osteoporosis.

Methods

It was conducted based on epidemiological descriptive methods on 732 Korean women at a public healthcare center in Seoul between July and November 2010. ANOVA, Pearson correlation, logistic regression analysis and receiver operating characteristics (ROC) curve were used for data analysis.

Results

There was an age-related correlation between bone mineral density (lumbar spine: F=37.88, p<.001; femur: F=54.27, p<.001) and estimated height loss (F=27.68, p<.001). Estimated height loss increased significantly with decreasing bone mineral density (lumbar spine: r=-.23, p<.001; femur: r=-.34, p<.001). The odds ratio for the point at which the estimated height loss affects the occurrence of osteoporosis was found to increase at a cut-off value of 2 cm and the area under ROC curve was .71 and .82 in lumbar spine and femur, respectively.

Conclusion

The optimal cut-off value of the estimated height loss for detection of osteoporosis was 2 cm. Height loss is therefore a useful indicator for the self-assessment and prognosis of osteoporosis.

Analysis & Interpretation

This may be the first type of evidence that I have found which shows that decrease bone mineral density leads to height loss. The type of subjects this experiment was tested on were East Asian/Korean adult females. Something that is well known is that East Asian females as a demographic suffer one of the highest rates of bone mineral loss. This means that Korean females have a very high risk of osteoporosis as they get older. The decreased height from bone density loss is very surprising.

We know that as people get older, the bone density level decreases in their bones. We also see the correlation between older age and height loss. People tend to loss at least around 1 inch of height for each decade that passes after their 40s. This report shows that for at least Korean females, maybe the reason they loss height is because they loss bone density. After the height loss reaches 2 cm, the chance of developing osteoporosis sharply rises.

This case is interesting since it shows a direct correlation to decreased bone density and height loss. It makes the height increase researcher wonder whether opposite might be right as well. if we increased bone mineral density in adult humans from taking bone growth pills like station, would that lead to increased height? That is something to think about.

Something that would be obvious is that to prevent such a high rate of height loss and stay around the same height even into later life for East Asian females, they would have to look for ways to keep the bone density at a reasonably healthy level.

The Connection Between Vascular Endothelial Growth Factor, VEGF And Growth Plate Senescence And Closure

From book “Regulators of Growth Plate Maturation” Chapter 11

VEGF expression

We already know that estrogen and it receptors interact with growth factors to control longitudinal growth. one of the growth factors is called Vascular Endothelial Growth Factor, VEGF. The Estrogen seems to upregulate the VEGF in bone tissue. In a previous section, it was said that both in vitro and vivo the administration of estrogen upregulated the concentration of VEGF. If the ovaries are removed, estrogen decreases by a huge amount and VEGF expression decreases. In addition growth plate maturation coincides with an increase in VEGF expression.

It is concluded that VEGF has a important role when endochondral ossification is close to finishing. If we can inhibit the VEGF expression then we can increase the longitudinal growth of the growth plates.

A Deeper Look Into The Multiple Pathologies Causing Gigantism Beyond Growth Hormone Excess

About 2 months ago I had wrote a very brief, superficial post on the multiple types of pathologies that would lead a person to develop extreme stature. It was entitled “A List Of The Types Of Disorders And Pathologies Which Can Cause Overgrowth, Excessive Height, And Gigantism”

This time I would find a more extensive page that goes much deeper into the medical science of the multiple causes for extremely tall stature from Endotext.org. This page seems to focus much more on the gigantism developed from growth hormone excess. 

The full page seems to be a page dedicated to gigantism as a general topic. The term gigantism refers to extreme large stature and physical size.

Let’s understand that when we are talking about stature and size, we are talking about height, not weight. Weight is something that can easily fluctuate and it seems that many americans can’t seem to stop getting bigger from increasing their weight. We are talking about height.

The way that the term gigantism is also defined is to assume that the cause or the process of gigantism starts in childhood or adolescence, while the growth plates are still open. Although the term gigantism is most often used to talk about growth hormone excess, it also is applied to non-hormonal causes of overgrowth in children.

Growth Hormone Excess

The link between gigantism and growth hormone excess was noticed even in the 19th century when giants that were big since childhood had their head, face, hands, and feet keep on getting larger in size in adulthood. The enlargement of these attributes would be termed acromegaly. Acromegaly has low rates of incidence around 3 per million people. As for growth hormone excess in childhood, that only occurs in a few hundred people. So Acromegaly and gigantism are two different things although they have some things in common. The first is that people who have acromegaly have around 10% chance of being tall statured. The acromegaly is deduced to be just the continual result of what the human body does after epiphyseal growth plate fusion when that individual also suffered from growth hormone excess giving them the tall stature. It seems that increased rate of growth hormone release is sporadic and there may be also a genetic predisposition for this type of disorder in some families.

Under the table for Etiologies of Growth Hormone Excess

  • Hypothalamic/Pituitary GH excess
  • Ectopic GH excess
  • Neurofibromatosis – I
  • McCune Albright Syndrome
  • Multiple Endocrine Neoplasia Type-1
  • Carney Complex
  • Familial Somatotrophinomas
  • Sotos Syndrome
  • Beckwith-Wiedemann Syndrome
  • Simpson-Golabi-Behmel Syndrome
  • Weaver Syndrome

All of these syndromes and pathologies seem to cause the adolescent who is still growing to have a higher rate of excess growth ending up with tall stature than a person without that pathology.

Analysis

When reading through the sections to see whether the different causes have anything in common, the main thing I noticed is that familial somatotrophinomas have a 100% chance of gigantism occuring. The term “familial somatotrophinomas is defined on the reference cite as “the development of GH hypersecretion in two or more members of a family that does not exhibit features of MEN-1 or CNC”. The other type of disorder that lead to high percentage of gigantism occurence is the multiple endocrine neoplasia type-1.

For the last four types of syndromes listed, they seem to cause not just postnatal excess growth but also prenatal excess growth. The occurence of macrocephaly is really high. Macroglossia is also a symptom of Bethwith Syndrome and Simpson Syndrome. For the mode of inheritance, all of the last 4 types of pathologies are extremely rare familial cases and sporadic.

 

Update #2: What Have I Been Doing To Grow Taller And Become Healthier – May 1st, 2013

In the last month I have started to add new exercises and ideas into my everyday schedule to optimize my body condition.

So this has been what resulted. Since I came back to the USA, Seattle specifically I went to see a new family doctor or someone who specialized in Internal Medicine. Since this is a new doctor, they took measurements of my stats.

The metal weight scale and stadiometer device in the doctor’s office said that in my socks, with me not really trying to stand up completely straight, I was at exactly 181 cms. I noted that in the doctors office they try to be very accurate on one’s measurements. I felt the metal edge touch the skin on the top of my head. So the measured value of 181 cms is sort of expected of where I am supposed to be. This was measured around 1:00 pm in the afternoon, after I had been awake for maybe 5-6 hours, so obviously I took into consideration the fact that my body did experience some time feeling the effects of vertebral decompression.

Height: 5′ 11.26″ or 1.81 meters tall

In terms of my weight, I weighed a ridiculous 219 lbs. That is 1 lb short of 100 kgs! Since my weight fluctuates so much due to different times of the day and whether I ate or not, I will just say that I weigh maybe 3 lbs less now, discounting the fact that during the weigh in I had my jeans and large belt on.

Weight: 216 lbs or 97. 98 kgs

I was very surprised with my weight since the last time I checked, which was more than 1 year ago I had weighed around 187-189 lbs. That means that I have gained around 30 extra lbs in the last year of my life. I guess it is true that one really does have trouble keeping the weight off as one grows older.

So what was my action plan to get healthier, loss weight, gain strength, and possibly regain any lost height back?

Well, the first thing I did was that after getting multiple car parking tickets, I decided to sell my car. So in terms of course of action.

1. I sold my car which I had for over 3 years. – Went on craigslist and managed to sell it for a reasonable price to a private buyer. The transaction went relatively smoothly.

2. I bought a 21 speed Diamondback Bike from Dick’s Sporting Goods store – I have been using the bike to get around anywhere within a 5 mile radius. The hardest part about getting this multiple gear bike is figuring out how to switch gears going up hill. Since I haven’t riden a bike in almost 12 years the process was really hard, painful, but very good overall for my health.

Since I used AirBnB.com to find a place for the short term, I ended up staying with a group of people who lived on a hill. The bicycling was really hard for the first week until I learned that there was a bus that was right beside the house.

For Height Increase purposes, I looked for the bike which had the largest wheels and I pushed the seat up high so that I would be forced to stretch out my legs out when I am pedaling.

3. I bought a Seattle and the Greater Puget Sound Public Transportation Pass. These are known as Orca Cards. They seem to be good for not just the bus, but also the Tram, the Light Rail, the train ,and the ferries. As it says on the website…“ORCA is accepted on: Community Transit, Everett Transit, King County Metro Transit, Kitsap Transit, Pierce Transit, Sound Transit and Washington State Ferries.” 

When I compare the cost of driving and the fact that gas seems to cost around $4.00 per gallon these days, it seems logical to choose the Bike + Public Transportation combination.

4. Just in case, there was no public transportation nearby and I had to get to places, I signed up an application for ZipCar and added the app Lyft to my iphone, which is similar to the function of Zipcar but the application process is much simpler.

5. I went to the local city Aquatic Center and bought a month or 30 day pass. – Everyday I spent around 1 hours riding the bike to the aquatic center and getting an hour of swimming.

The focus has been on stretching out the torso and doing the Butterfly Stroke. In combination, I would also add a round of stretching the back and torso twisting along with the swimming.

6. I noticed that my legs, lower back, knees, and butt area becoming very sore from so much bicycling so I found a mechanical massager that can help stimulate the muscles to relax. – I did notice that if one used the stronger massagers for a longer than average time, the vertebrae actually decompress since the muscles in the middle and lower back are not being decompressed so much. The massager that works amazingly well for me is Human Touch Swan Softouch HT-1280 Personal Massager.

As for height, I noticed that after a 20 minute application of the personal massager, the body feels looser and the vertebrate seems to decompress slightly.

7. Shaving my long hair to a very short length so that any measurements I do make will be much more accurate. I went for a very short buzz cut so now my hair is only a fraction of an inch in length. The measurements on height have been much more accurate and consistent.

So the things that I did to getting healthier and regain some lost height this months are…

  • Swimming 1 hour a day almost every day focusing on the butterfly stroke. 
  • Supplementing the swimming with back stretching exercises and torso twisting.
  • Using a bicycle with elevated seats for most of my transportation needs.
  • Using a strong hand held massager to decompress vertebrae.

Results:

I did a check on my height and noticed that my morning (right out of bed) height after just 2 weeks seemed to increase by a few millimeters (2-3) when I measured in front of the mirror and drawing a line horizontally at the place of my very first measurement. However that is my morning height.

That’s all for now today.

Two Major Breakthroughs In Research Made (Big Breakthrough!)

Something that I had discovered while I was doing research on the retinoic acid in the post “Endogenous Retinoic Acid Negatively Regulates Growth Plate Chondrogenesis And Longitudinal Growth” were two compounds which really got me excited in the research.

It seems that while retinoic acid inhibits longitudinal growth of the long bones, it’s antagonist known as the Retinoic Acid Receptor antagonist (aka RAC antagonist) seems to be able to actually reverse the inhibitory effects of RA. it seems to be able to make the mineralization, calcification, and chondrocyte maturation process go in reverse and turn cartilage extracellular matrix which have started to mineralize and accumulate with calcium deposits known as hydroxyapatite back to the collagenous and glycoaminoglycan filled tissue it was originally.

What makes the RAC antagonist so promising was the fact that the RA was fed to the lab rat of a single dosage orally and the effects on the growth plates and endochondral ossification became obvious after just a few days. If the RA can be taken orally, then it might be possible for the RAR antagonist to be taken orally as well.

If the RAR antagonist can indeed be taken orally, then what we have would be one of the first and only true scientifically validated compounds discovered which can actually accelerate growth in growing children. This would have huge implications for children around the world who developed stunted growth from bad nutrition. If the RAR antagonist can be separated and isolated, using chemistry devices like HPLCs, and then concentrated, we might be able to mass produce this compound element.

What is interesting is that the RAR antagonist can reverse the calcification and mineralization process so even if a person had a sliver of open growth plates left, they can start growing maybe even in a few weeks of a few millimeters.

Since the human body produces the retinoic acid and the retinoic acid receptor antagonist endogenously, it would be safe to intake orally/ ingest. It is safe for human oral consumption.

The 2nd compound which I discovered which may have evern bigger implications as I had researched in the previous post linked above is Parathyroid Hormone, PTH.

In that post, I had quoted a phrase from the study entitled “Retinoic acid induces rapid mineralization and expression of mineralization-related genes in chondrocytes.“

“Mineralization was completely abolished by treatment with parathyroid hormone; this profound effect…”

It seems that the PTH has the ability to break down the calcium deposits down. In terms of general biological and medical literature, the fact that PTH can cause calcium accumulation to be resorbed back into the blood is already a very well known point.

From a webpage from Colorado State University…

Parathyroid hormone accomplishes its job by stimulating at least three processes:

  • Mobilization of calcium from bone: Although the mechanisms remain obscure, a well-documented effect of parathyroid hormone is to stimulate osteoclasts to reabsorb bone mineral, liberating calcium into blood.
  • Enhancing absorption of calcium from the small intestine: Facilitating calcium absorption from the small intestine would clearly serve to elevate blood levels of calcium. Parathyroid hormone stimulates this process, but indirectly by stimulating production of the active form of vitamin D in the kidney. Vitamin D induces synthesis of a calcium-binding protein in intestinal epithelial cells that facilitates efficient absorption of calcium into blood.

Excessive secretion of parathyroid hormone is seen in two forms:

  • Primary hyperparathyroidism is the result of parathyroid gland disease, most commonly due to a parathyroid tumor (adenoma) which secretes the hormone without proper regulation. Common manifestations of this disorder are chronic elevations of blood calcium concentration (hypercalcemia), kidney stones and decalcification of bone.
  • Secondary hyperparathyroidism is the situation where disease outside of the parathyroid gland leads to excessive secretion of parathyroid hormone. A common cause of this disorder is kidney disease – if the kidneys are unable to reabsorb calcium, blood calcium levels will fall, stimulating continual secretion of parathyroid hormone to maintain normal calcium levels in blood. Secondary hyperparathyroidism can also result from inadequate nutrition – for example, diets that are deficient in calcium or vitamin D, or which contain excessive phosphorus (e.g. all meat diets for carnivores). A prominent effect of secondary hyperparathyroidism is decalcification of bone, leading to pathologic fractures or “rubber bones”.

There is no doubt that chronic secretion or continuous infusion of parathyroid hormone leads to decalcification of bone and loss of bone mass. However, in certain situations, treatment with parathyroid hormone can actually stimulate an increase in bone mass and bone strength.

Analysis & Interpretation:

Another great resource I have used to learn more about the Parathyroid Hormone is the website Parathyroid.com. The thing is that one can stimulate calcium mineral deposits to break apart using the PTH. If you can extract enough calcium, the bones turn into “rubber” (or become very easy to fracture as well) which means that we can then probably stretch the bones.

I had already concluded in two previous, pivotal posts that the compound PTHrP (Parathyroid Hormone related Peptide) is most likely the key to induce the first step for adults with no cartilage to possibly dissolve the hard bone matrix for cartilage replacement using other growth factors with more chondrogenic effects. This post seems to put more anecdotal, but still weak evidence in showing that either PTH or PTHrP can be used for our ultimate goal of achieving bone lengthening after the cartilages completely disappear.

It seems that we have quite  a few ways to demineralize bone and give it just enough elastic properties to strength the bones.

I like to conclude this pivotal post with the link for how one can actually turn bone into rubber-like using vinegar for an elementary school science project.

Non-Invasive Union Of Long Bone Fractures Using Electrical Stimulations, A Final Conclusion

Just today while I was doing research towards the patent and research done by Brighton on applying electrical stimulation and capacitative electrical fields to accelerate epiphyseal growth plate growth, I found another old article published showing that applying some type of electrical stimulation will lead to fractures in bones, whether long, short irregular to heal. Any non-unions because the fractures are too big are more likely to heal and join together.

Since I am having some trouble copy and pasting the title, author, and abstract below, I have clipped and pasted a pic of the top of the article below.

non invasive electrical stimulation

What is important to get out of this post is to realize that the idea of using PEMF or some type of capacitative electrical field would indeed help bone formation, bone healing, and bone growth, but it will not help our endeavor, unless the individual is willing to accept the idea of using some type of bone distraction method, where a fracture has to be first induced.

The researchers at the end in the section for “discussion” notes that the PEMF idea is a very simple and safe non-invasive approach to heal bone fractures that don’t heal very well. Before the application of the PEMF, the patients in cast has not had any union in bone segments. After the application of the PEMF, the union occurred in most of the broken bones around or before 6 months. The researchers at the time did not know what was the molecular mechanism which caused the bones to heal from the PEMF application. There doesn’t seem to be a lot of evidence that callus was formed on the outside. There was evidence however that blood vessels did develop though, and this was followed by gradual interfragmentary callus formation.

The conclusion is that PEMF works, and it will lead to bone growth, just not in the way that we are hoping for. It can always be used as a part of any proposed technique or method we might come up with, when it comes time to create revascularization, and callus formation.