The Desire To Become Beautiful, Feel Loved, And Be Accepted

I was once listening to this guy talk at a seminar and he stated something which I have since realized about people in general. People rarely are completely honest with others, and rarer still is being honest with themselves.

He stated it clearly by saying this “The problem you think you have is rarely the real problem you really have. The problem you say that you have in the beginning of a therapy session is almost never the problem you say you have at the end of a therapy session.” That stuck to me a lot because I realized that for so long, for many years I had been lying to myself and to others. I was lying because I was insecure and afraid. My ego was too proud and defensive to admit that I was making the wrong choices and hurting myself in the process.

When a person has lived enough of life and the years are mostly behind them, they develop a very clear 20/20 view on the past. They finally realize where they had make the biggest mistakes, the most critical moments that had the biggest influence, etc. When everything is stripped away, people find themselves naked to the truth.

Here is the real truth that I believe is what is really going on for people who desire to become taller. They  want to be loved and they are not getting that love. They secretly believe that by somehow adding the inches to their body, other people (and themselves) will finally be able to accept and love them. I know that I have always wanted to be taller to get both the respect of other men and the attraction and admiration of women. In the US, my height would be average. If this was many years ago, I would have been completely content with being just average in height. I could have gone through life with complete full acceptance of my height. It was not in my focus since other things were really bothering me.

Very early in this year, a girl I had been with for over a year left me. The way she did it was not in the best way. I found out later that she had started dating someone new the same day she left me. Now that hurt. It cut me like a blade. I missed her, and could not stop thinking about her for over 6 months. I would go to sleep and have nightmares about her leaving me. I would find myself waking up late at night in cold sweats. My sleep was completely destroyed and my business suffered.

I felt at those moments that I was not worthy of love, not good enough for someone as good as she was. I hated the way I looked, the person I saw in the mirror. Now, I don’t think she rejected me because of my height. She liked that I was sort of on the tall side. It wasn’t about my size that she left me, but from other reasons. I came from a good home, had a good degree from a respectable school, and was self employed making ok money. We got along so well in terms of personality. So for me, the only conclusion I could reach was that I was not good looking for her. She stated that she thinks this new guy is good looking and she didn’t think I was good looking.

I will admit for the first time that one of the main reasons that I am in Seoul, South Korea was to possibly get plastic surgery on my face. The plastic surgeons in this city I am in are the best in the world, veyr professional, and highly recommended by clients across the world. The service is great and the fee rates are rather cheap. I went to two of the most famous clinics and got my consultations. The entire process took two entire days of meetings, interviews, and medical checkups. The doctor I saw recommended that I get my eyes, eyelids, nose, jawline, and forehead all done, for around $12,000 for the entire process. I had the money and I was ready to get it done.

I actually got lost on the way to one of the clinics and one of the female strangers who helped me find the way actually commented that I was “good looking” and that “you don’t need the surgery”. I could see in her eyes that she was sort of attracted to me, but at the time I didn’t want to believe her. I felt I had to face the truth that I was not desirable or attractive. I didn’t want to believe that a girl could find me attractive. I felt ugly and I wanted to completely change myself, specifically my face and the way I looked.

Everyday, as I walk alongside the streets of Gangnam-gu I see dozens of people wearing eyepatches, face masks, nose masks, and botox pads, all showcasing that they had their face done. It is completely socially accepted to want to get plastic surgery to change one’s face in this city. People are also expected to be always unhappy with who they are. You must be striving everyday to become better, to be smarter, taller, prettier, richer than your peers. Competition is fierce and no one wants to be in the lower percentile. When you are are among the elite, your greatest fear is that you might drop down the social standing and be ridiculed and ostracized for your failures. In this country based on Confucian values, the need to be judged well by everyone around you is strong. You must always keep an image. If you are not accepted, that is like the kiss of death.

You look on the Korean TV and you see the music and tv stars being mobbed by adoring fans everywhere they go. People across the internet space are always either complimenting on how good looking they are, how thin they are, or how tall they are. I am sure those stars love the feeling knowing that they are loved by so many people. I secretly want to be loved by others as well. I am flawed in my desires to want to be beautiful, to be tall, to be special and unique. I feel that I can’t ever be good enough .What can be done then to feel that I am finally good enough to finally, fully accept and love myself?

I understand now. I would like to be taller, but I don’t need it. I don’t need to add another 10 cm to my height or change my face for someone else to find my acceptable and love me.

Decreasing Weight And Exercising Core Abdominal Muscles May Increase Morning Height And Decrease Height Lose Throughout The Day

So by now for most of us height increase seekers, we know that the height we have in the morning, after we get up from sleep is different than the height we have after we have been standing and walking around for the entire day and when we go to sleep. The drop in height can be upwards of even 3 cm for some really tall people. For me, the drop seems to be around 2 cm.

Recently I was looking through one of the posts on the GrowTallerForum and one person mentioned that apparently the combination of the decrease in weight, and exercise focused on developing the core and abdominal muscles can allow one to develop a higher morning height. At first I didn’t think much of the comment, until I was in the shower (don’t all the great ideas come along when we are in the bathroom) and I realized that from a physical therapist point of view that actually makes sense.

When we are talking about height, and the increase in height, we are almost always talking about the transformation and lengthening of the long bones, since the bones are the limiting factor. However, we sometimes forget that there is more to the lengthening than just the bones. We forget about the muscles as well. The bones is the primary thing that gives us the form we have and provides most of the support. However, the muscles are also used to support the body and the internal organs.

I recently met a college graduate who was trying to get into medical school. He was only 22 and he was already suffering from acute pain from his lower back. For anyone who knows anything about orthopaedics of the back, the L4-L5 intervertebral disk is the one that is more likely to rupture or bulge out causing either a bulged or hernitated disk. However, herniated disks often lead to After learning more about his situation, it turns out he actually has at least 3, possibly 4 herniated or bulged disks. There was the L5-L4, the L4-L3, the L6-L5, etc. When he told me he was not taking any form of medication, I suggested NSAIDs, non-steroidal anti-inflammatory pills. When it turns out he didn’t want to use medication, I suggested to him the Alexander method. After he learned about the alexander method, he asked me about it and I explained the concept of it to him. Then I put the two parts together.

The core muscles in our torso helps in the support of our body, but especially our vertebrate. When a person suffers a herniated disk, the suggestion given by most physical therapists is that one muscle exercise and develop the core abdominal muscles to be strong so they can support and hold up the upper body and head from compressing down on the disks any further causing more pain.

From using simple physics principles, we understand that lose of weight form the top means less work needed for the muscles to be done. So this is what I am suggesting.

1. Lose weight from upper body area, specifically fat.

2. Do exercises to help the core. Focus on the abdominals, delts, and pecs. I personally find swimming, in combination with yoga stretches, and crunches to be the most effective.

The stronger and more developed muscles around the core, not the top means the muscles around the middle should be able to support the upper body. In theory that would mean that the decrease of height because of the downward force of gravity over time during the day can be countered and minimized by the upperward work done by the cor muscles. That can be used to explain why the drop of height is decreased  and the overall height over through out the day has been increased.

In a horizontal direction, the core muscles which have grown bigger and thicker can be relaxed becoming wider, which can even pull the intervertebral disks farther in width when lying down. That can be used to explain why the morning height after we get up can be increased as well.

Personally, I can claim that I first noticed that I passed the 6 foot in height mark during the morning about 1 month after I started to get into my swimming obsession, which lasted for over 4 years. After just 2 weeks of swimming, I noticed that my body was transforming and that I felt lighter, taller, and more fit. 

Before I started swimming, I thought my maximum height was 5′ 11.75″ and my lowest was around 5′ 10.5″. After I started swimming, I found out that my maximum height was over 6 feet and the lowest height I could drop to was 5′ 11.25″

Hormonal Regulation Of Longitudinal Bone Growth, Different Pathways Of GH and IGF-1

This post will be more informative in nature. I had typed the term “estrogen bone growth” into google and one of the first ranked links was to this article written on pubmed entitled “Hormonal Regulation Of Longitudinal Bone Growth.”

The abstract is below. The article was found from PubMEd located HERE and the most important parts were highlighted.

Eur J Clin Nutr. 1994 Feb;48 Suppl 1:S150-8; discussion S158-60.

Hormonal regulation of longitudinal bone growth.

Nilsson A, Ohlsson C, Isaksson OG, Lindahl A, Isgaard J.

Source

Department of Orthopedics (Hand Surgery), Sahlgren’s Hospital, Sweden.

Abstract

The regulation of postnatal somatic growth is complex. Genetic, nutritional factors and hormones exert regulatory functions. Hormones that have an established role in the regulation include growth hormone (GH), thyroid hormone and sex steroids. GH promotes mainly the growth of the long bones in terms of final height, while the action of the sex steroids and thyroid hormone is less well known. Longitudinal bone growth is the result of chondrocyte proliferation and subsequent endochondral ossification in the epiphyseal growth-plates. The growth-plate is a cartilaginous template that is located between the epiphysis and the metaphysis of the long bones. GH and insulin-like growth factor-I (IGF-I) have different target cells in the epiphyseal growth-plate. GH stimulates the slowly dividing prechondrocytes in the germinative cell layer while IGF-I promotes the clonal expansion in the proliferative cell layer of a GH primed cell. Thyroid hormone blocks the clonal expansion and stimulates chondrocyte maturation. IGF-I mRNA is primarily regulated by GH, and IGF-I is produced in several tissues such as the liver, muscle, fat and epiphyseal growth plates. However, IGF-I mRNA is also increased during compensatory growth of heart and kidneys and by estrogen in the Fallopian tube in the rat. Nutrition, i.e. energy from fat and carbohydrates and proteins, also influences the final height, but the cellular mechanism of action is not known. The aim of this article is to review hormonal action on longitudinal bone growth.

Me: It is too bad that I can’t pay for a way to read the entire article. The thing I took away from the abstract was that the Gh and the IGF-1 have different target cells in the growth plates. The GH stimulates the prechondrocytes in the germinative cell layer while the IGF-1 promotes the clonal expansion in the proliferative cell layes of a GH primed cell. So, the Gh starts the chondrocytes out by getting ready and the IGF-1 helps the cells divide and multiply. This shows that both the GH and the IGF-1 are both needed to get the plates to proliferate and grow thicker from cell multiplication. 

As stated very clearly, the thyroid hormone (which one it is is not revealed in the abstract) causes the clonal expansion (aka cell division and growth) to be blocked and causes the chondrocytes to grow old. This suggests that if I can just figure out which thyroid hormone is causing the blocking of cell division and cell senescence, we can find another way to slow down the growth plate decrease and maturation process. 

 

 

Our Height Is Controlled By More Than Only The Genes (IMPORTANT)

I was looking through the news the last few days and one article really caught my eye and sort of gave me a new paradigm on thinking about how the human body would behave.

It was from NBC NEWS. Article was originally from HERE. It is posted below with the important parts highlighted.

New DNA project shows us living beyond our genes

According to recently released research papers, genes are only a very small piece of what makes the body work. Much more important is the stuff in between the genes – stuff once dismissed as “junk DNA.” NBC’s Robert Bazell reports.

By Robert Bazell and Maggie Fox, NBC News

In what many scientists say is a revolution in biology, a giant new project is rewriting our understanding not only of what causes diseases or what makes our eyes a certain color, but what makes us human. And it turns out scientists have been looking in the wrong place for a very long time.

The bounty of new discoveries, released in a batch of 40 research papers on Wednesday, shows the stretches of DNA that we call genes are only a very small piece of what makes the body work. Much more important is the stuff in between the genes – stuff once dismissed as “junk DNA”. It turns out that junk DNA is what is in control, they report in the series of papers in the journals Nature, Science and elsewhere.

“This has opened up whole new galaxies. It’s like having a bigger telescope,” says Dr. Bruce Stillman, president of Cold Spring Harbor Laboratory, which played a major role in the work.

Scientists already knew in 2003, as they finished the giant Human Genome Project, that they did not have the understanding they had hoped for.  It turned out that humans had just a measly 22,000 genes – fewer than some animals and far fewer even than a plant such as rice. How could something as complex and advanced as a human be boiled down into something so simple?

“We understood precious little about the processes that turns genes on and off. In short we had more questions than answers about how the human genome works,” said Dr. Eric Green, director of the National Human Genome Research Institute, which conducted the study.

The next phase of work, called ENCODE for Encyclopedia of DNA Elements, shows there’s nothing simple about it. As many as 40 million different switches are controlling these genes, turning them on and off in complex and subtle ways.

“The genome is loaded with gene controlling switches. There are literally millions of these,” Dr. John Stamatoyannopoulos of the University of Washington, who worked on the studies, told reporters in a telephone briefing.

Dr. Francis Collins, director of the National Institutes of Health, calls the findings “awesome and elegant.”

“This is the first truly comprehensive view, of how the three billion letter instruction book for human biology actually carries out its work, across many tissues and over the course of development,” he told NBC News in an interview.

Stanford University genomic expert Michael Snyder says it looks like gene mutations — the changes in DNA sequences that we associate with causing diseases — may only affect rare diseases. Common diseases, like heart disease, cancer, and allergy, are probably controlled elsewhere. “We think that most of the changes that affect disease don’t lie in the genes themselves, but the switches,” Snyder says.

So treating these common diseases may lie in trying to affect the switches. “The pharmaceutical industry has largely given up on genomics and the genome in favor of older approaches,” said Stamatoyannopoulos. These new findings may reinvigorate new drug research, he said. “Now we have a huge amount of genetic data about human disease that we can actually put to work to find the right kind of genes and proteins to target,” he said.

This new data will also help doctors diagnose disease in the first place, predict which treatments will work best for patients, and monitor their progress. It  points the way to studies to determine the causes of hundreds of diseases including  all kinds of cancer, Alzheimer’s disease, schizophrenia, heart disease, type 1 and type 2 diabetes, lupus, rheumatoid arthritis and asthma.  It also may lead to a better understanding of how our genetics determine such non-disease factors as height, weight and expected life span.

Not only that, it also can help explain why humans and chimpanzees share 98 percent or more of our genes, yet are so different.

“Genes occupy only a tiny fraction of the genome, and most efforts to map the genetic causes of disease were frustrated by signals that pointed away from genes. Now we know that these efforts were not in vain, and that the signals were in fact pointing to the genome’s ‘operating system’ — the instructions for which are hidden in millions of locations around the genome,” said Stamatoyannopoulos. “The findings provide a new lens through which to view the role of genetics and genome function in disease.”

Another surprising finding was that the regulatory circuitry blueprints could be used to pinpoint cell types that play a role in specific diseases — without requiring any prior knowledge about how the disease worked. For example, DNA changes associated with Crohn’s disease (a common type of inflammatory bowel disease) are concentrated in the switches controlling two types of immune cells.

Researchers can use this same method to identify cell types not previously known to play a role in a particular disease, expanding our understanding of the disease process and potentially leading to new therapies.

“We now have a parts list of what makes us human,” says Mark Gerstein of Yale university, who worked on the project. “What we are doing is figuring out the wiring diagram of how it all works.”

The findings rewrite biology 101 for most of us.  Each gene, we were taught, provided the code for a single protein. The proteins were the building blocks of cells, and the products made by the cells, from compounds called growth factors to signal-carrying chemicals. An intermediary genetic structure called RNA carried this information. ENCODE shows this is not quite so straightforward, that RNA generates the 40 million switches that can affect how and when many things happen within the cells.

“This is another grand chapter in the ongoing and historic research story that is unraveling the details about how life works, and how disease occurs,” Collins said.

Me: This is one of those articles that I would say comes along once every 5 years that brings to the public eye a completely new way of thinking and how to perceive the world. I personally view this type of news similar to when the scientists demoted Pluto from being a planet to a dwarf planet. Or when it turned out the universe was found to be expanding in size, instead of slowing down. It even stated in the article that the new paradigm can be used to explain non-disease factors such as HEIGHT. The fact that the writer of the article mentioned height as the first non pathological factor that the new paradigm can be used to understand shows that the public is well aware that height is primarily determined by the genetics, and that if we figure out the signals, the switches, and the genes that really affect height, we will eventually find a way to do real gene therapy to correct for short stature and increase in height. 

In a previous post I wrote entitled “the genetics of height” I noted that the human genome seemed to have an abnormally small number of genes, around 30,000-50,000. Now this report comes out and it seems we have even fewer, around 22,000. If we are by species 99% similar to the gorilla by looking only at the 22,000 genes, that means only 220 genes separate us from looking like a gorilla. That just seems too small. If we then look at race, then we could say we are 99.9% similar, which means only 22 gene mutation differences separate me from a african male who is living in a tribe in nambia. That for me seems very hard to believe. With this new discovery, nature seems to make a little more sense now. I would hardly could have believed that a person who looks quite different from me was only 22 genetic differences away from me. That would not even explain the reason why my nose is slightly bigger or longer than a male who looks very similar to me. It would seem that there HAD to be more that is controlling our phenotypical traits that just the 22,000 genes geneticists say there are. 

Overall, this article is BIG news and will only lead to a far, far better understanding of the genome and the real controlling nucleotide bases. I really believe this type of news could lead an entire new generation of biologists and geneticists into studying further for the clues to height increase through genetic engineering.

Create A Height Increase And Grow Taller Vegetable Juice

I remember reading the “grow taller 4 idiots” pdf and reading about this vegetable cocktail juice one can make just from ordinary grocery store vegetable that was supposed to help give you the needed types of amino acids. I didn’t really think the cocktail formula was worth adding to this site but since reading about it on the E-product, the juice cocktail seems to appear in other “how to grow taller” websites, specifically this blog.

So here it is.

This juice recipe is really simple. The ingredients are tomatoes , broad beans and cabbage. Why should these ingredients?
Tomatoes contain High In Gamma-Aminobutryic Acid (GABA ), this  is an amino acid, inhibitory neurotransmitter, responsible for inducing relaxation and sleep. It is usually ingested orally in powdered form. In a study from the First Medical Clinic at the University of Milan showed “In all of the 19 subjects studied, compared with 18 controls, plasma growth hormone levels were significantly Increased (above 5 mg/ml) by acute oral administration of 5 g of GABA”. This dramatic Increase In HGH levels can be put down to GABA5 ability to increase Deep Sleep In patients through Its neurotransmitter inhibitory response. Deep Sleep, as you will learn more of further on, is when large proportions of HGH is secreted naturally. Experts claim that powdered GABA should not cross the Blood-Brain-Barrier and therefore be ineffective, but many studies keep showing oral ingestion of GABA to have some effect on HGH levels.
Broad beans contain L-Dopa, an amino acid that has been used for years in the treatment of Parkinson Disease. L-dopa increases levels of dopamine in the brain and causes the secretion of growth hormone from the anterior pituitary gland. In 1970, Boyd and colleagues found that a 500mg oral dose “caused a significant rise in plasma growth hormone in PD patients, Initially starting therapy or on chronic L-dopa therapy for as long as 11 months. The rise in plasma growth hormone persisted for 120 minutes after the administration of the drug.” (4). Boden and his co-workers gave 500mg of the drug orally to four male and five female volunteers. “HGH levels rose sharply at 45 minutes from the basal value of 0.8mg/nil, to a maximum of 10.0mg/nil at 90 minutes (p<0.001) and declined thereafter. This rise occurred in eight of the nine subjects.” (5). Hayek and Crawford reported that six out of seven “constitutionally short children” responded to oral L-dopa (200-500mg), “…with elevations in HGH concentration above 7mg! ml, peak levels occurring between 30 and 120 minutes after drug administration.. “. (3). There have been many other study’s which also back up these results.
Cabbage contains L-Glutamine. This is the most abundant amino acid in the body. L-glutamine Is a readily available popular sport supplement. L-glutamines HGH level increasing ability’s may be a result of is its ability to boost protein manufacturing. A 1995 study by Tomas C. Welbourne of Louisiana State University College of Medicine in Shreveport. Welbourne showed that about  2 grams of glutamine raised HGH levels more than four times than when the  subjects were given a placebo. Another study showed a 5g dose of the mixture  L-lycine, L-glutamine and Niacin to increase serum HGH levels 70% (2).
Well, now you know what and why we should choose those ingredients. Then now let’s make it :
1.   3 Tomatoes –
2.   250 grams broad beans
3.   250 grams cabbage
Place those ingredients into blender and blend until liquid (add water to adjust consistency).
For daily consumption , you can make triple then put in your fridge . Drink them as your height program suggests.

From Source HERE

Me: One thing I have a problem with of this recipe is that in one of Hakker’s Old posts, he strictly said to avoid Tomatos because of a certain compound that is not helpful in height increase. I don’t remember the exact post or where it was from but tomatos was specified not be eaten for height increase.

Increase Height And Grow Taller Using Melatonin (BREAKTHROUGH, Getting Closer)

The compound Melatonin was always linked to Niacin as a supplement vitamin to take stated by Hakker and Cliff in their posts. There was believed to have been 4 main methods they created, but the other 3 methods beside the basic M.E.N.S. method was not found by me. A lot of people have asked about the H.U.S.S. method which was theoretically supposed to give a person up to 2.5 cm of extra height a month, which just sounds too incredible to believe.

I found more information on the bodybuilding boards of a person who started to describe the use of niacin and melatonin in helping people increase their height using the vitamin supplements.

Again, I will highlight the parts that are the most important

From the BodyBuilding Forum HERE

ABSTRACT:

Melatonin and resistance exercise alone have been shown to increase the levels of growth hormone (GH). The purpose of this study was to determine the effects of ingestion of a single dose of melatonin and heavy resistance exercise on serum GH, somatostatin (SST), and other hormones of the GH/insulin-like growth factor 1 (IGF-1) axis.*
Physically active males (n = 30) and females (n = 30) were randomly assigned to ingest either a melatonin supplement at 0.5 mg or 5.0 mg, or 1.0 mg of dextrose placebo. After a baseline blood sample, participants ingested the supplement and underwent blood sampling every 15 min for 60 min, at which point they underwent a single bout of resistance exercise with the leg press for 7 sets of 7 reps at 85% 1-RM. After exercise, participants provided additional blood samples every 15 min for a total of 120 min.*
Serum free GH, SST, IGF-1, IGFBP-1, and IGFBP-3 were determined with ELISA. Data were evaluated as the peak pre- and post-exercise values subtracted from baseline and the delta values analyzed with separate three-way ANOVA (p < 0.05). In males, when compared to placebo, 5.0 mg melatonin caused GH to increase (p = 0.017) and SST to decrease prior to exercise (p = 0.031), whereas both 0.5 and 5.0 mg melatonin were greater than placebo after exercise (p = 0.045) and less than placebo for SST. No significant differences occurred for IGF-1; however, males were shown to have higher levels of IGFBP-1 independent of supplementation (p = 0.004). The 5.0 mg melatonin dose resulted in higher IGFBP-3 in males (p = 0.017).*
In conclusion, for males 5.0 mg melatonin appears to increase serum GH while concomitantly lowering SST levels; however, when combined with resistance exercise both melatonin doses positively impacts GH levels in a manner not entirely dependent on SST.

Melatonin

The pineal gland, via melatonin, may also modulate GH secretion. Oral administration of melatonin to normal subjects increases basal GH levels and the GH response to GHRH (516), but marginally affects GH responses to hypoglycemia or apomorphine (517, 518). This suggests that melatonin might play a minimal (stimulatory) role in baseline GH secretion, possibly acting at the hypothalamic level via inhibition of somatostatin. The GH response to L-dopa is reduced in blind human subjects (519), who presumptively lack both light-mediated inhibition of melatonin release and the normal slow wave sleep-associated rise in plasma GH concentrations (520). Thus, it is possible, but entirely unproven, that variations in the release of endogenous melatonin could modulate GH secretion in humans.

From Source 1

Melatonin: A Hormone That Protects Against Breast Cancer and Aging

Thursday, April 10, 2008 by: Barbara L. Minton
(NaturalNews) Melatonin is nature’s sleeping pill. It is secreted by the light sensitive pineal gland which regulates our biological clock and synchronizes our hormonal-immune network. Our level of melatonin rises with darkness and falls with light. According to Dr. Uzzi Reiss, in his book Natural Hormone Balance, a healthy pineal gland produces 2.5 milligrams of melatonin every twenty-four hours. Melatonin plays a central role in the natural aging processes of the body. When pineal production begins to diminish, at around age 40, the decline sets off changes in the operation of the body’s cells. The physiology of the cell shifts from repair and rejuvenation to aging and degeneration.Recent studies are now showing that as our levels of melatonin sink, our chances for breast cancer rise. Many women with breast cancer have lower levels of melatonin than those without the disease. Laboratory experiments indicate that lower levels of melatonin stimulate growth of breast cancer cells. Adding melatonin to these cells inhibits their growth.Breast cancer and melatonin: studies and results

According to a study at the Department of Physiology, Faculty of Science, University of Extremadura, Badajoz, Spain, published in Molecular and Cellular Biochemistry, Oct. 2005, melatonin increases the survival time of animals with untreated mammary tumors.

The aim of the study was to evaluate the therapeutic effect of melatonin on rats with advanced and untreated mammary tumors. Mammary tumors were chemically induced in rats. Following appearance of the tumors, the effect of melatonin was evaluated based on the survival time, tumor multiplicity, and tumor volume up until the death of the animals. Additionally, the variations in prolactin, noradrenaline and adrenaline concentrations, and percentage of NK cells were evaluated after one month of the melatonin treatment.

Results indicate that daily administration of melatonin increased significantly the survival time of tumor bearing animals compared to the control non-melatonin receiving rats. However, the lengthened survival time did not correlate with changes in either tumor multiplicity or growth rates. Animals with mammary tumors exhibited increased levels of prolactin and catecholamine concentrations compared to the healthy animals. The administration of melatonin stabilized the hormone levels, returning them to the levels of the healthy animals. Rats with mammary tumors also presented lower percentages of NK cells, however these levels were not increased with the administration of melatonin. Researchers concluded that melatonin is beneficial during advanced breast cancer. It increases survival time, perhaps by improving the homeostatic and neuroendocrine equilibrium which is imbalanced during advanced breast cancer.

As published in the International Journal of Cancer, January, 2006, researchers at the Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, Santander, Spain, found that melatonin inhibits the growth of induced mammary tumors by decreasing the local biosynthesis of estrogens through the modulation of aromatase activity. They note that melatonin inhibits the growth ofbreast cancer cells by interacting with estrogen-responsive pathways, effectively behaving as an anti-estrogenic hormone. They had previously described that melatonin reduces aromatase expression and activity in human breast cancer cells, thus modulating local estrogen biosynthesis.

To investigate the in vivo aromatase-inhibitory properties of melatonin in the current study, the indoleamine was administered to rats bearing induced mammary tumors ovariectomized and treated with testosterone. In these castrated animals, the growth of the estrogen-sensitive tumors depended on the local aromatization of testosterone to estrogens. Ovariectomy significantly reduced the size of the tumors while the administration of testosterone to ovariectomized animals stimulated tumor growth, an effect that was suppressed by administration of melatonin or the aromatase inhibitor aminoglutethimide. Uterine weight of the rats, which depended on the local synthesis of estrogens, was increased by testosterone, except in those animals that were also treated with melatonin or aminoglutethimide. The growth-stimulatory effects of testosterone on the uterus and tumors depended exclusively on locally formed estrogens, since no changes in serum estradiol were appreciated in testosterone treated rats.

Tumors from animals treated with melatonin had lower microsomal aromatase activity than tumors of animals from other groups, and incubation with melatonin decreased the aromatase activity of microsomal fractions of tumors. Animals treated with melatonin had the same survival probability as the castrated animals and significantly higher survival probability than those not castrated.

Researchers conclude that melatonin could exert its antitumoral effects on hormone dependent mammary tumors by inhibiting the aromatase activity of the tumoral tissue.

And in the April, 2007 edition of Oncology Report, this same research team at the University of Cantabria, Santander, Spain, reports the effects of MT1 melatonin receptor over-expression on the aromatase-suppressive effect of melatonin in human breast cancer cells. They note that a major mechanism through which melatonin reduces the development of breast cancer is based on its anti-estrogenic actions by interfering at different levels with the estrogen-signaling pathways.

Transfection of the MT1 melatonin receptor in the breast cancer cells significantly decreased aromatase activity, and MT1-transfected cells showed a level of aromatase activity that was 50% of vector-transfected cells. The proliferation of estrogen-sensitive cells in an estradiol-free media but in the presence of testosterone (an indirect measure of aromatase activity) was strongly inhibited by melatonin in those cells over-expressing the MT1 receptor. This inhibitory effect of melatonin on cell growth was higher on MT1 transfected cells than in vector transfected cells. In MT1-transfected cells, aromatase activity was inhibited by melatonin. The same concentrations of melatonin did not significantly influence the aromatase activity of the vector-transfected cells. MT1 melatonin receptor transfection induced a 55% inhibition of aromatase expression in comparison to vector-transfected cells. Additionally, in MT1-transfected cells, melatonin treatment inhibited aromatase expression and induced a higher down-regulation of aromatase expression than in vector-transfected cells.

The researchers concluded that their findings point to the importance of the MT1 melatonin receptor in mediating the oncostatic action of melatonin in human breast cancer cells, and confirm the MT1 melatonin receptor as a major mediator in the melatonin signaling pathway in breast cancer.

Supplementing with melatonin

Since production of melatonin by the pineal gland begins to decline at age 40, it follows that anyone over the age of 40 may be melatonin deficient and may benefit from supplementation as a preventative. Since melatonin is produced while you sleep, it also follows that if you do not get enough sleep, your levels of melatonin may be deficient. Enough sleep is 8 or more hours. Supplementing with melatonin may also be indicated for those who now have or once had breast cancer.

Your melatonin level can be measured with a simple blood test.

According to Dr. Reiss, you should not take melatonin if you have exhausted adrenal glands, symptomized by constant fatigue, low blood pressure, feeling faint when standing up, and low tolerance for physical and emotional stress. Melatonin can reduce the production of cortisol and would be contraindicated for this condition. When adrenal glands are again healthy, supplementation can be started. Women who are trying to conceive should not take melatonin as it could negatively impact the ovulation process.

Melatonin supplements are synthesized to be bio-identical with your own melatonin. They are available at health food stores in capsules, sublingual drops, pills, and as an oral spray.

For anti-aging, Dr. Reiss recommends starting with 0.25 to 0.5 milligrams and increasing the dose gradually until you notice a side effect. The optimal dose is usually 1 to 5 milligrams.

Side effects from excess melatonin are drowsiness upon waking, wild dreams that are not pleasant, waking up nervous, sweating, or with palpitations, and decreased estrogen and progesterone levels.

There is disagreement among authorities as to whether higher doses of melatonin should be recommended for cancer prevention. Dr. Reiss recommends 20 to 40 milligrams daily for prevention. He notes that participants in studies using these very high doses did not develop the side effects seen at lower doses.

Dr. John Lee, in his book What Your Doctor May Not Tell You About Breast Cancer, says that high melatonin levels reduce the ovarian production of estrogens and progesterone, and this is the feedback that is thought to be protective against breast cancer. However, he stresses that all the body’s hormones must be in balance, and more is not better when it comes to melatonin. He recommends supplementing with no more than 1 milligram of melatonin sublingually just before bedtime.

If you choose to rely on you own production of melatonin, be aware that production of melatonin rises from bedtime until the middle of the night, and then slowly declines throughout the rest of the night. This production is dependent on you sleeping in a dark room. If you get up during the night and turn on the light or open the refrigerator door, your melatonin production will abruptly stop.

About the author

Barbara is a school psychologist, a published author in the area of personal finance, a breast cancer survivor using “alternative” treatments, a born existentialist, and a student of nature and all things natural.

Conclusion: In my personal opinion, this is another breakthrough in height increase research. The melatonin seems to promote GH release somehow, be an estrogen aromatization inhibitor, and seems to regulate our sleep patterns which means we can get better, longer, and deeper sleep effectively helping our brain to release even more Gh and our spines to decompress.

In addition, melatonin is supposed to give us some anti-aging properties. We are talking about another one of those medical miracle supplements which has so many positive benefits. As for whether it can help the adult with fused growth plates grow taller, I would be willing to bet that it might have the ability to do that, even if it is from getting better and more sleep and spinal decompression. 

{Here’s a new Melatonin study-Tyler

Melatonin regulates mesenchymal stem cell differentiation: a review

“Melatonin seems to regulate selected signaling responses that alternatively commit and drive MSC through differentiation into osteogenic, chondrogenic, adipogenic or myogenic lineages. Common pathways appear to function as master regulators of these processes acting at the earliest or irreversible steps of MSC signaling, such as the Wnt/β-catenin/PPARγ pathway, MAPKs, TGF-β signaling and others.”

“antioxidant effects of melatonin are just a component of the homeostatic and cell protective effects”

“melatonin can shift bone marrow precursor cells from an adipocytic to osteoblastic differentiation”<-We would want it to shift to chondrogenic differentiation.

“MSC express antigens detected on pericytes, endothelial and perivascular cells and that postcapillary venule pericytes from bone-marrow and peri-vascular cells from most tissues exhibit MSC-like characteristics”

“TWIST also plays an important role in lineage specification of MSC”<-Twist1 overexpression results in bone overgrowth.

“adult MSC [are in the] bone marrow. [But only account for] 0.001- 0.01% of total nucleated cells”<-Since mesenchymal condensation is key to form neo-growth plates this is an obstacle.

“The canonical Wnt/β-catenin signaling is a key regulator of bone formation and MSC differentiation to either the osteogenic or chondrogenic lineage through rather high or low Wnt
canonical activity, respectively”

“an appropriate level of β-catenin signaling is required for commitment to the chondrogenic lineage.”<-You need just enough B-Catenin signaling to induce chondrogenesis.

“activated Wnt/β-catenin pathway can induce MSC aging possibly by the activation of ROS generating pathways or lower control of their reactivity by antioxidant genes. Actually, ROS generation was increased in MSC when high levels of Wnt3a were expressed, whereas lower levels of this Wnt form were unable to induce ROS generation.”<-Thus maybe too elevated levels of Beta-Catenin inhibit neo growth plate formation in adults?

“melatonin is known to regulate ERK1/2 activity”

“Cells were induced during chondrogenic differentiation via high density micromass culture
in chondrogenic medium containing vehicle or 50 nM melatonin.”<-The melatonin group was more chondrogenic than the other group but other precursors were needed to induce chondrogenesis than the melatonin.    The cells used were human MSCs which is promising for height growth as they are the cells in the bone marrow unlike embryonic stem cells.

“Besides the collagen type II (COL2A1) and X (COL10A1), the genes involved in chondrogenic
differentiation up-regulated by the melatonin treatment included aggrecan (ACAN), SRY (Sex
determining Region Y), Sox 9 (SOX9), runt-related transcription factor 2 (RUNX2), and the potent
inducer of chondrogenic differentiation BMP2.”<-The study this points to was Forced expression of Sox2 or Nanog in human bone marrow derived mesenchymal stem cells maintains their expansion and differentiation capabilities.  However, I could not find the related melatonin information.