Monthly Archives: August 2012

Using Relativity To Define Size And Height And Finding Gratitude

When you are ever in one of those moods or states where you are focusing on your height or size, you will feel bad and get negative emotions. You can look at yourself naked in them mirror and wonder why is it that you have such a short torso, or short legs, or why your head is so much bigger than your body. You look at the Cosmo and Glamour magazines and feel envy towards the women on those covers and spreads. The women all seem to have the longest legs, and the most fit perfect bodies with not even an inch of cellulite showing.

Well, I can tell you without a shadow of a doubt that as for those taut, fit bodies in the pictures are almost all photoshopped. The picture gets edited after it is taken, and then reedited to enhance certain parts of the body (i.e. breasts) and to reduce other parts of the body (i.e. love handles).

As for the dimensions that are defined by the bone, like leg length, the photoshops even work on those. A legs can be slightly lengthened using a few photoshop tricks and one who looked like they were 6′ 0″ in the previous picture now look like they are 6′ 2″.

When you look in the mirror again, ask yourself this honest question, “Would I still have this negative image of my body and my size if everyone else in the world was only 4′ 6″?”

What if you were living with a tribe in the middle of Indonesia where the indigenous people were pygmies would you still think you are “short”? Of course, not. Like most objects and phenomenon in our world, everything is relative. There is almost no absolutes in this universe. When we say that we are rich, that does not mean that we have a billion dollars on our bank account. What we really said is more like “we have more money than 95% of the rest of the society we live in”. So when we say we are tall, we are saying that our height is really in the upper percentile of the society we live in.

If you really don’t like your size, you can always just move to a country where the average height of its people are lower than where you had come from. So if you are 5′ 8″ you can move to Vietnam and you would actually be more on the tall side after living there for a short while.

My whole point of this post is to say that our perception our what we think is a immutable fact like our height/size is actually not truly immutable. While It may be true we may never be able to change ourselves, we can change our surroundings to make ourselves on the big/tall percentile side of another nation or tribe in comparison if we decided to move. So, please learn to use the concept of relativity to define your size and you can actually learn to feel better about yourself. There are plenty of people in the world who are shorter than you and if we all tried, we can all find gratitude in all the inches in height we do have, not what height we do not have.

Update On The Height Of Jessica Pardoe

In a previous article post I did entitled “Tallest Female Teenager In The World – Who Is It?” I had mentioned that besides the original three female contenders, there was a new addition. That was Jessica Pardoe on the UK was at the age of 19 was 6′ 9″. Now, in that article I was really trying to figure out whether a girl can still be considered a teenager after she gets past the age of 18 since 2 of the 3 top contenders were 19 or older. Only the Brazilian Elisany Silva was still technically a teenager since she should be 16 at this time (late Aug. 2012).

However, it turns out that this website seems to get quite a bit of traffic from people who are searching up the name “Jessica Pardoe” on google and other search engine sites.

Well, it was recently reported that Jessica Pardoe had her height promoted once more, to a maximum height of 6′ 10″.

Here is Jessica meeting 6′ 9″ Caroline Welz, the tallest woman in Germany. From the video it look like Caroline may actually be taller than Jessica but a look at their shoes would show that Caroline is wearing thick high heeled boots which can often give more than 2″ in extra height, and Jessica is wearing Teenager Converse-like shoes which give more like 0.5-0.75″ in extra height.

From the video on Youtube below where the story was reported by The Daily Star UK, Jessica Pardoe has grown from the mid 2011 story of her being 6′ 9″ to 6′ 10″ by only october of 2011. My real question then becomes, did Jessica really grow another inch in height from July 2011 when the news stated she was 6’9″ to 6’10” by October? If that is true then that is quite an insane growth spurt to go through.

Do You Feel Insecure About Your Height?

This is just a question I always ask people who have expressed that they would like to be taller. So far in my life, I have met many family members, relatives, past girlfriends, and guy friends who have at some point proclaimed that they wished to be slightly taller.

However, for a few of these people, they were very adamant and almost obsessive about their desire to be taller. A girl I used to date who used to say that she was 5′ 1″ was really 5′ 0″ when I questioned her about it some more. When I asked her what she wished for more than anything in the world, she told me that she only wanted to be taller . I asked her about her professional dreams and what she wanted to do for a career and she didn’t have any desires and goals about them. I guess for her, she was insecure about her height.

I know that for a long time I was insecure about my height too. I tried to do some exercises and bought equipment to help me gain some extra inches (or centimeters) and I think for all of my work over 2 years, I got 0.25 of extra height, and I think I pushed from 5′ 11.75″ of height in the morning after I wake up to a height of 6′ 0″ (and slightly more) in the morning after waking up. I was very surprised the first time I measured myself and the tip of the top of my head hit the 6 foot mark. I was really glad and was not sure if it might have been a measurement error. So I double checked, and triple checked, and quadruple checked, and I found out that I had indeed grown or managed to push myself to over the 6 foot mark in height, at least in the morning after I wake up.

For me, I really wanted that extra quarter of an inch so that if I was ever on a first date with a girl and she asked me how tall I was, I could say that I was 6 foot and not lie about it. For so many girls these days, they have this strong cut off point in their own head of the minimum height their mate must be. On the internet/online dating websites, there are many women who actually set up their profile so that they can’t get emails or messages from men who are less than 6 foot tall. This means that some men on those sites will purposely lie and say that they are 6 foot when they are more like 5′ 11″ or 5′ 10″. For me, I have never used the internet or an online dating site to meet the opposite sex, but if I did, I would not want to lie about something like height. The people will eventually have to meet you, and at that moment, they know how tall you really are.

However, in the end it doesn’t matter and we all (the men and women) know that. A lot of guys like to joke that when they start doing the “horizontal tango” all issues of height disappear. I agree with these guys, but I can also point out that one can not always be doing the “horizontal tango” all the time. One does have to stand up again.

On my driver’s license when I got it first when I was 21 (I know, I was scared to drive and never took the driving test) I stated my height as 5′ 11″. After I lost that license and go a renewed license when I was 25, I decided to list my height as 6′ 0″. In the end, I am still to this day working on having good posture, walking correctly, and making sure I don’t lose the height I gained when I was younger when I get older. But that is really something that is beyond my control. For me, I do still sometimes feel insecure about my height. I feel I am too short. I feel that I am unattractive. I feel like I am not good enough. I feel like I may never be loved as much as I secretly desire inside. And all of this stuff just comes out and manifest in some bizarre behavior that other people might not understand and may find very strange.

So how about you, “Do you feel insecure about your height?

                                             “Why are you insecure about your height?”

    “How badly do you desire to be taller than you are now?”

The Largest Person In History, Mills Darden

I have written articles talking about 7 feet tall people, 8 feet tall people, the tallest natural giants, the tallest twins, the tallest couples, the tallest toddlers, the tallest teenagers, the fattest people in history, the biggest babies in history, and everything else you could possibly think of. However that is one question that I have wanted to answer for the longest time…”Who was the largest/biggest person in history?”

Now that question is hard because now you have to consider more than one variable. When it comes to figure out who is bigger with height or weight, that is easy to do since it is one variable. To find the heaviest, you put a scale underneath them and note the number.With height, you put them next to a vertical measuring tape.

With looking for big, you have to take the two factors of height and weight together and weigh them out. In history, there has one who was just a lot “bigger” than the rest of people around. That would be Mills Darden of North Carolina.

There are no picture of this giant of a man and of the pictures on the internet, they are not of Darden himself but of someone else.

He was said to have been 7′ 6″ and weighed up to 1000 lbs. Now that is a very big man. From the Tallest Man website HERE, I paste the article on his life below…

Mills Darden – 7 feet 6 inches (228.6 cm)

” N. Y., 1892, volume 2, page 77:DARDEN, Miles, giant, b. in North Carolina is 1798; d. in Henderson county, Tenn., 28 Jun, 1857. He wits seven feet six inches in height, and at his death weighed more than one thousand pounds. Until 1838 he was active, energetic, and able to labor, but from that time was obliged to remain at home, or be moved about in a wagon. In 1850 it required thirteen and is halt yards of cloth, one yard wide, to make him as coat. His coffin was eight feet long, thirty-five inches deep, thirty-two inches across the breast, eighteen across tie bead, and fourteen across the feet.”Mills Darden (October 7, 1799 – January 23, 1857) is alleged to have been one of the largest men in history. He was widely reported to have stood approximately 7 feet 6 inches (2.3 m) tall and is said to have weighed around 1,000 to 1,100 pounds (450 to 500 kg) at his heaviest. If the reported figures are correct, Darden was 30 percent taller and about six times as heavy as the average American male of today.

Mills (or Miles) Darden was born on October 7, 1799, near Rich Square, North Carolina, to John and Mary Darden. He was married at least once and had several children. His wife Mary, who died in 1837 aged about 40, was 4 feet 11 inches (1.5 m) tall and weighed 98 pounds (44 kg), and the tallest of their sons reached 5 feet 11 inches (1.8 m) (tall for an era when the average adult American male only stood about 5 feet 6 inches (1.7 m)).

Mills Darden made his living as a farmer and reportedly owned a saloon at some point. There are many tales of his enormous size and strength, although it is difficult to tell whether they are fact or fiction. A few cunning villagers once measured his weight by marking the exact point his one-horse cart (which had springs) lowered to as he sat on it. Later on, they placed large rocks on the cart to see just how much weight it would take to match Mills sitting on it. They concluded that he weighed over a thousand pounds.

He died on January 23, 1857. He was buried in Lexington, Tennessee. His grave, and his wife’s, have been restored by the local Development Authority. No known photo remains of him.

Me: When it comes to these types of stories of people who were from the 19th century or any time before that when the picture and photograph had not been invented yet, it is really hard for someone ilke me to completely take the story and dimensions of this guy seriously. People back then were much smaller (shorter) and for anyone who was probably over 6′ 6″ they would have looked tremendously tall and people might have thought they were much bigger than they really are. If this guy was alive today, I would have definitely have liked to get him checked on how big he really is. Does that mean that I don’t believe this guy was as tall and heavy as the people back then proclaimed? Yeah, I would guess that this guy was not the 7’6″ height he was claimed at, but probably more like 7’0″. 

However, this is all just my own personal opinion. I still wanted to pay my respects to this person and don’t want to get into any argument of whether Mills Darden deserves the title of being called the “biggest man in history”. For this post, I really just want to state the information I found and let you interpret it how you would like.

Dwarfism Through Achondroplasia

Let’s look at the condition that is the leading cause for dwarfism, Achondroplasia. I wanted to focus more on the genetics of the disorder to understand what is the mechanism that triggers the process. From PubMed Health at National Institute Of Health HERE 

Causes, incidence, and risk factors

Achondroplasia is one of a group of disorders called chondrodystrophies or osteochondrodysplasias.

Achondroplasia may be inherited as an autosomal dominant trait, which means that if a child gets the defective gene from one parent, the child will have the disorder. If one parent has achondroplasia, the infant has a 50% chance of inheriting the disorder. If both parents have the condition, the infant’s chances of being affected increase to 75%.

However, most cases appear as spontaneous mutations. This means that two parents without achondroplasia may give birth to a baby with the condition.

Signs and tests

During pregnancy, a prenatal ultrasound may show excessive amniotic fluid surrounding the unborn infant.

Examination of the infant after birth shows increased front-to-back head size. There may be signs of hydrocephalus (“water on the brain”).

X-rays of the long bones can reveal achondroplasia in the newborn.

From the Wikipedia Article on Achondroplasia HERE

Achondroplasia is a common cause of dwarfism. It occurs as a sporadic mutation in approximately 75% of cases (associated with advanced paternal age) or may be inherited as an autosomal dominant genetic disorder.

Achondroplastic dwarfs have short stature, with an average adult height of 131 centimeters (51.5 inches) for males and 123 centimeters (48.4 inches) for females. Achondroplastic adults are known to be as short as 62.8 cm (24.7 inches). The disorder itself is caused by a change in the DNA for fibroblast growth factor receptor 3 (FGFR3), which causes an abnormality of cartilage formation. If both parents of a child have achondroplasia, and both parents pass on the mutant gene, then it is very unlikely that the homozygous child will live past a few months of its life. The prevalence is approximately 1 in 25,000.

In normal figures, FGFR3 has a negative regulatory effect on bone growth. In achondroplasia, the mutated form of the receptor is constitutively active and this leads to severely shortened bones.


People with achondroplasia have one normal copy of the FGFR3 gene and one mutant copy. Two copies of the mutant gene are invariably fatal before or shortly after birth. Only one copy of the gene has to be present for the disorder to occur. Therefore, a person with achondroplasia has a 50% chance of passing on the gene to his or her offspring, meaning that there will be a 50% chance that each child will have achondroplasia. Since it is fatal to have two copies (homozygous), if two people with achondroplasia have a child, there is a 25% chance of the child dying shortly after birth, a 50% chance the child will have achondroplasia, and a 25% chance the child will have an average phenotype. People with achondroplasia can be born to parents that do not have the condition. This is the result of a new mutation.[2]

New gene mutations leading to achondroplasia are associated with increasing paternal age[3] (over 35 years old). Studies have demonstrated that new gene mutations for achondroplasia are exclusively inherited from the father and occur during spermatogenesis; it is theorized that oogenesis has some regulatory mechanism that hinders the mutation from originally occurring in females (although females are still readily able to inherit and pass on the mutant allele). More than 99% of achondroplasia is caused by two different mutations in the FGFR3. In about 98% of cases, a G to A point mutation at nucleotide 1138 of the FGFR3 gene causes a glycine to arginine substitution (Bellus et al. 1995, Shiang et al. 1994, Rousseau et al. 1996). About 1% of cases are caused by a G to C point mutation at nucleotide 1138. The mutant gene was discovered by John Wasmuth and his colleagues in 1994.

From the Achondroplasia website of UK found HERE

In early 1994, linkage studies placed the achondroplasia gene on the short arm of human chromosome 4, distal to an anonymous marker, D4S43.
This region on chromosome 4 had been scrutinized for more than 10 years by scientists searching for the Huntington’s disease gene, and among the genes already known to reside in this area was fibroblast growth factor receptor 3 (FGFR3).
Proteins in the family of fibroblast growth factor receptors have a highly conserved structure. The protein spans the cell membrane and consists of three extracellular immunoglobulin-like domains, a lipophilic transmembrane domain, and intracellular tyrosine kinase domains. FGFR3 is expressed in cartilage and brain, and the mouse homologue is known to mediate the effect of fibroblast growth factor on chondrocytes.
By virtue of its known function and chromosomal localization, therefore, the gene encoding FGFR3 was a strong candidate for the achondroplasia gene.

Two groups of investigators have recently reported analyses of the FGFR3 gene in people with achondroplasia. Both groups found FGFR3 mutations in the DNA from affected persons and found no such mutations in the DNA from unaffected persons. In families with multiple affected members the identified mutations were inherited with the disorder. Amazingly, both groups found that every mutation was at exactly the same nucleotide in the transmembrane domain of the FGFR3 gene. In all but a very few other genetic disorders studied thus far, different affected families have different mutations in the disease gene. Shiang et al. found that 15 of the 16 achondroplasia mutations they analyzed had a guanine-to-adenine (G-to-A) transition at nucleotide 1138; the 16th mutation was a guanine-to-cytosine (G-to-C) transversion at the same nucleotide. (A point mutation is called a “transition” when a purine replaces a purine or a pyrimidine replaces a pyrimidine; it is called a “transversion” when a purine replaces a pyrimidine or vice versa.) Both mutations resulted in the substitution of arginine for glycine at amino acid 380 of the protein. Similarly, Rousseau et al. found that all 23 achondroplasia mutations in their series resulted in the same substitution at the same amino acid of the transmembrane domain of the FGFR3 protein. This high proportion of identical mutations (100 percent for the amino acid change), which is unprecedented for an autosomal dominant disorder in which more than 80 percent of cases represent new mutations, may explain the consistency of the phenotype in achondroplasia.

The achondroplasia mutations occur in a cytidine phosphate guanosine (CpG) dinucleotide in the FGFR3 gene sequence. CpG dinucleotides are known to be mutational “hot spots”; the cytosine residues adjacent to a guanine have a tendency to be methylated and then deaminated, resulting in the substitution of thymine for cytosine. This event will change a guanine to an adenine on the opposite (sense) strand which was the observed event in 37 of the 39 FGFR3 mutations reported to date. The mutation rate at nucleotide 1138 of the FGFR3 gene is therefore two to three orders of magnitude higher than the mutation rates calculated for CpG-mutation hot spots in the factor IX gene, making nucleotide 1138 the most highly mutable nucleotide currently known in the human genome. The reason for the exceptionally high mutation rate at this nucleotide, as well as the phenotypic effects of other mutations in the FGFR3 gene, remains to be explored.

Both the G-to-A transition and the G-to-C transversion at FGFR3 nucleotide 1138 create new recognition sites for restriction enzymes, making it exceptionally easy to test for the presence or absence of the mutations in genomic DNA. As a result, prenatal diagnosis of heterozygous achondroplasia, homozygous achondroplasia, and the homozygous unaffected state is now possible. The availability of prenatal diagnosis raises complex ethical issues concerning reproductive options for couples with achondroplasia. Since adults with achondroplasia are always heterozygous for the abnormal gene, it is possible for two affected parents to have children who are homozygous affected, heterozygous, or homozygous unaffected (i.e., of average stature). If only one parent is affected, the children will be either heterozygous or homozygous unaffected.

Other important advances have recently been made in our understanding of skeletal dysplasias. Hypochondroplasia, a skeletal disorder similar to but distinct from achondroplasia, seems to be linked to the same region on chromosome 4 as is achondroplasia, but no FGFR3 mutations have yet been identified in DNA from people with this condition. Reardon et al. recently reported FGFR2 mutations in patients with the Crouzon syndrome, the most common form of craniosynostosis. Through the use of positional cloning techniques, the gene for diastrophic dysplasia, an autosomal recessive skeletal dysplasia, was recently found to encode a sulfate transporter. Diastrophic dysplasia, like achondroplasia, is characterized by dwarfism, and it is especially common in Finland. Headway is being made in the identification of the genes causing several other skeletal dysplasias, including pseudoachondroplasia, multiple epiphyseal dysplasia, and cartilage hair hypoplasia. Thus, we appear to be on the threshold of a revolution in our understanding of the role of specific genes in normal and pathologic skeletal growth and development.

From MedScape Reference HERE


Achondroplasia, a nonlethal form of chondrodysplasia, is the most common form of short-limb dwarfism. It is inherited as a mendelian autosomal dominant trait with complete penetrance. Approximately 80% of cases are due to new or de novo dominant mutations with a mutation rate estimated to be 0.000014 per gamete per generation. Salient phenotypic features include disproportionate short stature, megalencephaly, a prominent forehead (frontal bossing), midface hypoplasia, rhizomelic shortening of the arms and legs, a normal trunk length, prominent lumbar lordosis, genu varum, and a trident hand configuration.


Achondroplasia is caused by mutations in the fibroblast growth factor receptor-3 (FGFR3) gene. At present, FGFR3 is the only gene known to cause achondroplasia.[1] This gene has been mapped to chromosome 4, band p16.3 (4p16.3). All causal mutations occur at the exact same location within the gene; hence molecular testing by targeted mutational analysis is easily done and interpreted. The mutations (G1138A, G1138C) cause an increased function of theFGFR3 gene, resulting in decreased endochondral ossification, inhibited proliferation of chondrocytes in growth plate cartilage, decreased cellular hypertrophy, and decreased cartilage matrix production.

The nucleotide G1138A and G1138C mutations of FGFR3 account for 99% of the mutations resulting in a specific point mutation, hence an amino acid substitution.[2] About 98% of cases have the G1138A mutation resulting from a G-to-A point change. One percent of cases have a G-to-C point change at nucleotide 1138, causing the G1138C mutation. A rare missense mutation (Lys650Met) in the tyrosine kinase region of FGFR3 causes a disorder termed severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) . See Differentials.

Genetics of Achondroplasia

  • Author: Germaine L Defendi, MD, MS, FAAP; Chief Editor: Bruce Buehler, MD



United States

Frequency has not been documented in the United States.


Frequency is believed to be 1 case per 15,000-40,000 births worldwide. In 1986, Orioli et al reported on the frequency of all skeletal dysplasias in a study population of 349,470 live births and stillbirths.  Based on their study, the prevalence rate for achondroplasia was estimated to be 0.5-1.5 cases per 10,000 births and the mutation rate to be 1.72-5.57 x 10-5 per gamete per generation.


Sudden death within the first year of life is attributed to abnormalities at the craniocervical junction causing spinal cord compression. Central apnea occurs due arterial compression at the cervical level of the foramen magnum. The small foramen magnum present in these patients may also cause a high cervical myelopathy.

The risk of sudden death for infants with achondroplasia is 2-5%. This risk can be minimized with appropriate assessment of the craniocervical junction, which includes a thorough neurological history and examination, neuroimaging (either CT scanning or MRI), and polysomnography. If neurological abnormalities are detected, referral to medical center with neurosurgical consultation services is indicated.

Caregivers should use an infant carrier with a firm back that gives good neck support and to use a rear-facing car seat for travel as long as possible. Use of mechanical swings and carrying slings should be avoided to limit the potential for uncontrolled head movement.

Thoracolumbar kyphosis occurs in most infants with achondroplasia. Severe kyphosis is related to unsupported sitting of the infant before adequate trunk muscle strength has developed. Angular deformities of the extremities, premature degenerative joint disease, and spinal disorders are common clinical features.

Cervical instability is present in a large number of patients. Great care must be taken with manipulation of the neck, as would occur for preparation of intubation in general anesthesia. Uncontrolled neck movements could cause significant neurological compromise with spinal cord compression.

Obesity, when present, aggravates the morbidity related to lumbar stenosis, nonspecific joint problems, and cardiovascular risks. Based on the weight/height (W/H) curves developed by Hunter et al for boys and girls with achondroplasia, the mean W/H curve in children with achondroplasia matches the control curve until the children reach 75 cm in height. Beyond 75 cm, the weight in children with achondroplasia increases disproportionately to height. The Quetelet index or body mass index (BMI=W/H2) can be used to estimate weight excess in children ages 3-6 years; after that, the Rohrer index (RI=W/H3) should be used for children and adolescents ages 6-18 years.

Respiratory disorders are seen frequently, including apnea and abnormalities of gas exchange. Studies report that as many as 75% of children with achondroplasia have a pathologic apnea index (>30 episodes). Brainstem compression may contribute to central apnea whereas obstructive apnea may be due to midface structural abnormalities such as hypoplasia.

Severe upper airway obstruction occurs in less than 5% in children with achondroplasia. Tonsillectomy and adenoidectomy do not help resolve this obstruction very well in children with achondroplasia. Hypotonicity, a narrow trunk with a small thoracic cage and adenotonsillar hypertrophy all contribute to confining the airway and causing upper airway obstruction.

Children with achondroplasia who have respiratory dysfunction and obstructive sleep apnea (OSA) detected by polysomnography have associated cognitive deficits, as evident in children with OSA within the general population. Restrictive pulmonary disease, with or without restrictive airway disease, occurs in less than 5% of children younger than 3 years old. This risk is greater for those who live at higher elevations.

A study of school-aged children with achondroplasia reported CT findings, including kinking of the medulla and neuroanatomic abnormalities consistent with arrested hydrocephalus, including enlarged ventricles and hypoplasia of the corpus callosum. These CT findings are similar to those seen in children with compensated, unshunted hydrocephalus. The hydrocephalus may be due to increased intracranial venous pressure secondary to stenosis of the sigmoid sinus at the level of the narrowed jugular foramina.

Although their overall cognitive scores are within normal, children with achondroplasia may show mild deficits in visual-spatial tasks. This deficit has been identified in children with arrested hydrocephalus.

Motor milestones are usually delayed for the first year of life due to a large cranium and poor overall muscle tone (hypotonia). Language development is normal, if no conductive hearing loss is present.

Me: Overall I felt that the studying of the genetics and the mechanism that causes the disorder was something that I and the readers needed to do to understand.

What Type Of Diet Leads To The Most Growth And Height?

This question I wanted to answer is really more for the pre-epiphyseal plate closure crowd than the ones who are looking for extra height in their adult years. If you are a parent, you might be concerned and wonder whether your child will be getting the right nutrition so that they can reach their full growth and height potential. This can be a particularly worrying subject if you are of short stature yourself and so is your spouse.

We all know that on average, taller people in life are treated better, are liked more, have more romantic partners, and get more career advancement and financial rewards than their shorter counterparts. A teenager who is shorter than his/her peers and classmates may be particularly worried about this situation. If one is too short (or even too tall) they might be the victim of ridicule by others. So how does one make sure in terms of diet that they are getting everything they can to push their growth and height to the maximum?

First, we have to understand that diet makes up only a small part of the equation. What is even more important than diet is sleep and genetics. I showed in a previous post entitled”How much of human height is genetic and how much is due to nutrition?” that our genetics make up 60%-80% of what will become of our height so it is a very big factor. After that comes sleep, which is when most of our longitudinal lengthening of the long bones happen.

There is a post I had originally written entitled “The Effect On Height And Growth Being A Vegetarian“. I particularly focused on the need to get protein because the meat that vegetarians purposely choose not to eat is often the main source of protein in one’s diet. Protein is critical and essential for the human to live.

So the first thing we need to do to make sure the factor of diet is not inhibiting our growth and height is to get proteins, and as much good proteins as possible.

There is sort of a concern going around the US that most of the meat we eat came from cows, pigs, and chicken which had been fed growth hormones so that they can grow fatter faster. The fatter the animals are, the more meat there is. We american love to eat and we do had an obesity problem so it is possible that the meat we buy from the supermarket is filled with growth hormones. From a previous post I did looking at the effects of growth hormones on height, the general conclusion is that one consumes too much GH, it can theoretically speed up the growing process so that the growth plates will actually fuse earlier than they are supposed to so you end up shorter than if you had not taken the GH.

So the 2nd thing is that we need to make sure is that we are not eating meat from animals that is not been injected with GH. That is hard to do because we don’t know what type of treatment the beef we are eat is from a cow that was treated well or not. The suggestion is then to go to a place like “Whole Foods” and buy the beef that is is “grass fed”.

As for Carbohydrates, a lot of the flour made from wheat, rye, and corn these days have been processed with many forms of preservatives. Those flour are then used to make our bread, donuts, cake ,etc. In terms of how processes food will affect our overall height, I am guessing that the processed food like the flour we use to make our breads and cakes have certain compounds that are not eh healthiest in the world. The does take away from the food from having real vitamins and minerals.

However, one thing that I would say is a casual observation is that families who eat more natural food like from “Whole Foods” seem to be more on the short side. Now, I might be burned for that last comment by people who want to rebuff that with their own anecdotes and heights of people they might know and who is also big. But I am just stating an observation. We all know that foods that have not been genetically altered are usually smaller in quantity. If you have ever seen a carrot or watermelon that is grown in the wild, they look nothing like what we find in our supermarket. The fruits we see in nature are often much smaller and even a different color.

Since the cost of the stuff we buy in say “Whole Foods” can be 30-50% more expensive than the processed, genetically engineered food. I would make sense that people who are militant on only eating the most natural organic food are eating less than the people who don’t. If we wanted to correlate weight to the type of food eaten, it is obvious that people who DON’T eat organic natural food is bigger, but can we say the same about height as well. Do people who eat non-organic processed food become slightly taller than the people who don’t. That is a very hard question to answer, but I would guess it is true. So the big take away is that going in the natural organic direction may be healthier but it might be the option that leads to the greater height.

As for fiber, there is not a lot of scientific research or data that correlates to the amount of fiber we take and the height we reach. What is known is that from taking sufficient fiber, one is less likely to get slow stool or get constipation. There does seem to be some relationship with having a high fiber diet at old age with a lower mortality risk. That means that eating more vegetables has a correlation with overall health and longevity. So if you get enough fiber, your digestive system overall will be cleaner.

However, from what I have seen over my lifetime, from evolutionary theory, there seems to be an inverse correlation between longevity and height. Often it is the shorter people who outlive their taller counterparts. Taller people are more likely to develop cancer, since they have more mass in their body. The Japanese who are among the shortest group of people in the Developed world also have some of the shortest average heights of its people. In contrast, the people of the dynamic alps like Bosnia, Herzegovina, Croatia, and Serbia who have experienced so much ethnic conflict in the last century are among the tallest in the world.  They have lower lifespan than the Japanese from so much conflict but they are bigger. Of course if you even thought over my last argument, you realize that my argument is not completely logical.

In terms of fat, the human body needs fat (the good kind) to survive. Fat is made of lipids and in the human body, it is the adipose tissue. I am too lazy to do the research right now and pull out a scientific article on some study, but if I was to guess, I would say that not getting enough of the right type of fat in one’s diet will lead to a decrease in height.

Conclusion: So after going on for so long, what is the conclusion on the best type of diet needed to lead to the most growth and height? The best type of diet will involve at least 5 main parts

1. Getting all the neseccary types of vitamins and minerals, especially the type that involve in bone creation and growth and cartilage creation.

2. Getting enough of the right proteins, so eat a lot of meat like grilled chicken, fish ,grass fed cows, and eggs

3. Getting as much water as possible.

4. Eat enough fiber to have a rather clean gut to be healthier but don’t eat too much fiber.

5. Eat a lot of the good fat.

6. Try to find meat that was not injected with growth hormones

7. Eating some processed food is okay