One day, it just happens.

You look over at your younger sibling and realize that to meet their  eye, you’ve gotta look up. The horror dawns as you understand that your days of pushing them around are over.

What’s that about? You two have the same parents, so why is your little sibling  suddenly taller than you? It turns out the why of human  stature is pretty complicated.

It’s not just genetic, though  that’s a big part of it. Here’s the long and short of it all. [♪INTRO] To understand height, we need to  bone up on anatomy, specifically… bones. We were all born smaller than we are today, and our bones go through a lot to  get us to our full adult sizes.

But when you’re born, your bones  aren’t just mini versions of the full-sized ones. A lot of  them aren’t even just one bone. Lots of our long bones, like the femur or humerus, are formed when three or  more pieces fused together.

You’ve got the diaphysis, which is  the middle shaft part, the epiphysis, which is the very end, and the metaphysis, which is just the name for the part  of the shaft closest to the epiphysis. And right between the metaphysis and epiphysis, you’ve got a growth plate made up of cartilage cells called chondrocytes. During early years and adolescence, these growth plate cells are hyperactive, dividing and making loads of  cartilage in intricate patterns.

Blood vessels start to occupy this  cartilage matrix, bringing in cells called osteoblasts which work to  turn the matrix into solid bone. Keeping the epiphysis separate  means that there’s more room to get that shaft section of the  bone as long as possible, because your growth plate is able  to just build on that free end of the bone, instead of having  to stretch from the middle. All that long bone growth winds  down at the end of puberty.

That’s when the growth plates  settle down into maintenance mode, and all the separate parts of the  bones have started fusing together. Your body’s hormones are what  trigger all this bone growth. The one creatively named  “growth hormone” is the biggie, and that comes from the pituitary gland.

Growth hormone tells the chondrocytes and osteoblasts to make more of themselves, and the more growth hormone you  have, the more they’ll grow. Another important hormone is  Insulin-like growth factor I, which promotes survival and  migration of our bone-making cells. Hormones often modulate each other, and this is the case for growth hormone and IGF-I.

Sex hormones, like testosterone and estrogen, also play a role in bone growth. Testosterone does this a  bit more than estrogen does, which is part of why people assigned male at birth are usually taller than those  assigned female at birth. Now that we know the mechanics of it all, let’s get into why not everyone gets  to be pro-basketball player sized.

And the answer is your parents. One of the first researchers  to spend time studying height variation was Francis Galton in the 1880s. He noted that height seems to  be really heritable in families, meaning that children would usually grow to within a couple standard deviations of  their parents’ adult heights.

With modern gene sequencing,  we can put a number on how much of our stature is genetic,  and as it turns out, it’s a lot. Some researchers estimate that 80-90% of height is controlled by genetics. Height is polygenic, meaning lots  of genes contribute to the trait.

All of the small variations in  those genes have an additive impact. For starters, some height-determining genes are found on the X and Y chromosomes, so that can contribute to  sex-related differences in height. It's hard to know exactly  how many genes play a role, but a 2025 review estimated that there's about 600 genes with a known contribution.

Plus, sometimes variations in  the DNA around genes can affect height too, because these  bits of DNA can influence how often those height-controlling genes get read. That 600-gene number doesn't include  those non-coding bits of DNA, which means there are possibly thousands of spots on your genome that work together to determine whether you can  reach the top shelf or not. These variants can be super  subtle, sometimes just a single nucleotide change.

Many of these  subtle DNA variants that influence height have been found using  genome-wide association studies. These studies compare the genomes of loads of people to identify any sequences that show up more in taller people  than shorter, or vice versa. With statistical data analysis,  it’s possible to see correlations between height and DNA variations,  even if the effect is pretty small.

But we also know there are genes  that play a much bigger role. However, when a single gene is known  to have a big impact on height, those genes tend to be associated with syndromes, meaning that height impact can  come with a few side effects. Some mutations are dominant, meaning a mutation in just one gene copy is sufficient  to cause the syndrome.

Sometimes, these mutations arise spontaneously, rather than being passed down from parents. An example is Marfan syndrome, which results in increased height, but often causes heart defects, too. People with Marfan syndrome  have a mutation where their bodies don’t make enough of  a protein called fibrillin-1, which is a major component of our  connective tissues like cartilage.

But Fibrillin-1 is part of  the bone protein matrix too, and based on studies in mouse models, scientists think fibrillin-1’s  role in the bones is to slow down bone growth, not speed it up. That’s why decreasing the amount of it that you have can lead to increased height. Another height-related syndrome is achondroplasia, one of the most common  causes of dwarfism in humans.

Quick note here, we’re using the word dwarfism because that’s the medical term, but most people with these conditions prefer to use terms like little person or short statured  to describe themselves. In the case of achondroplasia, the mutation causes the bones not to produce enough chondrocytes. And since those are most active in our long bones, that’s why people with this  mutation tend to have shorter limbs.

Other gene mutations affecting  height are recessive, meaning the condition only manifests if you have mutations in both copies of the mutated gene. An example of this is Laron syndrome, where there are mutations  in both copies of the gene that makes your growth hormone receptors, so they won’t respond to growth hormone. This leads to shorter stature and delayed puberty.

The type of gene mutation is pretty important too. For instance, different  mutations in the HMGA2 gene can cause extreme shortness, extreme  tallness or influence normal height variation, depending on  which part of the gene is mutated. So genetics is pretty important when it comes to height, but it’s not everything.

That’s especially clear when you  look at twins, since identical twins have the same genes, but  are often different heights. It’s kind of like cooking. The genes that go into determining height are like your body’s recipe, giving cells the instructions to make the proteins that do the work of growing your bones.

But to make those proteins,  your body needs raw materials. Ingredients, if you will. And this  is where your environment comes in.

But before we get to that, all  research needs funding, even ours. So here’s a quick ad break. Thanks to our Presidents of Science,  Harry Plumley, Charlie Stanley,   and TJ Steyn, for supporting this SciShow video!

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Donate responsibly When we say that the  environment affects our height, we’re not just talking about pollution, though that does seem to be  linked to a decrease in stature. We’re talking about the environment more broadly. Things like the conditions a person  grows up in or their nutrition all add up and play parts in  determining adulthood height.

You can only reach the height that your genes want you to if your body has all  the building blocks it needs. Growing takes calories, and  making your bones correctly also requires the right vitamin  and mineral building blocks. Calcium is the most obvious one.

Our bones need it to mineralize, so low calcium intake can lead to shorter stature. Low Vitamin D intake can also decrease growth, because vitamin D actually helps your body absorb as much calcium as possible from your food. Too little vitamin D during  childhood can cause rickets, which causes the bones to curve and buckle under the body’s weight.

Not good! This is also why most commercially available milk is fortified with vitamin D,  since that helps you get the most calcium out of every glass, whether  it’s cow’s milk or plant-based. And when it comes to calories  and overall macronutrients, you need both quantity and quality.

A 2014 study found that the greatest environmental factor in determining adult stature for Europeans was the ratio of high quality  protein, like dairy, fish and meat to low quality protein, primarily wheat. People living in countries with  lower GDPs tend to have limited access to varied, nutrient-dense  diets, and the nutrient deficiencies that come with poverty can end  up reducing someone's stature. But fortunately, the inverse is true too.

We’ve seen a worldwide increase  in average human height over the last century, partially  thanks to improved nutrition. That’s actually plateauing now,  and there’s still plenty of places where food access is  insufficient, but it’s still nice to see. For environmental factors, the  influence can begin pretty early.

Like, in utero, early. There  are some studies that show a correlation between consuming  caffeine and smaller babies at birth. While the current recommendation  says up to 200 mg of caffeine per day is okay during pregnancy, a  2022 study found that people who consumed even less caffeine than  that while pregnant had smaller babies than people who’d had no  caffeine during their pregnancy.

Plus, those smaller babies were still shorter than the control group at age eight, although, like the children themselves,  that effect wasn’t huge. By the way, there doesn’t seem to be any evidence that caffeine consumption by  children affects their growth, but it does appear to stunt bone  growth in mice going through puberty. But since caffeine isn’t great  for kids for other reasons, you might not want to caffeinate your kiddos.

Plus, things that result in  lower birth weight can sometimes be hard to come back from even outside the womb. One study on size differences in  twins found that 91% of the twins that were smaller at birth were still  the shorter one, even years later. Researchers think this is a  reflection of differences in nutrient access in utero, meaning that the conditions we’re all exposed to in utero can  affect our height forever.

Another part of your environment that  can affect your height is disease. Identical twin studies show that  infections in early years of life lead to differences in height of more  than 2 centimeters by adulthood. And according to one study, that trend held when including less serious conditions in the infection calculation too, like diarrhea or stomach bugs.

Just being sick more often  can result in reduced stature. And here is where my cooking metaphor  from earlier gets complicated. Your environment can affect how  well your body makes hormones, meaning that your ingredients alter  the ability to execute the recipe.

I guess it’s kinda like, if you want  to make cookies but your recipe calls for brown sugar and you don’t have  any. You can swap to white sugar, but going off book means that the  cookies you make aren’t identical to what the recipe would have  made without substitutions. The genes tell your body what hormones to make and how much, and environmental factors determine if your body can  actually follow those orders.

And then these hormones regulate  how your skeleton grows, and when it decides to call  it a day and stop growing. So, your genes set up your stature  trajectory before you’re even born. Then environmental influences from  pre-birth to puberty, play their part, mediating your hormones and all  adding up to your final adult height.

It’s worth mentioning that while  you gain height in your youth, you’ll likely lose height in your later years. That’s because spinal discs wear down over time, and they compact with age. Gravity  plus friction.

Stupid physics. And hey, if the fact that your  height is basically entirely up to chance is a bummer, I get it.  There are perks to being tall. There’s a positive correlation  between height and income, which is likely because of  social biases towards tallness.

But despite what popular culture may tell you, being tall isn’t always worth it. Taller people are at greater risk  of developing cancer overall,  particularly breast and  colorectal cancers in women. Why this is, we’re not quite  sure, though there are theories.

It could just be that tall  people just have more cells, therefore more potential  for something to go wrong. And the hormones that affect our height are often doing more than one thing in our bodies. For example, growth hormone regulates height, but also regulates cell proliferation in general.

So it’s not that surprising  that people with growth hormone receptor deficiency are both shorter,  and less likely to get cancer. That said, being short isn’t some kind of protection against all disease, all the time. Shorter heights are sometimes  correlated with greater risk of type 2 diabetes,  hypertension, and osteoarthritis.

We don’t know whether it’s the predisposition to these diseases that slows your growth, or whether being short itself puts  you at risk for these conditions. So there’s still plenty of work  to be done to understand it all. To make a long story short, height is complicated.

There’s a lot going on to make  your body the size that it is, whether you’re a short king or future NBA player. Whatever it says on your driver’s license, you can stand tall knowing that  we like you just the way you are. [♪OUTRO]