Biology Explainer: The big 4 building blocks of life–carbohydrates, fats, proteins, and nucleic acids

The short version
  • The four basic categories of molecules for building life are carbohydrates, lipids, proteins, and nucleic acids.
  • Carbohydrates serve many purposes, from energy to structure to chemical communication, as monomers or polymers.
  • Lipids, which are hydrophobic, also have different purposes, including energy storage, structure, and signaling.
  • Proteins, made of amino acids in up to four structural levels, are involved in just about every process of life.                                                                                                      
  • The nucleic acids DNA and RNA consist of four nucleotide building blocks, and each has different purposes.
The longer version
Life is so diverse and unwieldy, it may surprise you to learn that we can break it down into four basic categories of molecules. Possibly even more implausible is the fact that two of these categories of large molecules themselves break down into a surprisingly small number of building blocks. The proteins that make up all of the living things on this planet and ensure their appropriate structure and smooth function consist of only 20 different kinds of building blocks. Nucleic acids, specifically DNA, are even more basic: only four different kinds of molecules provide the materials to build the countless different genetic codes that translate into all the different walking, swimming, crawling, oozing, and/or photosynthesizing organisms that populate the third rock from the Sun.


Big Molecules with Small Building Blocks

The functional groups, assembled into building blocks on backbones of carbon atoms, can be bonded together to yield large molecules that we classify into four basic categories. These molecules, in many different permutations, are the basis for the diversity that we see among living things. They can consist of thousands of atoms, but only a handful of different kinds of atoms form them. It’s like building apartment buildings using a small selection of different materials: bricks, mortar, iron, glass, and wood. Arranged in different ways, these few materials can yield a huge variety of structures.

We encountered functional groups and the SPHONC in Chapter 3. These components form the four categories of molecules of life. These Big Four biological molecules are carbohydrates, lipids, proteins, and nucleic acids. They can have many roles, from giving an organism structure to being involved in one of the millions of processes of living. Let’s meet each category individually and discover the basic roles of each in the structure and function of life.

You have met carbohydrates before, whether you know it or not. We refer to them casually as “sugars,” molecules made of carbon, hydrogen, and oxygen. A sugar molecule has a carbon backbone, usually five or six carbons in the ones we’ll discuss here, but it can be as few as three. Sugar molecules can link together in pairs or in chains or branching “trees,” either for structure or energy storage.

When you look on a nutrition label, you’ll see reference to “sugars.” That term includes carbohydrates that provide energy, which we get from breaking the chemical bonds in a sugar called glucose. The “sugars” on a nutrition label also include those that give structure to a plant, which we call fiber. Both are important nutrients for people.

Sugars serve many purposes. They give crunch to the cell walls of a plant or the exoskeleton of a beetle and chemical energy to the marathon runner. When attached to other molecules, like proteins or fats, they aid in communication between cells. But before we get any further into their uses, let’s talk structure.

The sugars we encounter most in basic biology have their five or six carbons linked together in a ring. There’s no need to dive deep into organic chemistry, but there are a couple of essential things to know to interpret the standard representations of these molecules.

Check out the sugars depicted in the figure. The top-left molecule, glucose, has six carbons, which have been numbered. The sugar to its right is the same glucose, with all but one “C” removed. The other five carbons are still there but are inferred using the conventions of organic chemistry: Anywhere there is a corner, there’s a carbon unless otherwise indicated. It might be a good exercise for you to add in a “C” over each corner so that you gain a good understanding of this convention. You should end up adding in five carbon symbols; the sixth is already given because that is conventionally included when it occurs outside of the ring.

On the left is a glucose with all of its carbons indicated. They’re also numbered, which is important to understand now for information that comes later. On the right is the same molecule, glucose, without the carbons indicated (except for the sixth one). Wherever there is a corner, there is a carbon, unless otherwise indicated (as with the oxygen). On the bottom left is ribose, the sugar found in RNA. The sugar on the bottom right is deoxyribose. Note that at carbon 2 (*), the ribose and deoxyribose differ by a single oxygen.

The lower left sugar in the figure is a ribose. In this depiction, the carbons, except the one outside of the ring, have not been drawn in, and they are not numbered. This is the standard way sugars are presented in texts. Can you tell how many carbons there are in this sugar? Count the corners and don’t forget the one that’s already indicated!

If you said “five,” you are right. Ribose is a pentose (pent = five) and happens to be the sugar present in ribonucleic acid, or RNA. Think to yourself what the sugar might be in deoxyribonucleic acid, or DNA. If you thought, deoxyribose, you’d be right.

The fourth sugar given in the figure is a deoxyribose. In organic chemistry, it’s not enough to know that corners indicate carbons. Each carbon also has a specific number, which becomes important in discussions of nucleic acids. Luckily, we get to keep our carbon counting pretty simple in basic biology. To count carbons, you start with the carbon to the right of the non-carbon corner of the molecule. The deoxyribose or ribose always looks to me like a little cupcake with a cherry on top. The “cherry” is an oxygen. To the right of that oxygen, we start counting carbons, so that corner to the right of the “cherry” is the first carbon. Now, keep counting. Here’s a little test: What is hanging down from carbon 2 of the deoxyribose?

If you said a hydrogen (H), you are right! Now, compare the deoxyribose to the ribose. Do you see the difference in what hangs off of the carbon 2 of each sugar? You’ll see that the carbon 2 of ribose has an –OH, rather than an H. The reason the deoxyribose is called that is because the O on the second carbon of the ribose has been removed, leaving a “deoxyed” ribose. This tiny distinction between the sugars used in DNA and RNA is significant enough in biology that we use it to distinguish the two nucleic acids.

In fact, these subtle differences in sugars mean big differences for many biological molecules. Below, you’ll find a couple of ways that apparently small changes in a sugar molecule can mean big changes in what it does. These little changes make the difference between a delicious sugar cookie and the crunchy exoskeleton of a dung beetle.

Sugar and Fuel

A marathon runner keeps fuel on hand in the form of “carbs,” or sugars. These fuels provide the marathoner’s straining body with the energy it needs to keep the muscles pumping. When we take in sugar like this, it often comes in the form of glucose molecules attached together in a polymer called starch. We are especially equipped to start breaking off individual glucose molecules the minute we start chewing on a starch.

Double X Extra: A monomer is a building block (mono = one) and a polymer is a chain of monomers. With a few dozen monomers or building blocks, we get millions of different polymers. That may sound nutty until you think of the infinity of values that can be built using only the numbers 0 through 9 as building blocks or the intricate programming that is done using only a binary code of zeros and ones in different combinations.

Our bodies then can rapidly take the single molecules, or monomers, into cells and crack open the chemical bonds to transform the energy for use. The bonds of a sugar are packed with chemical energy that we capture to build a different kind of energy-containing molecule that our muscles access easily. Most species rely on this process of capturing energy from sugars and transforming it for specific purposes.

Polysaccharides: Fuel and Form

Plants use the Sun’s energy to make their own glucose, and starch is actually a plant’s way of storing up that sugar. Potatoes, for example, are quite good at packing away tons of glucose molecules and are known to dieticians as a “starchy” vegetable. The glucose molecules in starch are packed fairly closely together. A string of sugar molecules bonded together through dehydration synthesis, as they are in starch, is a polymer called a polysaccharide (poly = many; saccharide = sugar). When the monomers of the polysaccharide are released, as when our bodies break them up, the reaction that releases them is called hydrolysis.

Double X Extra: The specific reaction that hooks one monomer to another in a covalent bond is called dehydration synthesis because in making the bond–synthesizing the larger molecule–a molecule of water is removed (dehydration). The reverse is hydrolysis (hydro = water; lysis = breaking), which breaks the covalent bond by the addition of a molecule of water.

Although plants make their own glucose and animals acquire it by eating the plants, animals can also package away the glucose they eat for later use. Animals, including humans, store glucose in a polysaccharide called glycogen, which is more branched than starch. In us, we build this energy reserve primarily in the liver and access it when our glucose levels drop.

Whether starch or glycogen, the glucose molecules that are stored are bonded together so that all of the molecules are oriented the same way. If you view the sixth carbon of the glucose to be a “carbon flag,” you’ll see in the figure that all of the glucose molecules in starch are oriented with their carbon flags on the upper left.

The orientation of monomers of glucose in polysaccharides can make a big difference in the use of the polymer. The glucoses in the molecule on the top are all oriented “up” and form starch. The glucoses in the molecule on the bottom alternate orientation to form cellulose, which is quite different in its function from starch.

Storing up sugars for fuel and using them as fuel isn’t the end of the uses of sugar. In fact, sugars serve as structural molecules in a huge variety of organisms, including fungi, bacteria, plants, and insects.

The primary structural role of a sugar is as a component of the cell wall, giving the organism support against gravity. In plants, the familiar old glucose molecule serves as one building block of the plant cell wall, but with a catch: The molecules are oriented in an alternating up-down fashion. The resulting structural sugar is called cellulose.

That simple difference in orientation means the difference between a polysaccharide as fuel for us and a polysaccharide as structure. Insects take it step further with the polysaccharide that makes up their exoskeleton, or outer shell. Once again, the building block is glucose, arranged as it is in cellulose, in an alternating conformation. But in insects, each glucose has a little extra added on, a chemical group called an N-acetyl group. This addition of a single functional group alters the use of cellulose and turns it into a structural molecule that gives bugs that special crunchy sound when you accidentally…ahem…step on them.

These variations on the simple theme of a basic carbon-ring-as-building-block occur again and again in biological systems. In addition to serving roles in structure and as fuel, sugars also play a role in function. The attachment of subtly different sugar molecules to a protein or a lipid is one way cells communicate chemically with one another in refined, regulated interactions. It’s as though the cells talk with each other using a specialized, sugar-based vocabulary. Typically, cells display these sugary messages to the outside world, making them available to other cells that can recognize the molecular language.

Lipids: The Fatty Trifecta

Starch makes for good, accessible fuel, something that we immediately attack chemically and break up for quick energy. But fats are energy that we are supposed to bank away for a good long time and break out in times of deprivation. Like sugars, fats serve several purposes, including as a dense source of energy and as a universal structural component of cell membranes everywhere.

Fats: the Good, the Bad, the Neutral

Turn again to a nutrition label, and you’ll see a few references to fats, also known as lipids. (Fats are slightly less confusing that sugars in that they have only two names.) The label may break down fats into categories, including trans fats, saturated fats, unsaturated fats, and cholesterol. You may have learned that trans fats are “bad” and that there is good cholesterol and bad cholesterol, but what does it all mean?

Let’s start with what we mean when we say saturated fat. The question is, saturated with what? There is a specific kind of dietary fat call the triglyceride. As its name implies, it has a structural motif in which something is repeated three times. That something is a chain of carbons and hydrogens, hanging off in triplicate from a head made of glycerol, as the figure shows.  Those three carbon-hydrogen chains, or fatty acids, are the “tri” in a triglyceride. Chains like this can be many carbons long.

Double X Extra: We call a fatty acid a fatty acid because it’s got a carboxylic acid attached to a fatty tail. A triglyceride consists of three of these fatty acids attached to a molecule called glycerol. Our dietary fat primarily consists of these triglycerides.

Triglycerides come in several forms. You may recall that carbon can form several different kinds of bonds, including single bonds, as with hydrogen, and double bonds, as with itself. A chain of carbon and hydrogens can have every single available carbon bond taken by a hydrogen in single covalent bond. This scenario of hydrogen saturation yields a saturated fat. The fat is saturated to its fullest with every covalent bond taken by hydrogens single bonded to the carbons.

Saturated fats have predictable characteristics. They lie flat easily and stick to each other, meaning that at room temperature, they form a dense solid. You will realize this if you find a little bit of fat on you to pinch. Does it feel pretty solid? That’s because animal fat is saturated fat. The fat on a steak is also solid at room temperature, and in fact, it takes a pretty high heat to loosen it up enough to become liquid. Animals are not the only organisms that produce saturated fat–avocados and coconuts also are known for their saturated fat content.

The top graphic above depicts a triglyceride with the glycerol, acid, and three hydrocarbon tails. The tails of this saturated fat, with every possible hydrogen space occupied, lie comparatively flat on one another, and this kind of fat is solid at room temperature. The fat on the bottom, however, is unsaturated, with bends or kinks wherever two carbons have double bonded, booting a couple of hydrogens and making this fat unsaturated, or lacking some hydrogens. Because of the space between the bumps, this fat is probably not solid at room temperature, but liquid.

You can probably now guess what an unsaturated fat is–one that has one or more hydrogens missing. Instead of single bonding with hydrogens at every available space, two or more carbons in an unsaturated fat chain will form a double bond with carbon, leaving no space for a hydrogen. Because some carbons in the chain share two pairs of electrons, they physically draw closer to one another than they do in a single bond. This tighter bonding result in a “kink” in the fatty acid chain.

In a fat with these kinks, the three fatty acids don’t lie as densely packed with each other as they do in a saturated fat. The kinks leave spaces between them. Thus, unsaturated fats are less dense than saturated fats and often will be liquid at room temperature. A good example of a liquid unsaturated fat at room temperature is canola oil.

A few decades ago, food scientists discovered that unsaturated fats could be resaturated or hydrogenated to behave more like saturated fats and have a longer shelf life. The process of hydrogenation–adding in hydrogens–yields trans fat. This kind of processed fat is now frowned upon and is being removed from many foods because of its associations with adverse health effects. If you check a food label and it lists among the ingredients “partially hydrogenated” oils, that can mean that the food contains trans fat.

Double X Extra: A triglyceride can have up to three different fatty acids attached to it. Canola oil, for example, consists primarily of oleic acid, linoleic acid, and linolenic acid, all of which are unsaturated fatty acids with 18 carbons in their chains.

Why do we take in fat anyway? Fat is a necessary nutrient for everything from our nervous systems to our circulatory health. It also, under appropriate conditions, is an excellent way to store up densely packaged energy for the times when stores are running low. We really can’t live very well without it.

Phospholipids: An Abundant Fat

You may have heard that oil and water don’t mix, and indeed, it is something you can observe for yourself. Drop a pat of butter–pure saturated fat–into a bowl of water and watch it just sit there. Even if you try mixing it with a spoon, it will just sit there. Now, drop a spoon of salt into the water and stir it a bit. The salt seems to vanish. You’ve just illustrated the difference between a water-fearing (hydrophobic) and a water-loving (hydrophilic) substance.

Generally speaking, compounds that have an unequal sharing of electrons (like ions or anything with a covalent bond between oxygen and hydrogen or nitrogen and hydrogen) will be hydrophilic. The reason is that a charge or an unequal electron sharing gives the molecule polarity that allows it to interact with water through hydrogen bonds. A fat, however, consists largely of hydrogen and carbon in those long chains. Carbon and hydrogen have roughly equivalent electronegativities, and their electron-sharing relationship is relatively nonpolar. Fat, lacking in polarity, doesn’t interact with water. As the butter demonstrated, it just sits there.

There is one exception to that little maxim about fat and water, and that exception is the phospholipid. This lipid has a special structure that makes it just right for the job it does: forming the membranes of cells. A phospholipid consists of a polar phosphate head–P and O don’t share equally–and a couple of nonpolar hydrocarbon tails, as the figure shows. If you look at the figure, you’ll see that one of the two tails has a little kick in it, thanks to a double bond between the two carbons there.

Phospholipids form a double layer and are the major structural components of cell membranes. Their bend, or kick, in one of the hydrocarbon tails helps ensure fluidity of the cell membrane. The molecules are bipolar, with hydrophilic heads for interacting with the internal and external watery environments of the cell and hydrophobic tails that help cell membranes behave as general security guards.

The kick and the bipolar (hydrophobic and hydrophilic) nature of the phospholipid make it the perfect molecule for building a cell membrane. A cell needs a watery outside to survive. It also needs a watery inside to survive. Thus, it must face the inside and outside worlds with something that interacts well with water. But it also must protect itself against unwanted intruders, providing a barrier that keeps unwanted things out and keeps necessary molecules in.

Phospholipids achieve it all. They assemble into a double layer around a cell but orient to allow interaction with the watery external and internal environments. On the layer facing the inside of the cell, the phospholipids orient their polar, hydrophilic heads to the watery inner environment and their tails away from it. On the layer to the outside of the cell, they do the same.
As the figure shows, the result is a double layer of phospholipids with each layer facing a polar, hydrophilic head to the watery environments. The tails of each layer face one another. They form a hydrophobic, fatty moat around a cell that serves as a general gatekeeper, much in the way that your skin does for you. Charged particles cannot simply slip across this fatty moat because they can’t interact with it. And to keep the fat fluid, one tail of each phospholipid has that little kick, giving the cell membrane a fluid, liquidy flow and keeping it from being solid and unforgiving at temperatures in which cells thrive.

Steroids: Here to Pump You Up?

Our final molecule in the lipid fatty trifecta is cholesterol. As you may have heard, there are a few different kinds of cholesterol, some of which we consider to be “good” and some of which is “bad.” The good cholesterol, high-density lipoprotein, or HDL, in part helps us out because it removes the bad cholesterol, low-density lipoprotein or LDL, from our blood. The presence of LDL is associated with inflammation of the lining of the blood vessels, which can lead to a variety of health problems.

But cholesterol has some other reasons for existing. One of its roles is in the maintenance of cell membrane fluidity. Cholesterol is inserted throughout the lipid bilayer and serves as a block to the fatty tails that might otherwise stick together and become a bit too solid.

Cholesterol’s other starring role as a lipid is as the starting molecule for a class of hormones we called steroids or steroid hormones. With a few snips here and additions there, cholesterol can be changed into the steroid hormones progesterone, testosterone, or estrogen. These molecules look quite similar, but they play very different roles in organisms. Testosterone, for example, generally masculinizes vertebrates (animals with backbones), while progesterone and estrogen play a role in regulating the ovulatory cycle.

Double X Extra: A hormone is a blood-borne signaling molecule. It can be lipid based, like testosterone, or short protein, like insulin.


As you progress through learning biology, one thing will become more and more clear: Most cells function primarily as protein factories. It may surprise you to learn that proteins, which we often talk about in terms of food intake, are the fundamental molecule of many of life’s processes. Enzymes, for example, form a single broad category of proteins, but there are millions of them, each one governing a small step in the molecular pathways that are required for living.

Levels of Structure

Amino acids are the building blocks of proteins. A few amino acids strung together is called a peptide, while many many peptides linked together form a polypeptide. When many amino acids strung together interact with each other to form a properly folded molecule, we call that molecule a protein.

For a string of amino acids to ultimately fold up into an active protein, they must first be assembled in the correct order. The code for their assembly lies in the DNA, but once that code has been read and the amino acid chain built, we call that simple, unfolded chain the primary structure of the protein.

This chain can consist of hundreds of amino acids that interact all along the sequence. Some amino acids are hydrophobic and some are hydrophilic. In this context, like interacts best with like, so the hydrophobic amino acids will interact with one another, and the hydrophilic amino acids will interact together. As these contacts occur along the string of molecules, different conformations will arise in different parts of the chain. We call these different conformations along the amino acid chain the protein’s secondary structure.

Once those interactions have occurred, the protein can fold into its final, or tertiary structure and be ready to serve as an active participant in cellular processes. To achieve the tertiary structure, the amino acid chain’s secondary interactions must usually be ongoing, and the pH, temperature, and salt balance must be just right to facilitate the folding. This tertiary folding takes place through interactions of the secondary structures along the different parts of the amino acid chain.

The final product is a properly folded protein. If we could see it with the naked eye, it might look a lot like a wadded up string of pearls, but that “wadded up” look is misleading. Protein folding is a carefully regulated process that is determined at its core by the amino acids in the chain: their hydrophobicity and hydrophilicity and how they interact together.

In many instances, however, a complete protein consists of more than one amino acid chain, and the complete protein has two or more interacting strings of amino acids. A good example is hemoglobin in red blood cells. Its job is to grab oxygen and deliver it to the body’s tissues. A complete hemoglobin protein consists of four separate amino acid chains all properly folded into their tertiary structures and interacting as a single unit. In cases like this involving two or more interacting amino acid chains, we say that the final protein has a quaternary structure. Some proteins can consist of as many as a dozen interacting chains, behaving as a single protein unit.

A Plethora of Purposes

What does a protein do? Let us count the ways. Really, that’s almost impossible because proteins do just about everything. Some of them tag things. Some of them destroy things. Some of them protect. Some mark cells as “self.” Some serve as structural materials, while others are highways or motors. They aid in communication, they operate as signaling molecules, they transfer molecules and cut them up, they interact with each other in complex, interrelated pathways to build things up and break things down. They regulate genes and package DNA, and they regulate and package each other.

As described above, proteins are the final folded arrangement of a string of amino acids. One way we obtain these building blocks for the millions of proteins our bodies make is through our diet. You may hear about foods that are high in protein or people eating high-protein diets to build muscle. When we take in those proteins, we can break them apart and use the amino acids that make them up to build proteins of our own.

Nucleic Acids

How does a cell know which proteins to make? It has a code for building them, one that is especially guarded in a cellular vault in our cells called the nucleus. This code is deoxyribonucleic acid, or DNA. The cell makes a copy of this code and send it out to specialized structures that read it and build proteins based on what they read. As with any code, a typo–a mutation–can result in a message that doesn’t make as much sense. When the code gets changed, sometimes, the protein that the cell builds using that code will be changed, too.

Biohazard!The names associated with nucleic acids can be confusing because they all start with nucle-. It may seem obvious or easy now, but a brain freeze on a test could mix you up. You need to fix in your mind that the shorter term (10 letters, four syllables), nucleotide, refers to the smaller molecule, the three-part building block. The longer term (12 characters, including the space, and five syllables), nucleic acid, which is inherent in the names DNA and RNA, designates the big, long molecule.

DNA vs. RNA: A Matter of Structure

DNA and its nucleic acid cousin, ribonucleic acid, or RNA, are both made of the same kinds of building blocks. These building blocks are called nucleotides. Each nucleotide consists of three parts: a sugar (ribose for RNA and deoxyribose for DNA), a phosphate, and a nitrogenous base. In DNA, every nucleotide has identical sugars and phosphates, and in RNA, the sugar and phosphate are also the same for every nucleotide.

So what’s different? The nitrogenous bases. DNA has a set of four to use as its coding alphabet. These are the purines, adenine and guanine, and the pyrimidines, thymine and cytosine. The nucleotides are abbreviated by their initial letters as A, G, T, and C. From variations in the arrangement and number of these four molecules, all of the diversity of life arises. Just four different types of the nucleotide building blocks, and we have you, bacteria, wombats, and blue whales.

RNA is also basic at its core, consisting of only four different nucleotides. In fact, it uses three of the same nitrogenous bases as DNA–A, G, and C–but it substitutes a base called uracil (U) where DNA uses thymine. Uracil is a pyrimidine.

DNA vs. RNA: Function Wars

An interesting thing about the nitrogenous bases of the nucleotides is that they pair with each other, using hydrogen bonds, in a predictable way. An adenine will almost always bond with a thymine in DNA or a uracil in RNA, and cytosine and guanine will almost always bond with each other. This pairing capacity allows the cell to use a sequence of DNA and build either a new DNA sequence, using the old one as a template, or build an RNA sequence to make a copy of the DNA.

These two different uses of A-T/U and C-G base pairing serve two different purposes. DNA is copied into DNA usually when a cell is preparing to divide and needs two complete sets of DNA for the new cells. DNA is copied into RNA when the cell needs to send the code out of the vault so proteins can be built. The DNA stays safely where it belongs.

RNA is really a nucleic acid jack-of-all-trades. It not only serves as the copy of the DNA but also is the main component of the two types of cellular workers that read that copy and build proteins from it. At one point in this process, the three types of RNA come together in protein assembly to make sure the job is done right.

 By Emily Willingham, DXS managing editor 
This material originally appeared in similar form in Emily Willingham’s Complete Idiot’s Guide to College Biology

Childbirth and C-sections in pre-modern times

[Today's post first appeared at Dr. Kristina Killgrove's blog, Powered by Osteons. Kristina is a bioarchaeologist who studies the skeletons of ancient Romans to learn more about how they lived. Her biography at her blog begins, "When your life's passion is to study dead Romans, you often get asked for your 'origin story,' something that explains a long, abiding and, frankly, slightly creepy love for skeletons." Now that you undoubtedly want to know more, read the rest of her bio here, and then read below to learn why childbirth is so difficult and what the archaeological record has to tell us about outcomes for mother and child in the ancient world. For more about Kristina and her work, you can see her academic Website at  and find out about her latest research project at You can also find her at her G+ page and on Twitter as @BoneGirlPhD.]

Basically since we started walking upright, childbirth has been difficult for women.  Evolution selected for larger and larger brains in our hominin ancestors such that today our newborns have heads roughly 102% the size of the mother’s pelvic inlet width (Rosenberg 1992).

Yes, you read that right. Our babies’ heads are actually two percent larger than our skeletal anatomy

Fetal head and mother’s pelvic inlet width
Photo credit:

Obviously, we’ve also evolved ways to get those babies out.  Biologically, towards the end of pregnancy, a hormone is released that weakens the cartilage of the pelvic joints, allowing the bones to spread; and the fetus itself goes through a complicated movement to make its way down the pelvic canal, with its skull bones eventually sliding around and overlapping to get through the pelvis.  Culturally, we have another way to deliver these large babies: the so-calledcaesarean section.

Up until the 20th century, childbirth was dangerous.  Even today, in some less developed countries, roughly 1 maternal death occurs for every 100 live births, most of those related to obstructed labor or hemorrhage (WHO Fact Sheet 2010).  If we project these figures back into the past, millions of women must have died during or just after childbirth over the last several millennia.  You would think, then, that the discovery of childbirth-related burial – that is, of a woman with a fetal skeleton within her pelvis – would be common in the archaeological record.  It’s not.

Archaeological Evidence of Death in Childbirth

Two recent articles in the International Journal of Osteoarchaeology start the exact same way, by explaining that “despite this general acceptance of the vulnerability of young females in the past, there are very few cases of pregnant woman (sic) reported from archaeological contexts” (Willis & Oxenham, In Press) and ”archaeological evidence for such causes of death is scarce and therefore unlikely to reflect the high incidence of mortality during and after labour” (Cruz & Codinha 2010:491).

The examples of burials of pregnant women that tend to get cited include two from Britain (both published in the 1970s), four from Scandinavia (published in the 1970s and 1980s), three from North America (published in the 1980s), one from Australia (1980s), one from Israel (1990s), six from Spain (1990s and 2000s), one from Portugal (2010), and one from Vietnam (2011) (most of these are cited in Willis & Oxenham).  Additionally, I found some unpublished reports: a skeleton from Egypt, a body from the Yorkshire Wolds in England, and a skeleton from England.

The images of these burials are impressive: even more than child skeletons, these tableaux are pathos-triggering, they’re snapshots of two lives cut short because of an evolutionary trade-off.

The wide range of dates and geographical areas illustrated in the slideshow demonstrates quite clearly that death of the mother-fetus dyad is a biological consequence of being human.  But what we have from archaeological excavations is still fewer than two dozen examples of possible childbirth-related deaths from all of human history.

Where are all the mother-fetus burials?

As with any bioarchaeological question, there are a number of reasons that we may or may not find evidence of practices we know to have existed in the past.  Some key issues at play in recovering evidence of death in childbirth include:
  • Archaeological Theory and Methodology.  From the dates of discovery of maternal-fetal death cited above, it’s obvious that these examples weren’t discovered until the 1970s.  Why the 70s?  It could be that the rise of feminist archaeology focused new attention on the graves of females, with archaeologists realizing the possibility that they would find maternal-fetal burials.  Or it could be that the methods employed got better around this time: archaeologists began to sift dirt with smaller mesh screens and float it for small particles like seeds and fetal bones.
  • Death at Different Times.  Although some women surely perished in the middle of childbirth, along with a fetus that was obstructed, in many cases delivery likely occurred, after which the mother, fetus, or both died.  In modern medical literature, there are direct maternal deaths (complications of pregnancy, delivery, or recovery) and indirect maternal deaths (pregnancy-related death of a woman with preexisting or newly arisen health problems) recorded up to about 42 days postpartum.  An infection related to delivery or severe postpartum hemorraging could easily have killed a woman in antiquity, leaving a viable newborn.  Similarly, newborns can develop infections and other conditions once outside the womb, and infant mortality was high in preindustrial societies.  With a difference between the time of death of the mother and child, a bioarchaeologist can’t say for sure that these deaths were related to childbirth.  Even finding a female skeleton with a fetal skeleton inside it is not always a clear example, as there are forensic cases of coffin birth or postmortem fetal extrusion, when the non-viable fetus is spontaneously delivered after the death of the mother.
  • Cultural Practices.  Another condition of being human is the ability to modify and mediate our biology through culture.  So the final possibility for the lack of mother-fetus burials is a specific society’s cultural practices in terms of childbirth and burial.  In the case of complicated childbirth (called dystocia in the medical literature), this is done through caesarean section (or C-section), a surgical procedure that dates back at least to the origins of ancient Rome.

Cultural Interventions in Childbirth

It’s often assumed that the term caesarean/cesarean section comes from the manner of birth ofJulius Caesar, but it seems that the Roman author Pliny may have just made this up. The written record of the surgical practice originated as the Lex Regia (royal law) with the second king of Rome, Numa Pompilius (c. 700 BC), and was renamed the Lex Caesarea (imperial law) during the Empire.  The law is passed down through Justinian’s Digest (11.8.2) and reads:

Negat lex regia mulierem, quae praegnas mortua sit, humari, antequam partus ei excidatur: qui contra fecerit, spem animantis cum gravida peremisse videtur.

The royal law forbids burying a woman who died pregnant until her offspring has been excised from her; anyone who does otherwise is seen to have killed the hope of the offspring with the pregnant woman. [Translation mine]
Example of Roman gynaecological equipment: speculum
From the House of the Surgeon, Pompeii (1st c AD)
Photo credit: UVa Health Sciences Library

There’s discussion as to whether this law was instituted for religious reasons or for the more practical reason of increasing the population of tax-paying citizens.  In spite of this law, though, there isn’t much historical evidence of people being born by C-section.  Many articles claim the earliest attested C-section as having produced Gorgias, an orator from Sicily, in 508 BC (e.g., Boley 1991), but Gorgias wasn’t actually born until 485 BC and I couldn’t find a confirmatory source for this claim.  Pliny, however, noted that Scipio Africanus, a celebrated Roman general in the Second Punic War, was born by C-section (Historia Naturalis VII.7); if this fact is correct, the earliest confirmation that the surgery could produce viable offspring dates to 236 BC.

This practice in the Roman world is not the same as our contemporary idea of C-section.  That is, the mother was not expected to survive and, in fact, most of the C-sections in Roman times were likely carried out following the death of the mother.  Until about the 1500s, when the French physician François Rousset broke with tradition and advocated performing C-sections on living women, the procedure was performed only as a last-ditch effort to save the neonate.  Some women definitely survived C-sections from the 16th to 19th centuries, but it was still a risky procedure that could easily lead to complications like endometritis or other infection.  Following advances in antibiotics around 1940, though, C-sections became more common because, most importantly, they were much more survivable.

Caesarean Sections and Roman Burials

Roman relief showing a birthing scene
Tomb of a Midwife (Tomb 100), Isola Sacra
Photo credit: magistrahf on Flickr

In spite of the Romans’ passion for recordkeeping, there’s very little evidence of C-sections.  It’s unclear how religiously the Lex Regia/Caesarea was followed in Roman times, which means it’s unclear how often the practice of C-section occurred.  Would all women have been subject to these laws?  Just the elite or just citizens?  How often did the section result in a viable newborn?  Who performed the surgery?  It probably wasn’t a physician (since men didn’t generally attend births), but a midwife wouldn’t have been trained to do it either (Turfa 1994).

Whereas we can supplement the historical record with bioarchaeological evidence to understand Romans’ knowledge of anatomy, their consumption of lead sugar, or the practice of crucifixion, this isn’t possible with C-sections – the surgery is done in soft tissue only, meaning we’d have to find a mummy to get conclusive evidence of an ancient C-section.

We can make the hypothesis, though, that because of the Lex Regia/Caesarea, we should findno evidence in the Roman world of a woman buried with a fetus still inside her.  This hypothesis, though, is quickly negated by two reported cases – one from Kent in the Romano-British period and one from Jerusalem in the 4th century AD. The burial from Kent hasn’t been published, although there is a photograph in the slide show above.

Interestingly, the Jerusalem find was studied and reported by Joe Zias, who also analyzed theonly known case of crucifixion to date.  Zias and colleagues report on the find in Nature(1993) and in an edited volume (1995), but their primary goal was to disseminate information about the presence of cannabis in the tomb (and its supposed role in facilitating childbirth), so there’s no picture and the information about the skeletons is severely lacking:

We found the skeletal remains of a girl (sic) aged about 14 at death in an undisturbed family burial tomb in Beit Shemesh, near Jerusalem.  Three bronze coins found in the tomb dating to AD 315-392 indicate that the tomb was in use during the fourth century AD.  We found the skeletal remains of a full-term (40-week) fetus in the pelvic area of the girl, who was lying on her back in an extended position, apparently in the last stages of pregnancy or giving birth at the time of her death… It seems likely that the immature pelvic structure through which the full-term fetus was required to pass was the cause of death in this case, due to rupture of the cervix and eventual haemorrhage (Zias et al. 1993:215).

Both Roman-era examples involve young women, and it is quite interesting that they were already fertile.  Age at menarche in the Roman world depended on health, which in turn depended on status, but it’s generally accepted that menarche happened around 14-15 years old and that fertility lagged behind until 16-17, meaning for the majority of the Roman female population, first birth would not occur until at least 17-19 years of age (Hopkins 1965, Amundsen & Diers 1969).  These numbers have led demographers like Tim Parkin (1992:104-5) to note that pregnancy was likely not a major contributor to premature death among Roman women.  But the female pelvis doesn’t reach skeletal maturity until the late teens or early 20s, so complications from the incompatibility in pelvis size versus fetal head size are not uncommon in teen pregnancies, even today (Gilbert et al. 2004).

More interesting than the young age at parturition is the fact that both of these young women were likely buried with their fetuses still inside them, in direct violation of the Lex Caesarea.  So it remains unclear whether this law was ever prosecuted, or if the application of the law varied based on location (these young women were both from the provinces), social status (both young women were likely higher status), or time period.  Why wasn’t medical intervention, namely C-section, attempted on these young women?  It’s possible that further context clues from the cemeteries and associated settlements could give us more information about medical practices in these specific locales, but neither the Zias articles nor the Kent report make this information available.

Childbirth – Biological or Cultural?

Childbirth is both a biological and a cultural process.  While biological variation is consistent across all human populations, the cultural processes that can facilitate childbirth are quite varied.  The evidence that bioarchaeologists use to reconstruct childbirth in the past includes skeletons of mothers and their fetuses; historical records of births, deaths, and interventions; artifacts that facilitate delivery; and context clues from burials.  The brief case study of death in childbirth in the Roman world further shows that history alone is insufficient to understand the process of childbirth, the complications inherent in it, and the form of burial that results.  In order to develop a better understanding of childbirth through time, it’s imperative that archaeologists pay close attention when excavating graves, meticulously document their findings, and publish any evidence of death in childbirth.

Further Reading:

This post was chosen as an Editor's Selection for ResearchBlogging.orgD.W. Amundsen, & C.J. Diers (1969). The age of menarche in Classical Greece and Rome. Human Biology, 41 (1), 125-132. PMID: 4891546.

J.P. Boley (1991). The history of caesarean section. Canadian Medical Association Journal, 145 (4), 319-322. [PDF]

S. Crawford (2007). Companions, co-incidences or chattels? Children in the early Anglo-Saxon multiple burial ritual.  In Children, Childhood & Society, S. Crawford and G. Shepherd, eds.  BAR International Series 1696, Chapter 8. [PDF]

C. Cruz, & S. Codinha (2010). Death of mother and child due to dystocia in 19th century Portugal. International Journal of Osteoarchaeology, 20, 491-496. DOI: 10.1002/oa.1069.

W. Gilbert, D. Jandial, N. Field, P. Bigelow, & B. Danielsen (2004). Birth outcomes in teenage pregnancies. Journal of Maternal-Fetal and Neonatal Medicine, 16 (5), 265-270. DOI:10.1080/14767050400018064.

K. Hopkins (1965). The age of Roman girls at marriage. Population Studies, 18 (3), 309-327. DOI: 10.2307/2173291.

E. Lasso, M. Santos, A. Rico, J.V. Pachar, & J. Lucena (2009). Postmortem fetal extrusion. Cuadernos de Medicina Forense, 15 (55), 77-81. [HTML - Warning: Graphic images!]

T. Parkin (1992).  Demography and Roman society.  Baltimore: Johns Hopkins University Press.

K. Rosenberg (1992). The evolution of modern human childbirth. American Journal of Physical Anthropology, 35 (S15), 89-124. DOI: 10.1002/ajpa.1330350605
J.M. Turfa (1994). Anatomical votives and Italian medical traditions. In: Murlo and the Etruscans, edited by R.D. DePuma and J.P. Small. University of Wisconsin Press.

C. Wells (1975). Ancient obstetric hazards and female mortality. Bulletin of the New York Academy of Medicine, 51 (11), 1235-49. PMID: 1101997.

A. Willis, & M. Oxenham (In press). A Case of Maternal and Perinatal Death in Neolithic Southern Vietnam, c. 2100-1050 BCE. International Journal of Osteoarchaeology, 1-9. DOI:10.1002/oa.1296.

J. Zias, H. Stark, J. Seligman, R. Levy, E. Werker, A. Breuer & R. Mechoulam (1993). Early medical use of cannabis. Nature, 363 (6426), 215-215. DOI: 10.1038/363215a0.

J. Zias (1995). Cannabis sativa (hashish) as an effective medication in antiquity: the anthropological evidence. In: S. Campbell & A. Green, eds., The Archaeology of Death in the Ancient Near East, pp. 232-234.

Note: Thanks to Marta Sobur for helping me gain access to the Zias 1995 article, and thanks toSarah Bond for helping me track down the Justinian reference.

Miscarriage: When a beginning is not a beginning

The “Pregnant Woman” statue
at Ireland Park, Toronto, by Rowan Gillespie

Photo credit: Benson Kua.
[Editor's note: We are pleased to be able to run this post by Dr. Kate Clancy that first appeared at Clancy's Scientific American blog, the wonderful Context and Variation. Clancy is an Assistant Professor of Anthropology at the University of Illinois. She studies the evolutionary medicine of women’s reproductive physiology, and blogs about her field, the evolution of human behavior and issues for women in science. You can follow her on Twitter--which we strongly recommend, particularly if you're interested in human behavior, evolutionary medicine, and ladybusiness--@KateClancy.]
Over the course of my training to become a biological anthropologist with a specialty in women’s reproductive ecology and life history theory, or ladybusiness expert, I have learned a lot about miscarriage. Only it wasn’t miscarriage, it was spontaneous abortion. Except that some didn’t like the term spontaneous abortion and used intrauterine mortality (Wood, 1994). Or fetal loss. Fetal loss is probably the most common.
There is also pregnancy loss (Holman and Wood, 2001). You can use that term, too. Oh, or a Continue reading

The Vampire of Venice Returns, or What Is that Brick Doing in that Skull’s Mouth?

[We're delighted to feature another post from our favorite bioarchaeologist, Kristina Killgrove, who first blogged about the Vampire of Venice at her site, Powered by Osteons. Kristina previously told DSXers about the history of childbirth and caesarian sections.]
It seems like every spring there is renewed coverage of a partial skeleton that was found on the island of Lazaretto Nuovo (one of two 15th-16th century leper colonies near Venice) in 2009. I’ve never covered it here, but since I was alerted to an airing of a documentary about the skeleton on Italian TV this week, I thought it may be time to track the progress of the so-called Vampire of Venice (“il vampiro di Venezia” in Italian, and not to be confused with a similarly named Dr. Who episode).

Immediately upon excavating this individual from what appears to have been a plague cemetery dating to 1576, archaeologists realized that something was very, very different about the burial treatment: there was a heavy brick placed in the person’s mouth. [BBC news video clip, March 13, 2009] A photograph from National Geographic [March 10, 2009 news story] prior to complete excavation:

During the 16th century, as plague raged around Europe, many people were buried hastily, in mass graves. Without modern forensic knowledge, people didn’t understand how the body decomposed. For example, as the bacteria present in the gut start consuming the internal organs, fluid can be produced and chest cavities can bulge and sink, making the bodies seem to sigh; as the skin dries out and recedes from the fingernails, they can appear to grow longer; and as the muscles go through stages of rigor mortis, bodies can seem to move. Mass plague graves were often reopened to inter more individuals, so seeing corpses that had changed since burial confused and scared the living.

The National Geographic article suggests that a plague victim who was buried in a shroud may have emitted some bodily fluids, staining and dissolving the shroud, making the undertakers think that the person was undead: a vampire who transmitted plague through this fluid. The way to prevent the vampire from continuing to spread the plague was to insert a brick or stone into the person’s mouth. Archaeologists believe that this individual suffered that fate; however, it’s unclear to me if the brick was placed at the time of burial or at a later time, such as on reopening of the grave to bury more people. [More photos of the excavation at KataWeb (labels in Italian)]

A year after excavation, the Vampire of Venice got her own documentary in the National Geographic series Mysterious Science, in an episode entitled “Vampire Forensics” (really, NatGeo? I expect more from you than this sort of pandering). You can actually watch the entire documentary in segments on YouTube: Part 1Part 2Part 3Part 4, and Part 5. (Warning: Part 5 has some very graphic forensic images, which may be re-creations but which are even more graphic than what I normally show my forensic anthropology students.) Or you can watch this less gruesome preview from National Geographic’s website:

Based on anthropological analysis, the Vampire of Venice was, surprisingly, an older woman in her 60s. Forensic specialists have reconstructed her face using her skull and the knowledge of her sex, age, and European ancestry [National Geographic, February 26, 2010]:

Using carbon and nitrogen isotope analysis of a bit of postcranial skeleton, anthropologists discovered that she ate a lot of vegetables and grains, likely a lower-class diet. I’m assuming from reading between the lines of the NatGeo article that C/N isotope analysis of a rib was done, which would have given them information about the protein component of the diet and thus told them that she didn’t eat a lot of meat or fish. Since it wasn’t remarked on and since DNA analysis said she was European, I’m also guessing the C isotope analysis revealed C3 plant consumption (wheat and barley, e.g.).

The discovery of a skeleton of an older female in a 16th century Italian plague cemetery with an anomalous burial practice that correlates to superstitions about disease and the occult is extremely cool, whether or not she was “il vampiro di Venezia”. Italian archaeologists and anthropologists are learning both about the biology of plague victims and about their cultural explanations for disease prior to modern germ theory. The analysis of this individual is an excellent example of using historical records and biological remains to understand what life was like centuries ago. I wish that National Geographic hadn’t resorted to the “Vampire Forensics” title and that they hadn’t resorted to blatant pandering and sensationalism in making the documentary, because there is some very good science behind the story. But perhaps it’s the marriage of vampires and forensic science that explains why this story keeps surfacing in my news feed and why friends and colleagues keep sending me links to it.

Footnote (7/2/12) – Since I originally wrote this post, a bit of an argument has been kicked off in the academic literature about this burial.  The discovery was published in 2010 in the Journal of Forensic Sciences by Nuzzolese and Borrini, although the article seems to be a conference paper rather than a full-length explication of the find.  It’s in this brief communication that Nuzzolese and Borrini lay out their argument that the community may have thought of and treated this woman (at least in death) as a vampire.

A few months ago, another group of Italian bioarchaeologists, led by Simona Minozzi, wrote acommentary about this also in the Journal of Forensic Sciences.  In essence, they argue that the brick in the mouth, the misaligned collarbones, and other aspects of Nuzzolese and Borrini’s case are simply taphonomic – that is, normal processes that happen by chance after death and burial.  They also take issue with Nuzzolese and Borrini’s interpretation of the historical record as well.  Minozzi and colleagues don’t buy the vampire interpretation at all, and go so far in this LiveScience article as saying that Borrini is making it up to bring more attention to the perpetually underfunded state of Italian bioarchaeology.

I don’t know if Minozzi or others have been able to take a look at the skeleton itself, but I’m not sure it would help since most of the vampire interpretation lies in the context of the burial rather than in the biological elements.  And as we all know, as soon as you excavate something, you destroy the context forever.  We may never solve the mystery of whether or not this woman was considered a vampire, but the arguments about the interpretation indicate that researchers need to be meticulous and seek additional input from knowledgeable colleagues before committing on paper to an interpretation as dramatic as “vampire.”

Biology Xplainer: Evolution and how it happens

Evolution: a population changes over time
First of all, in the context of science, you should never speak of evolution as a “theory.” There is no theory about whether or not evolution happens. It is a fact.

Scientists have, however, developed tested theories about how evolution happens. Although several proposed and tested processes or mechanisms exist, the most prominent and most studied, talked about, and debated, is Charles Darwin’s idea that the choices of nature guide these changes. The fame and importance of his idea, natural selection, has eclipsed the very real existence of other ways that populations can change over time.

Evolution in the biological sense does not occur in individuals, and the kind of evolution we’re talking about here isn’t about life’s origins. Evolution must happen at least at the populationlevel. In other words, it takes place in a group of existing organisms, members of the same species, often in a defined geographical area.

We never speak of individuals evolving in the biological sense. The population, a group of individuals of the same species, is the smallest unit of life that evolves.

To get to the bottom of what happens when a population changes over time, we must examine what’s happening to the gene combinations of the individuals in that population. The most precise way to talk about evolution in the biological sense is to define it as “a change in the allele frequency of a population over time.” A gene, which contains the code for a protein, can occur in different forms, or alleles. These different versions can mean that the trait associated with that protein can differ among individuals. Thanks to mutations, a gene for a trait can exist in a population in these different forms. It’s like having slightly different recipes for making the same cake, each producing a different version of the cake, except in this case, the “cake” is a protein.
Natural selection: One way evolution happens

Charles Darwin, a smart, thoughtful,
observant man. Via Wikimedia.
Charles Darwin, who didn’t know anything about alleles or even genes (so now you know more than he did on that score), understood from his work and observations that nature makes certain choices, and that often, what nature chooses in specific individuals turns up again in the individuals’ offspring. He realized that these characteristics that nature was choosing must pass to some offspring. This notion of heredity–that a feature encoded in the genes can be transmitted to your children–is inherent now in the theory of natural selection and a natural one for most people to accept. In science, an observable or measurable feature or characteristic is called a phenotype, and the genes that are the code for it are called its genotype. The color of my eyes (brown) is a phenotype, and the alleles of the eye color genes I have are the genotype.

What is nature selecting any individual in a population to do? In the theory of natural selection, nature chooses individuals that fit best into the current environment to pass along their “good-fit” genes, either through reproduction or indirectly through supporting the reproducer. Nature chooses organisms to survive and pass along those good-fit genes, so they have greater fitness.

Fitness is an evolutionary concept related to an organism’s reproductive success, either directly (as a parent) or indirectly (say, as an aunt or cousin). It is measured technically based on the proportion of an individual’s alleles that are represented in the next generation. When we talk about “fitness” and “the fittest,” remember that fittest does not mean strong. It relates more to a literal fit, like a square peg in a square hole, or a red dot against a red background. It doesn’t matter if the peg or dot is strong, just whether or not it fits its environment.

One final consideration before we move onto a synthesis of these ideas about differences, heredity, and reproduction: What would happen if the population were uniformly the same genetically for a trait? Well, when the environment changed, nature would have no choice to make. Without a choice, natural selection cannot happen–there is nothing to select. And the choice has to exist already; it does not typically happen in response to a need that the environment dictates. Usually, the ultimate origin for genetic variation–which underlies this choice–is mutation, or a change in a DNA coding sequence, the instructions for building a protein.

Don’t make the mistake of saying that an organism adapts by mutating in response to the environment. The mutations (the variation) must already be present for nature to make a choice based on the existing environment.

The Modern Synthesis

When Darwin presented his ideas about nature’s choices in an environmental context, he did so in a book with a very long title that begins, On the Origin of Species by Means of Natural Selection. Darwinknew his audience and laid out his argument clearly and well, with one stumbling block: How did all that heredity stuff actually work?

We now know–thanks to a meticulous scientist named Gregor Mendel (who also was a monk), our understanding of reproductive cell division, and modern genetics–exactly how it all works. Our traits–whether winners or losers in the fitness Olympics–have genes that determine them. These genes exist in us in pairs, and these pairs separate during division of our reproductive cells so that our offspring receive one member or the other of the pair. When this gene meets its coding partner from the other parent’s cell at fertilization, a new gene pair arises. This pairing may produce a similar outcome to one of the parents or be a novel combination that yields some new version of a trait. But this separating and pairing is how nature keeps things mixed up, setting up choices for selection.

Ernst Mayr, via PLoS.
With a growing understanding in the twentieth century of genetics and its role in evolution by means of natural selection, a great evolutionary biologist named Ernst Mayr (1904–2005) guided a meshing of genetics and evolution (along with other brilliant scientists including Theodosius Dobzhansky, George Simpson, and R.A. Fisher) into what is called The Modern Synthesis. This work encapsulates (dare I say, “synthesizes?”) concisely and beautifully the tenets of natural selection in the context of basic genetic inheritance. As part of his work, Mayr distilled Darwin’s ideas into a series of facts and inferences.

Facts and Inferences

Mayr’s distillation consists of five facts and three inferences, or conclusions, to draw from those facts.
  1. The first fact is that populations have the potential to increase exponentially. A quick look at any graph of human population growth illustrates that we, as a species, appear to be recognizing that potential. For a less successful example, consider the sea turtle. You may have seen the videos of the little turtle hatchlings valiantly flippering their way across the sand to the sea, cheered on by the conservation-minded humans who tended their nests. What the cameras usually don’t show is that the vast majority of these turtle offspring will not live to reproduce. The potential for exponential growth is there, based on number of offspring produced, but…it doesn’t happen.
  2. The second fact is that not all offspring reproduce, and many populations are stable in size. See “sea turtles,” above.
  3. The third fact is that resources are limited. And that leads us to our first conclusion, or inference: there is a struggle among organisms for nutrition, water, habitat, mates, parental attention…the various necessities of survival, depending on the species. The large number of offspring, most of which ultimately don’t survive to reproduce, must compete, or struggle, for the limited resources.
  4. Fact four is that individuals differ from one another. Look around. Even bacteria of the same strain have their differences, with some more able than others to with stand an antibiotic onslaught. Look at a crowd of people. They’re all different in hundreds of ways.
  5. Fact five is that much about us that is different lies in our genes–it is inheritable. Heredity undeniably exists and underlies a lot of our variation.
So we have five facts. Now for the three inferences:

  1. First, there is that struggle for survival, thanks to so many offspring and limited resources. See “sea turtle,” again.
  2. Second, different traits will be passed on differentially. Put another way: Winner traits are more likely to be passed on.
  3. And that takes us to our final conclusion: if enough of these “winner” traits are passed to enough individuals in a population, they will accumulate in that population and change its makeup. In other words, the population will change over time. It will be adapted to its environment. It will evolve.
Other mechanisms of evolution

A pigeon depicted in Charles Darwin’s
Variation of Animals and Plants
Under Domestication
, 1868. U.S.
public domain image, via Wikimedia.
When Darwin presented his idea of natural selection, he knew he had an audience to win over. He pointed out that people select features of organisms all the time and breed them to have those features. Darwin himself was fond of breeding pigeons with a great deal of pigeony variety. He noted that unless the pigeons already possessed traits for us to choose, we not would have that choice to make. But we do have choices. We make super-woolly sheep, dachshunds, and heirloom tomatoes simply by selecting from the variation nature provides and breeding those organisms to make more with those traits. We change the population over time.

Darwin called this process of human-directed evolution artificial selection. It made great sense for Darwinbecause it helped his reader get on board. If people could make these kinds of choices and wreak these kinds of changes, why not nature? In the process, Darwin also described this second way evolution can happen: human-directed evolution. We’re awash in it today, from our accidental development of antibiotic-resistant bacteria to wheat that resists devastating rust.

Genetic drift: fixed or lost

What about traits that have no effect either way, that are just there? One possible example in us might be attached earlobes. Good? Bad? Ugly? Well…they don’t appear to have much to do with whether or not we reproduce. They’re just there.

When a trait leaves nature so apparently disinterested, the alleles underlying it don’t experience selection. Instead, they drift in one direction or another, to extinction or 100 percent frequency. When an allele drifts to disappearance, we say that it is lost from the population. When it drifts to 100 percent presence, we say that it has become fixed. This process of evolution by genetic drift reduces variation in a population. Eventually, everyone will have it, or no one will.

Gene flow: genes in, genes out

Another way for a population to change over time is for it to experience a new infusion of genes or to lose a lot of them. This process of gene flow into or out of the population occurs because of migration in or out. Either of these events can change the allele frequency in a population, and that means that gene flow is another was that evolution can happen.

If gene flow happens between two different species, as can occur more with plants, then not only has the population changed significantly, but the new hybrid that results could be a whole new species. How do you think we get those tangelos?

Horizontal gene transfer

One interesting mechanism of evolution is horizontal gene transfer. When we think of passing along genes, we usually envision a vertical transfer through generations, from parent to offspring. But what if you could just walk up to a person and hand over some of your genes to them, genes that they incorporate into their own genome in each of their cells?

Of course, we don’t really do that–at least, not much, not yet–but microbes do this kind of thing all the time. Viruses that hijack a cell’s genome to reproduce can accidentally leave behind a bit of gene and voila! It’s a gene change. Bacteria can reach out to other living bacteria and transfer genetic material to them, possibly altering the traits of the population.

Evolutionary events

Sometimes, events happen at a large scale that have huge and rapid effects on the overall makeup of a population. These big changes mark some of the turning points in the evolutionary history of many species.

Cheetahs underwent a bottleneck that
has left them with little genetic variation.
Photo credit: Malene Thyssen, via
Bottlenecks: losing variation

The word bottleneck pretty much says it all. Something happens over time to reduce the population so much that only a relatively few individuals survive. A bottleneck of this sort reduces the variability of a population. These events can be natural–such as those resulting from natural disasters–or they can be human induced, such as species bottlenecks we’ve induced through overhunting or habitat reduction.

Founder effect: starting small

Sometimes, the genes flow out of a population. This flow occurs when individuals leave and migrate elsewhere. They take their genes with them (obviously), and the populations they found will initially carry only those genes. Whatever they had with them genetically when they founded the population can affect that population. If there’s a gene that gives everyone a deadly reaction to barbiturates, that population will have a higher-than-usual frequency of people with that response, thanks to this founder effect.

Gene flow leads to two key points to make about evolution: First, a population carries only the genes it inherits and generally acquires new versions through mutation or gene flow. Second, that gene for lethal susceptibility to a drug would be meaningless in a natural selection context as long as the environment didn’t include exposure to that drug. The take-home message is this: What’s OK for one environment may or may not be fit for another environment. The nature of Nature is change, and Nature offers no guarantees.

Hardy-Weinberg: when evolution is absent

With all of these possible mechanisms for evolution under their belts, scientists needed a way to measure whether or not the frequency of specific alleles was changing over time in a given population or staying in equilibrium. Not an easy job. They found–“they” being G. H. Hardy and Wilhelm Weinberg–that the best way to measure this was to predict what the outcome would be if there were no change in allele frequencies. In other words, to predict that from generation to generation, allele frequencies would simply stay in equilibrium. If measurements over time yielded changing frequencies, then the implication would be that evolution has happened.

Defining “Not Evolving”

So what does it mean to not evolve? There are some basic scenarios that must exist for a population not to be experiencing a change in allele frequency, i.e., no evolution. If there is a change, then one of the items in the list below must be false:

·       Very large population (genetic drift can be a strong evolutionary mechanism in small populations)

·       No migrations (in other words, no gene flow)

·       No net mutations (no new variation introduced)

·       Random mating (directed mating is one way nature selects organisms)

·       No natural selection

In other words, a population that is not evolving is experiencing a complete absence of evolutionary processes. If any one of these is absent from a given population, then evolution is occurring and allele frequencies from generation to generation won’t be in equilibrium.

Convergent Evolution

Arguably the most famous of the
egg-laying monotremes, the improbable-
seeming platypus. License.
One of the best examples of the influences of environmental pressures is what happens in similar environments a world apart. Before the modern-day groupings of mammals arose, the continent of Australiaseparated from the rest of the world’s land masses, taking the proto-mammals that lived there with it. Over the ensuing millennia, these proto-mammals in Australiaevolved into the native species we see today on that continent, all marsupialsor monotremes.

Among mammals, there’s a division among those that lay eggs (monotremes), those that do most gestating in a pouch rather than a uterus (marsupials), and eutherians, which use a uterus for gestation (placental mammals).

Elsewhere in the world, most mammals developed from a common eutherian ancestor and, where marsupials still persisted, probably outcompeted them. In spite of this lengthy separation and different ancestry, however, for many of the examples of placental mammals, Australiahas a similar marsupial match. There’s the marsupial rodent that is like the rat. The marsupial wolf that is like the placental wolf. There’s even a marsupial anteater to match the placental one.

How did that happen an ocean apart with no gene flow? The answer is natural selection. The environment that made an organism with anteater characteristics best fit in South America was similar to the environment that made those characteristics a good fit in Australia. Ditto the rats, ditto the wolf.

When similar environments result in unrelated organisms having similar characteristics, we call that process convergent evolution. It’s natural selection in relatively unrelated species in parallel. In both regions, nature uses the same set of environmental features to mold organisms into the best fit.

By Emily Willingham, DXS managing editor

Note: This explanation of evolution and how it happens is not intended to be comprehensive or detailed or to include all possible mechanisms of evolution. It is simply an overview. In addition, it does not address epigenetics, which will be the subject of a different explainer.

Are your children always on your mind? They may be IN your mind

Hmm. Do I have any cells in there?
On Mother’s Day this year, we told you why, if you have biological children, those children are literally a part of you for life thanks to a phenomenon called microchimerism. When a woman is pregnant, some of the fetal cells slip past the barrier between mother and fetus and take up residence in the mother. What researchers hadn’t turned up in humans before now was that some of those cells can end up in the mother’s brain. Once there, according to a study published today in PLoS ONE, they can stick around for decades and, the researchers suggest, might have a link to Alzheimer’s disease. Note that is a big “might.”

The easiest way to tell if a fetal cell’s made it into a maternal tissue is to look for cells carrying a Y chromosome or a Y gene sequence (not all fetuses developing as male carry a Y chromosome, but that’s a post for another time). As you probably know, most women don’t carry a Y chromosome in their own cells (but some do; another post for another time). In this study, researchers examined postmortem brain tissue from 26 women who had no detectable neurological disease and 33 women who’d had Alzheimer’s disease; the women’s ages at death ranged from 32 to 101. They found that almost two thirds (37) of all of the women tested had evidence of the Y chromosome gene in their brains, in several brain regions. The blue spots in the image below highlight cells carrying these “male” genes a woman’s brain tissue.

Photo Credit: Chan WFN, Gurnot C, Montine TJ, Sonnen JA, Guthrie KA, et al. (2012)
Male Microchimerism in the Human Female Brain. 
PLoS ONE 7(9): e45592. doi:10.1371/journal.pone.0045592

The researchers also looked at whether or not these blue spots were more (or less) frequent in the brains of women with Alzheimer’s disease compared to women who’d had no known neurological disease. Although their results hint at a possible association, it wasn’t significant. Because the pregnancy history of the women was largely unknown, there’s no real evidence here that pregnancy can heighten your Alzheimer’s risk or that being pregnant with or bearing a boy can help or hinder. As I discuss below, you can end up with some Y chromosome-bearing cells without ever having been pregnant.

Also, age could be an issue. Based on the reported age ranges of the group, the women without Alzheimer’s were on average younger at death (70 vs 79), with the youngest being only 32 (the youngest in Alzheimer’s group at death was 54). No one knows if the women who died at younger ages might later have developed Alzheimer’s. 

Indeed, most of this group–Alzheimer’s or not–had these Y-chromosome cells present in the brain. The authors say that 18 of the 26 samples from women who’d had no neurologic disease were positive for these “male” cells–that’s 69%–while 19 of the 33 who had Alzheimer’s were. That’s 58%. In other words, a greater percentage of women who’d not had Alzheimer’s in life were carrying around these male-positive cells compared to women who had developed Alzheimer’s. The age difference might also matter here, though, if these microchimeric cells tend to fade with age, although the researchers did get a positive result in the brain of a woman who was 94 when she died.

Thus, the simple fact of having male-positive cells (ETA: or not enough of them) in the brain doesn’t mean You Will Develop Alzheimer’s, which is itself a complex disease with many contributing factors. The researchers looked at this potential link because some studies have found a higher rate of Alzheimer’s among women who’ve been pregnant compared to women who have not and an earlier onset among women with a history of pregnancy. The possible reasons for this association range from false correlation to any number of effects of pregnancy, childbearing, or parenting.

Nothing about this study means that migration of fetal cells to the brain is limited to cells carrying Y chromosomes. It’s just that in someone who is XX, it’s pretty straightforward to find a Y chromosome gene. Finding a “foreign” X-linked gene in an XX person would be much more difficult. Also, a woman doesn’t have to have borne a pregnancy to term to have acquired these fetal cells. As the authors observe, even women without sons can have these Y-associated cells from pregnancies that were aborted or ended prematurely or from a “vanished” male twin in a pregnancy that did go to term. 

In fact, a woman doesn’t even have to have ever been pregnant at all to be carrying some cells with Y chromosomes. Another way you can end up with Y chromosome cells in an XX chromosome body is–get this–from having an older male sibling who, presumably, left a few cellular gifts behind in the womb where you later developed. As the oldest sibling, I can only assume I could have done the same for the siblings who followed me. So, if you’ve got an older sibling and have been pregnant before–could you be a double microchimera? 

But wait. You could even be a triple microchimera! This microchimerism thing can be a two-way street. If you’re a woman with biological children, those children already carry around part of you in the nuclear DNA you contributed and all of the mitochondria (including mitochondrial DNA) in all of their cells. Yes, they get more DNA from you than from the father. But they might also be toting complete versions of your cells, just as you have cells from them, although fetus–>mother transfer is more common than mother–>fetus transfer. The same could have happened between you and your biological mother. If so, a woman could potentially be living with cells from her mother, older sibling, and her children mixed in with her own boring old self cells.

The triple microchimera thing might be a tad dizzying, particularly the idea that you could be walking around with your mother’s and sibling’s cells hanging out in You, a whole new level of family relationships. But if you’re a biological mother, perhaps you might find it comforting to know that a cellular part of you may accompany your child everywhere, even as your child is always on your mind–and possibly in it, too.