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.

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

Are children today really suffering nature deficit disorder (TM)?

Children working in a London hosiery mill
around the turn of the century. Did they have
“Nature-Deficit Disorder (TM)”? Source.

Maybe you’ve heard of the scourge plaguing modern-day children, the one known as Nature Deficit Disorder (TM). You won’t find it in any of the standard diagnostic manuals used to identify true disorders, but the “disorder” arises, so the story goes, as a result of keeping children inside for fear of their safety and “stranger danger,” loss of natural surroundings in cities and neighborhoods, and increased attractions indoors that prevent spending time outdoors. 

This “disorder” is supposed to be an effect of modern times, the combined effects of controlling and fearful parents along with the irresistible screen-based attractions indoors. As a result of this “disorder,” children can allegedly be susceptible to any number of ills, including less respect for and understanding of nature, depression, shorter life spans, and obesity.

Concerns like these, it seems, have arisen with the advent of each new technological advance. One wonders if the invention of the wheel raised alarms that children might move through their natural surroundings too quickly to take them in. At any rate, while the person who invented this disorder, Richard Louv, has actually trademarked the term, it doesn’t seem to have made a big splash in the scientific literature. Given that studies are lacking–i.e., completely absent–about “nature deficit disorder,” one thing we can do is take a look back at how children lived before the technological age to see if their indoor-outdoor lives and exposure to the natural world were substantially different.

Go far enough back in human history, and of course, we all spent a lot of time outside. But how did we spend our time with the rise of civilization? Children in agrarian societies then and now worked from dawn to dusk as part of the family to put food on the table. In such a position, they certainly had no lack of exposure to nature, although how much they appreciated that endless grind could be in question. That is, of course, if they didn’t die in infancy or early childhood, as a large percentage of them did in spite of all that fresh air and time outside.

But what happened with children and how they spent their time with the rise of towns and cities? In early times, many of those cities were walled compounds, not necessarily hives of scum and villainy, but generally stacks upon stacks of living quarters existing solely for functionality. Nature? Outside the walls, where danger–including the most extreme kind of “stranger danger”–lurked. Cities that lacked walls, as ancient Rome did for a long period, still were more focused on efficient crowding and function far more than on nature, with only the wealthy having gardens, the modern equivalent of today’s back yards. In general, there were people, there were buildings, and there were more people. Not wildly different from, say, Manhattan today–except for that whole natural jewel known as Central Park.

This piling on of people, brick, mortar, more people, and wood continued for children who didn’t live in agrarian societies. With the Industrial Revolution, what may have really been a nature deficit disorder for a child living, in, say, London, became a genuine threat to health. While they certainly didn’t have television to keep them indoors, they also didn’t have child labor laws. The result was that children who once might have been at work at age 4 in a field were now at work at age 3 or 4 in a factory, putting in 12 or so hours a day before stepping out into the coal-smoked, animal-dung-scented air of the city. 

Child labor wasn’t something confined to Industrial Revolution Britain, and it continues today, both for agriculture and industry. I do wonder if the children harvesting oranges in Brazil feel any closer to nature than the children weaving carpets in Egypt. Likely, there are deficits more profound for them to worry about.

The trigger for this overview of whether or not things have really changed over recorded history in terms of children’s exposure to the natural world is this series of articles in the New York Times (NYT). In case you hit the paywall, it is the NYT’s “Room for Debate” series and includes four articles addressing whether or not nature shows and films connect people to the natural world or “contribute to ‘nature deficit disorder’” by keeping people glued to screens instead of being outside.

Louv, the coiner of “Nature deficit disorder TM”, is one of the four contributors to the debate. He argues that viewing nature documentaries can inspire us to go outside. He also thinks many of us grew up watching “Lassie” instead of the “Gilligan’s Island” my generation watched, but perhaps there’s not a huge difference between Timmy in the well and Gilligan in the lagoon and consequent outdoor inspiration. At any rate, Louv does argue in favor of viewing nature shows, although from a very first-world perspective (like the Romans and gardens, we don’t all have back yards, for example). 

Perhaps the least-defensible perspective is the argument that Ming (Frances) Kuo, an associate professor of natural resources and environmental sciences, has to offer. She compares nature documentaries to “junk food” and offers the obvious: They’re no comparison for the real world. For some reason, she implies that someone has argued that when you have access to TV, you don’t need access to nature, saying, “Scientists have been discovering that even in societies where just about everyone has access to a TV, Internet, or both, having access to nature matters.” I honestly don’t think anyone’s ever argued against that.

Does “nature deficit disorder” exist and is indoor screen time with nature documentaries to blame? In addition to the historical observations I’ve made above suggesting that children from previous eras haven’t necessarily been wandering the glades and meadows like wayward pixies, all I have to offer is a bit of anecdata, and I’m curious about the experiences of others. Historical comparisons suggest that city-dwelling children are no more deficient nature-wise today than city-dwelling children of yesteryear. But do nature documentaries help… or hinder?

When I was young and watching too much “Sesame Street,” “Gilligan’s Island,” and “Star Trek,” the only nature show available to me was “Wild Kingdom” (Mutual of Omaha’s, natch). Other than that, we had nothing unless a periodic NOVA episode came on public television. 

I was interested in science and nature, but acquiring knowledge outside of what I read in a book was difficult. As a resident of the great metropolis of Waco, Tex., yes, I had a natural world to explore, but let’s face it: The primates there weren’t that interesting, and bluebonnets get you only so far. I had no access to real-life live-motion visuals, auditory inputs, or information delivered in any form except what I could read in a book. Talk about sensory limitations.

These days, my children have a nature documentary library that extends to dozens and dozens of choices. And they have watched every single one, some of them repeatedly. That’s not to say that they don’t also have dozens of well-thumbed field guides and encyclopedias covering fossils, dinosaurs, plants, bugs, sharks, rocks–the usual obsessions of the young who are interested in nature. Our “movie nights” often kick off with a nature documentary, and our pick of choice will frequently be one involving narration from David Attenborough. My children want to be David Attenborough–so do I, for that matter–and I can’t recall ever really having that feeling about Marlin Perkins or Jim Fowler

And the upshot of that access to an expanse of nature documentaries I never had is that their knowledge of nature is practically encyclopedic. I’m the biologist in the family–or at least the one who has the biology degree–but my children often know more than I do about a specific plant or animal or ecosystem or area of the world, all thanks to these documentaries they watch. And when we’re outside, they extrapolate what they’ve learned, generalizing it to all kinds of local natural situations.

Do children today just need to be moving around more, somewhere, somehow? Oh, yes. But watching nature shows hasn’t exacerbated some kind of “nature deficit” my children might have, Minecraft obsessed as they are. And these documentaries haven’t replaced “real” nature with televised nature. Instead, the shows have expanded on and given context to the nature my children encounter, wherever that is–city, country, farm, sky, ocean, parking lot, grocery store, or even inside their own home, which is currently the scene of a sci-fi-like moth infestation that has triggered much excitement. I’d hazard that far from causing a deficit, nature shows have given my children a nature literacy that was unknown in previous generations. 

What is your take on nature deficits and nature documentaries?

By Emily Willingham, DXS managing editor 

Science, health, medical news freaking you out? Do the Double X Double-Take first

Handy short-form version.

Have you seen the headlines? Skip them
You’ve probably seen a lot of headlines lately about autism and various behaviors, ways of being, or “toxins” that, the headlines tell you, are “linked” to it. Maybe you’re considering having a child and are mentally tallying up the various risk factors you have as a parent. Perhaps you have a child with autism and are now looking back, loaded with guilt that you ate high-fructose corn syrup or were overweight or too old or too near a freeway or not something enough that led to your child’s autism. Maybe you’re an autistic adult who’s getting a little tired of reading in these stories about how you don’t exist or how using these “risk factors” might help the world reduce the number of people who are like you.

Here’s the bottom line: No one knows precisely what causes the extremely diverse developmental difference we call autism. Research from around the world suggests a strong genetic component [PDF]. What headlines in the United States call an “epidemic” is, in all likelihood, largely attributable to expanded diagnostic inclusion, better identification, and, ironically, greater awareness of autism. In countries that have been able to assess overall population prevalence, such as the UK, rates seem to have held steady at about 1% for decades, which is about the current levels now identified among 8-year-olds in the United States. 

What anyone needs when it comes to headlines honking about a “link” to a specific condition is a mental checklist of what the article–and whatever research underlies it–is really saying. Previously, we brought you Real vs Fake Science: How to tell them apart. Now we bring you our Double X Double-Take checklist. Use it when you read any story about scientific research and human health, medicine, biology, or genetics.

The Double X Double-Take: What to do when reading science in the news
1. Skip the headline. Headlines are often misleading, at best, and can be wildly inaccurate. Forget about the headline. Pretend you never even saw the headline.

2. What is the basis of the article? Science news originates from several places. Often it’s a scientific paper. These papers come in several varieties. The ones that report a real study–lots of people or mice or flies, lots of data, lots of analysis, a hypothesis tested, statistics done–is considered “original research.” Those papers are the only ones that are genuinely original scientific studies. Words to watch for–terms that suggest no original research at all–are “review,” “editorial,” “perspective,” “commentary,” “case study” (these typically involve one or only a handful of cases, so no statistical analysis), and “meta-analysis.” None of these represents original findings from a scientific study. All but the last two are opinion. Also watch for “scientific meeting” and “conference.” That means that this information was presented without peer review at a scientific meeting. It hasn’t been vetted in any way.

3. Look at the words in the article. If what you’re reading contains words like “link,” “association,” “correlation,” or “risk,” then what the article is describing is a mathematical association between one thing (e.g., autism) and another (e.g., eating ice cream). It is likely not describing a biological connection between the two. In fact, popular articles seem to very rarely even cover scientific research that homes in on the biological connections. Why? Because these findings usually come in little bits and pieces that over time–often quite a bit of time–build into a larger picture showing a biological pathway by which Variable 1 leads to Outcome A. That’s not generally a process that’s particularly newsworthy, and the pathways can be both too specific and extremely confusing.

4. Look at the original source of the information. Google is your friend. Is the original source a scientific journal? At the very least, especially for original research, the abstract will be freely available. A news story based on a journal paper should provide a link to that abstract, but many, many news outlets do not do this–a huge disservice to the interested, engaged reader. At any rate, the article probably includes the name of a paper author and the journal of publication, and a quick Google search on both terms along with the subject (e.g., autism) will often find you the paper. If all you find is a news release about the paper–at outlets like ScienceDaily or PhysOrg–you are reading marketing materials. Period. And if there is no mention of publication in a journal, be very, very cautious in your interpretation of what’s being reported.

5. Remember that every single person involved in what you’re reading has a dog in the hunt. The news outlet wants clicks. For that reason, the reporter needs clicks. The researchers probably want attention to their research. The institutions where the researchers do their research want attention, prestige, and money. A Website may be trying to scare you into buying what they’re selling. Some people are not above using “sexy” science topics to achieve all of the above. Caveat lector

6. Ask a scientist. Twitter abounds with scientists and sciencey types who may be able to evaluate an article for you. I receive daily requests via email, Facebook, and Twitter for exactly that assistance, and I’m glad to provide it. Seriously, ask a scientist. You’ll find it hard to get us to shut up. We do science because we really, really like it. It sure ain’t for the money. [Edited to add: But see also an important caveat and an important suggestion from Maggie Koerth-Baker over at Boing Boing and, as David Bradley has noted over at ScienceBase, always remember #5 on this list when applying #6.] 


Case Study
Lately, everyone seems to be using “autism” as a way to draw eyeballs to their work. Below, I’m giving my own case study of exactly that phenomenon as an example of how to apply this checklist.

1. Headline: “Ten chemicals most likely to cause autism and learning disabilities” and “Could autism be caused by one of these 10 chemicals?” Double X Double-Take 1: Skip the headline. Check. Especially advisable as there is not one iota of information about “cause” involved here.

2. What is the basis of the articleEditorialConference. In other words, those 10 chemicals aren’t something researchers identified in careful studies as having a link to autism but instead are a list of suspects the editorial writers derived, a list that they’d developed two years ago at the mentioned conference. 

3. Look at the words in the articles. Suspected. Suggesting a link. In other words, what you’re reading below those headlines does not involve studies linking anything to autism. Instead, it’s based on an editorial listing 10 compounds [PDF] that the editorial authors suspect might have something to do with autism (NB: Both linked stories completely gloss over the fact that most experts attribute the rise in autism diagnoses to changing and expanded diagnostic criteria, a shift in diagnosis from other categories to autism, and greater recognition and awareness–i.e., not to genetic changes or environmental factors. The editorial does the same). The authors do not provide citations for studies that link each chemical cited to autism itself, and the editorial itself is not focused on autism, per se, but on “neurodevelopmental” derailments in general.

4. Look at the original source of information. The source of the articles is an editorial, as noted. But one of these articles also provides a link to an actual research paper. The paper doesn’t even address any of the “top 10″ chemicals listed but instead is about cigarette smoking. News stories about this study describe it as linking smoking during pregnancy and autism. Yet the study abstract states that they did not identify a link, saying “We found a null association between maternal smoking and pregnancy in ASDs and the possibility of an association with a higher-functioning ASD subgroup was suggested.” In other words: No link between smoking and autism. But the headlines and how the articles are written would lead you to believe otherwise. 

5. Remember that every single person involved has a dog in this hunt. Read with a critical eye. Ask yourself, what are people saying vs what real support exists for their assertions? Who stands to gain and in what way from having this information publicized? Think about the current culture–does the article or the research drag in “hot” topics (autism, obesity, fats, high-fructose corn syrup, “toxins,” Kim Kardashian) without any real basis for doing so? 

6. Ask a scientist. Why, yes, I am a scientist, so I’ll respond. My field of research for 10 years happens to have been endocrine-disrupting compounds. I’ve seen literally one drop of a compound dissolved in a trillion drops of solvent shift development of a turtle from male to female. I’ve seen the negative embryonic effects of pesticides and an over-the-counter antihistamine on penile development in mice. I know well the literature that runs to the thousands of pages indicating that we’ve got a lot of chemicals around us and in us that can have profound influences during sensitive periods of development, depending on timing, dose, species, and what other compounds may be involved. Endocrine disruptors or “toxins” are a complex group with complex interactions and effects and can’t be treated as a monolith any more than autism should be.

What I also know is that synthetic endocrine-disruptors have been around for more than a century and that natural ones for far, far longer. Do I think that the “top 10″ chemicals require closer investigation and regulation? Yes. But not because I think they’re causative in some autism “epidemic.” We’ve got sufficiently compelling evidence of their harm already without trying to use “autism” as a marketing tool to draw attention to them. Just as a couple of examples: If coal-burning pollution (i.e., mercury) were causative in autism, I’d expect some evidence of high rates in, say, Victorian London, where the average household burned 11 tons of coal a year. If modern lead exposures were causative, I’d be expecting records from notoriously lead-burdened ancient Rome containing descriptions of the autism epidemic that surely took it over. 

Bottom line: We’ve got plenty of reasons for concern about the developmental effects of the compounds on this list. But we’ve got very limited reasons to make autism a focal point for testing them. Using the Double X Double-Take checklist helps demonstrate that.

By Emily Willingham, DXS managing editor 

Dinosaur Aunts, Bacterial Stowaways, & Insect Milk

Today’s guest post (originally posted here) is from Katie Hinde, an Assistant Professor in Human Evolutionary Biology at Harvard University.  Katie studies how variation in mother’s milk influences infant development in rhesus monkeys.  You can learn more about Katie and mammalian lactation by visiting her blog, Mammals Suck… Milk!.  Follow Katie on Twitter @Mammals_Suck.

Dinosaur Aunts, Bacterial Stowaways, & Insect Milk

Milk is everywhere. From the dairy aisle at the grocery store to the explosive cover of the Mother’s Day issue of Time magazine, the ubiquity of milk makes it easy to take for granted. But surprisingly, milk synthesis is evolutionarily older than mammals. Milk is even older than dinosaurs. Moreover, milk contains constituents that infants don’t digest, namely oligosaccharides, which are the preferred diet of the neonate’s intestinal bacteria (nom nom nom!)  And milk doesn’t just feed the infant, and the infant’s microbiome; the symbiotic bacteria are IN mother’s milk. 

Evolutionary Origins of Lactation
The fossil record, unfortunately, leaves little direct evidence of the soft-tissue structures that first secreted milk. Despite this, paleontologists can scrutinize morphological features of fossils, such as the presence or absence of milk teeth (diphyodonty), to infer clues about the emergence of “milk.” Genome-wide surveys of the expression and function of mammary genes across divergent taxa, and experimental evo-devo manipulations of particular genes also yield critical insights. As scientists begin to integrate information from complementary approaches, a clearer understanding of the evolution of lactation emerges.

In his recent paper, leading lactation theorist Dr. Olav Oftedal discusses the ancient origins of milk secretion (2012). He contends the first milk secretions originated ~310 million years ago (MYA) in synapsids, a lineage ancestral to mammals and contemporaries with sauropsids, the ancestors of reptiles, birds, and dinosaurs. Synapsids and sauropsids produced eggs with multiple membrane layers, known as amniote eggs. Such eggs could be laid on land. However, synapsid eggs had permeable, parchment-like shells and were vulnerable to water loss. Burying these eggs in damp soil or sand near water resources- like sea turtles do- wasn’t an option, posits Oftedal. The buried temperatures would have likely been too cold for the higher metabolism of synapsids. But incubating eggs in a nest would have evaporated water from the egg. The synapsid egg was proverbially between a rock and a hard place: too warm to bury, too permeable to incubate. 

Ophiacodon by Dmitri Bogdanov

Luckily for us, a mutation gave rise to secretions from glandular skin on the belly of the synapsid parent. This mechanism replenished water lost during incubation, allowing synapsids to lay eggs in a variety of terrestrial environments. As other mutations randomly arose and were favored by selection, milk composition became increasingly complex, incorporating nutritive, protective, and hormonal factors (Oftedal 2012). Some of these milk constituents are shunted into milk from maternal blood, some- although also present in the maternal blood stream- are regulated locally in the mammary gland, and some very special constituents are unique to milk. Lactose and oligosaccharides (a sugar with lactose at the reducing end) are two constituents unique to mammalian milk, but are interestingly divergent among mammals living today. 

Illustration by Carl Buell
Mammalian and Primate Divergences:  Milk Composition
Among all mammals studied to date, lactose and oligosaccharides are the primary sugars in milk. Lactose is synthesized in mammary glands only. Urashima and colleagues explain that lactose synthesis is contingent on the mammalian-specific protein alpha-lactalbumin (2012). Alpha-lactalbumin is very similar in amino-acid structure to C-type lysozyme, a more ancient protein found throughout vertebrates and insects. C-type lysozyme acts as an anti-bacterial agent. Oligosaccharides are predominant in the milks of marsupials and egg-laying monotremes (i.e. the platypus), but lactose is the most prevalent sugar in the milk of most placental (aka eutherian) mammals. Interestingly, the oligosaccharides in the milk of placental mammals are most similar to the oligosaccharides in the milk of monotremes. Unique oligosaccharides in marsupial milk emerged after the divergence of placental mammals. 

Marsupial and monotreme young seemingly digest oligosaccharides. Among placental mammals, however, young do not have the requisite enzymes in their stomach and small intestine to utilize oligosaccharides themselves. Why do eutherian mothers synthesize oligosaccharides in milk, if infants don’t digest them?

In May, Anna Petherick’s post “Multi-tasking Milk Oligosaccharides” revealed that oligosaccharides serve a number of critical roles for supporting the healthy colonization and maintenance of the infant’s intestinal microbiome. Beneficial bacterial symbionts contribute to the digestion of nutrients from our food. Just as importantly, they are an essential component of the immune system, defending their host against many ingested pathogens. The structures of milk oligosaccharides have been described for a number of primates, including humans, and data are now available from all major primate clades; strepsirrhines (i.e. lemurs), New World monkey (i.e. capuchin), Old World monkey (i.e. rhesus), and apes (i.e. chimpanzee). 

Among all non-human primates studied to date, Type II oligosaccharides are most prevalent (Type II oligosaccharides contain lacto-N-biose I). Type I oligosaccharides (containing N-acetyllactosamine) are absent, or in much lower concentrations than Type II(Taufik et al. 2012). 

In human milk, there is a much greater diversity and higher abundance of milk oligosaccharides than found in the milk of other primates. Most primate taxa have between 5-30 milk oligosaccharides; humans have ~200. Even more astonishingly, humans predominantly produce Type I oligosaccharides, the preferred food of the most prevalent bacterium in the healthy human infant gut- Bifidobacteria (Urashima et al 2012, Taufik et al. 2012).

Human infants have bigger brains and an earlier age at weaning than do our closest ape relatives. Many anthropologists have hypothesized that constituents in mother’s milk, such as higher fat concentrations or unique fatty acids, underlie these differences in human development. But only oligosaccharides, a constituent that the human infant does not itself utilize, are demonstrably derived from our primate relatives (Hinde and Milligan 2011). At some point in human evolution there must have been strong selective pressure to optimize the symbiotic relationship between the infant microbiome and the milk mothers synthesize to support it. The human and Bifidobacteria genomes show signatures of co-evolution, but the selective pressures and their timing remain to be understood.

Vertical Transmission of Bacteria via Milk
In the womb, the infant is largely protected from maternal bacteria due to the placental barrier. But upon birth, the infant is confronted by a teeming microbial milieu that is both a challenge and an opportunity. The first inoculation of commensal bacteria occurs during delivery as the infant passes through the birth canal and is exposed to a broad array of maternal microbes. Infants born via C-section are instead, and unfortunately, colonized by the microbes “running around” the hospital. But exposure to the mother’s microbiome continues long after birth. Evidence for vertical transmission of maternal bacteria via milk has been shown in rodents, monkeys(Jin et al. 2011), humans(Martin et al. 2012), and… insects. 


A number of insects have evolved the ability to rely on nutritionally incomplete food sources. They are able to do so because bacteria that live inside their cells provide what the food does not. These bacteria are known as endosymbionts and the specialized cells the host provides for them to live in are called bacteriocytes. For example, the tsetse fly has a bacterium, Wigglesworthia glossinidia,* that provides B vitamins not available from blood meals. Um, if you are squeamish, don’t read the previous sentence.     
 *I submit the tsetse fly and its bacterial symbiont (Wigglesworthia glossinidia
for consideration as the number one mutualism in which the common name of the host 
and the Latin name of the bacteria are awesome to say out loud! 
Bring on your challenger teams.
Hosokawa and colleagues recently revealed the Russian nesting dolls that are bats (Miniopterus fuliginosus), bat flies (Nycteribiidae), and endosymbiotic bacteria (proposed name Aschnera chenzii)(2012). Bat flies are the obligate ectoparasites of bats (Peterson et al. 2007). They feed on the blood of their bat hosts, and for nearly their entire lifespan, bat flies live in the fur of their bat hosts. Females briefly leave their host to deposit pupae on stationary surfaces within the bat roost. 

Bat flies are even more crazy amazing because they have a uterus and provide MILK internally through the uterus to larva! Male and female bat flies have endosymbiotic bacteria living in bacteriocytes along the sides of their abdominal segments (revealed by 16S rRNA). Additionally, females host bacteria inside the milk gland tubules, “indicating the presence of endosymbiont cells in milk gland secretion”. 

The authors are not yet certain of the specific nutritional role that these bacterial endosymbionts play in the bat fly host. The bacteria may provide B vitamins, as other bacterial symbionts of blood-consuming insects are known to do. My main question is what is the exact role of the bacteria in the milk gland tubules? Are they there to add nutritional value to the milk for the larva, to stowaway in milk for vertical transmission to larva, or both?  

The studies described above represent new frontiers in lactation research. The capacity to secrete “milk” has been evolving since before the age of dinosaurs, but we still know relatively little about the diversity of milks produced by mammals today. Even less understood are the consequences and functions of various milk constituents in the developing neonate. Despite the many unknowns, it is increasingly evident that mother’s milk cultivates the infant’s gut bacterial communities in fascinating ways. A microbiome milk-ultivation, if you will, that has far reaching implications for human development, nutrition, and health.  Integrating an evolutionary perspective into these newly discovered complexities of milk dynamics allows us to reimagine the world of “dairy” science.


Hinde & Milligan. 2011. Primate milk synthesis: Proximate mechanisms and ultimate perspectives. Evol Anthropol 20:9-23.
Hosokawa et al. 2012. Reductive genome evolution, host-symbiont co-speciation, and uterine transmission of endosymbiotic bacteria in bat flies. ISME Journal. 6: 577-587
Jin et al. 2011. Species diversity and abundance of lactic acid bacteria in the milk of rhesus monkeys (Macaca mulatta). J Med Primatol. 40: 52-58
Martin et al. 2012. Sharing of Bacterial Strains Between Breast Milk and Infant Feces. J Hum Lact. 28: 36-44
Oftedal 2012. The evolution of milk secretion and its ancient origins. Animal. 6: 355-368.
Peterson et al. 2007. The phylogeny and evolution of host choice in the Hippoboscoidea(Diptera) as reconstructed using four molecular markers. Mol Phylogenet Evol. 45 :111-22
Taufik et al. 2012. Structural characterization of neutral and acidic oligosaccharides in the milks of strepsirrhine primates: greater galago, aye-aye, Coquerel’s sifaka, and mongoose lemur. Glycoconj J. 29: 119-134.
Urashima, Fukuda, & Messer. 2012. Evolution of milk oligosaccharides and lactose: a hypothesis. Animal. 6: 369-374.

Happy belated birthday, Mary Anning!

Mary Anning and a small, non-fossilized dog. (Source)

[Today, we're featuring a post by Mike Rendell, author and keeper of Georgian Gentleman, a blog chronicling aspects of 18th century life. Mike spent 30 years as a lawyer--poor fellow--before he retired to time travel in his mind back to the 18th century, where he has set up mental shop permanently. By what he calls a "curious stroke of luck," he has all of the 18th century papers of his great-great-great-great (that's four) grandfather, including diaries, accounts, letters, and even shopping lists. In 2011, he published the story of this ancestor's life as a social history, "The Life of a Georgian Gentleman,' and thus, a blog was also born. We thank Mike for having graciously given us permission to publish his post here because we are huge fans of Mary Anning, who, as was typical, did not receive recognition from or entree into male scientific society of her day. We have added in a few explanatory links, too.]
Today the spotlight is turned not on a well-educated man, or a wealthy daughter with aristocratic connections, but on a girl who was amongst the poorest of the poor; who in many ways led a miserably hard and short life; who could barely read and write, and yet was someone who amazed the scientific world in the first half of the nineteenth century.
Her name was Mary Anning, born in Lyme Regis in Dorset on 21st May 1799. She cannot be said to have had an auspicious start in life. She was one of ten children – but eight died in childhood. An elder sister had already been called Mary but she had perished in a fire when her clothes were ignited from some burning wood shavings. Our heroine was born five months after this tragic death, and was named Mary in memory of her dead sibling.
Mary had luck, of a sort, on her side. When she was eighteen months old she was being held in the arms of a neighbour called Elizabeth Haskings who was in a group of women watching a travelling show. A storm sprang up and the group took shelter beneath an elm tree, but a bolt of lightning struck the tree, killing three of the women including Elizabeth. Yet Mary was apparently unscathed. Fate had something quite remarkable in store for the young girl…
Mary’s parents were Dissenters, meaning that education opportunities were limited and the family were subject to legal discrimination. A member of the Congregationalist Church, she attended Sunday School and here learned the rudiments of reading and writing. The Congregational Church, unlike the Anglican Church, attached great importance to education, particularly for young girls, and she was encouraged in her development by the pastor Revd James Wheaton. Her prized possession was apparently a copy of theDissenters’ Theological Magazine and Review Continue reading

Fighting the stereotype that math is only for boys

Does she look like an engineer to you?
She should. She is one.

[Ed. note: This post first appeared at our beloved Steminist and is reprinted here with permission.]
by Patricia Valoy
When I take a look around my office I see a lot of men, mostly older White men. There are also women, mostly administrative assistants, accountants, and marketing personnel, but few like me. I am an engineer, and I am young, female, Ivy League educated, and Hispanic. I took the same science and mathematics classes all my male peers took. I was given the same tests, the same homework assignments, and the same projects. Yet, every day I have to battle stereotypes of what some think women should be.
Courtesy of Indiana University.
Engineering, and most science fields, have long been male-dominated professions. Yet, in spite of traditional gender roles pigeonholing women to domestic duties, women haven’t necessarily settled into domesticity without first making many great advances in the science fields. We cannot forget Merit-Ptah, an ancient Egyptian physician, and also the first woman to be known by name in the history of the field of Medicine. Or the ancient Greek philosopher Hypatia, also the first historically noted woman in Mathematics. These women were not given positions in Science to fill a status quo, they earned it, just like women today.
Stereotypes are part of my daily life. In high school I was discouraged by a school teacher to apply to Engineering school, because she claimed it was “harder than I was imagining it to be.” She told me that I wanted to pursue a degree in Engineering because of the money I would earn, but it was clear to her that I did not have a passion for it. Never mind that I outperformed all my classmates, including all my male peers, and that I was about to graduate at the top of my class. As a professional adult, I still face these misconceptions about women in science fields. I get my bosses’ mail delivered to me every day because the delivery man, after four years, still thinks that I am a secretary. I politely remind him every day that I am in fact, also an engineer, like my boss, but it seems to fall on deaf ears. So I find myself not only doing my work, but also delivering mail. A week ago I was asked by a new employee which department I belonged in, and the conversation went like this:
Me: “Hi, are you new to our office?”

New Employee: “Yes, I work in the Marketing department. Do you work with Corporate?”

Me: “No, I work in the Transportation and Infrastructure department.”
New Employee: “Are you an administrative assistant?”
Me: “No, an Engineer.”
New Employee: “Oh, you’re an Accountant.”
Me: “Noooo, an Engineer, a Civil Engineer!”
New Employee: “Oh, wow! I would have never guessed…you don’t look like one.”
Me: “Umm…thanks?”

While I admit to becoming irritated, it was more disconcerting that this co-worker was also a young woman like myself. She reacted in a way that was natural and all too common, because there really aren’t enough women being positively represented in the fields of Science, Technology, Engineering, and Mathematics (STEM). I quite enjoy shaking up perceived ideas of what society assumes I should be, as a woman, a woman of color, and a woman in a male-dominated field, but when will all this shock and awe over women in science fields end? Nonetheless, I love the work I do and the feeling of accomplishment I get when I finish a project. And contrary to 18th century views of the female brain, we have shown that when given the same curriculum as men, we can equally excel.
According to a research study done by the University of Washington, the main culprit for girls not becoming enthusiastic about careers in mathematics and science is gender-stereotyping. The study speaks of the widespread cultural belief in the “girls don’t do math” stereotype. In the study, 247 school-age children (126 girls and 121 boys) were asked to sort four kinds of words: boy names, girl names, math words and reading words, into categories, with the use of an adapted keyboard on a laptop. The lead author of the study, Dario Cvencek, concluded that: “Not only do girls identify the stereotype that math is for boys, but they apply that to themselves. That’s the concerning part. Girls are translating that to mean, ‘Math is not for me.’”
While the study found that both genders equate mathematics with boys, it is unclear why this stereotype is so pronounced at such a young age, though there seems to be a connection with the way in which we speak to young children about mathematics. Dario Cvencek explains: “When a girl does poorly on a math test, often she’s told, ‘That’s fine. You did your best.’ When a boy does poorly, he is more likely to be told, ‘You can do better. Try harder next time.’”
Stereotypes are hurtful, and I believe that stereotype threat, the notion that we experience anxiety in a situation where we have the potential to confirm a negative stereotype, is all too real. We cannot expect young girls to be interested in pursuing careers in science, technology, engineering, and mathematics, if we continue to associate them with one gender. Stereotyping career choices is not in our best interest as we cannot achieve success if we believe that half of our population is not capable of contributing to the betterment of our society. I challenge every educator and parent to reevaluate the way they educate their children. Think about the toys we give them. Building blocks and other shape-sorting toys are equally entertaining for girls as they are for boys, and they help develop cognitive skills, something Barbie and Easy-Bake Ovens will never achieve. Teaching is powerful, and encouraging children to challenge themselves should not depend on the child’s gender.
I am passionate about increasing the number of women represented in STEM fields, not merely because I believe we should be equally represented in all career fields, but because I know we can positively contribute to the advancement of our society. Having both sexes equally represented opens the door for a more diverse range of ideas, which in turn can result in a more robust range of services and products. Additionally, having more women in STEM fields ensures that women’s health and well-being become common practice, and not women’s issues.
Careers in STEM fields require high-level skills and earn higher wages, they are also always in high demand, and experts predicts an even stronger demand for professionals in STEM fields in the future. Our economy is in crisis and 60% of women are the breadwinners or co-breadwinners in their families. If we continue to believe that these high paying careers are only for men, we are not cashing in on the earning power of women. Ultimately, it is not about filling a status quo, it is about using our population, men and women, to the best of their abilities.
Patricia Valoy is a Civil Engineer and an Assistant Project Manager at STV, an architectural, engineering, planning, environmental and construction management firm based in New York City. She is a graduate of the Columbia University School of Engineering in Applied Science, where she majored in Civil Engineering with a concentration in Construction Management. Patricia also is a co-host of a weekly radio show called, “Let Your Voice Be Heard.” The show’s mission is to spread awareness of social and political issues. In addition, she writes a blog about feminist issues and mentors high school and college students interested in pursuing careers in STEM fields. You can follow Patricia on Twitter at @besito86 and read her blog at