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.
Carbohydrates

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.

Proteins

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

Modern Astronomers

This edition of the Notable Women in Science series presents modern astronomers. Many of these women are currently working in fields of research or have recently retired. As before, pages could be written about each of these women, but I have limited information to a summary of their education, work, and selected achievements. Many of these blurbs have multiple links, which I encourage you to visit to read extended biographies and learn about their current research interests.

From L to R: Anne Kinney, NASA Goddard Space Flight Center, Greenbelt, Md.; Vera Rubin, Dept. of Terrestrial Magnetism, Carnegie Institute of Washington; Nancy Grace Roman Retired NASA Goddard; Kerri Cahoy, NASA Ames Research Center, Moffett Field, Calif.; Randi Ludwig. University of Texas, Austin, Texas.
Vera Cooper Rubin was making advancements decades ahead of popularity of her research topic.  She received her B.A. from Vassar College, M.A. from Cornell University, and her Ph.D. from Georgetown University in the 1940s and 50s. She continued at Georgetown University as a research astronomer then assistant professor, and then moved to the Carnegie Institution. Among her honors is her election to the National Academy of Sciences and receiving the National Medal of Science, Gold Medal of the Royal Astronomical Society. She was only the second female recipient of this medal, the first being Caroline Herschel. She has had an asteroid and the Rubin-Ford effect named after her. She is currently enjoying her retirement.

Dr. Nancy Roman
Nancy Grace Roman has a lifetime love for astronomy. She received her B.A. from Swarthmore College and Ph.D. from the University of Chicago in the 1940s. She started her career as a research associate and instructor at Yerkes Observatory, but moved on due to a low likelihood of tenure because of her gender. She eventually moved through chief and scientist positions to Head of the Astronomical Data Center at NASA. She was the first female to hold an executive position at NASA. She has received honorary D.Sc. from several colleges and has received several awards, including the American Astronautical Society’s William Randolf Lovelace II Award and the Women in Aerospace’s LIfetime Achievement Award. She is currently continuing to inspire young girls to dream big by consulting and lecturing by invitation at venues across the U.S.

Catharine (Katy) D. Garmany researches the hottest stars. Dr. Garmany earned her B.S. from Indiana University and her M.A. and Ph.D. from the University of Virginia in the 1960s and 70s. She continued with research and teaching at several academic institutions. She has served as past president of the Astronomical Society of the Pacific and received the Annie Jump Cannon Award. She is currently associated with the National Optical Astronomy Observatory with several projects.

Dr. Elizabeth Roemer
Elizabeth Roemer is a premier recoverer of “lost” comets. She received her B.A.  and Ph.D. from University of California – Berkeley in the 1950s. She spent some time as a researcher at U.S. Observatories before going to the University of Arizona and moving through the professorial ranks. She has received several awards, including Mademoiselle Merit Award, one of only four recipients of the Benjamin Apthorp Gould Prize from the National Academy of Sciences, and a NASA Special Award. She is currently Professor Emerita at the University of Arizona with research interests in comets and minor planets (“asteroids”), including positions (astrometry), motions, and physical characteristics, especially of those objects that approach the Earth’s orbit.

Margaret Joan Geller is a widely respected cosmologist. She received her A.B. from the University of California-Berkeley, and M.A. and Ph.D. from Princeton University in the 1970s. She moved through the professorial ranks at Harvard University and is currently an astrophysicist at the Smithsonian Astrophysical Observatory. Some of her awards include the MacArthur “Genius” Award and the James Craig Watson Award from the National Academy of Sciences. She continues to provide public education in science through written, audio, and video media.

In 1995, the majestic spiral galaxy NGC 4414 was imaged by the Hubble Space Telescope as part of the HST Key Project on the Extragalactic Distance Scale. An international team of astronomers, led by Dr. Wendy Freedman of the Observatories of the Carnegie Institution of Washington, observed this galaxy on 13 different occasions over the course of two months.


Wendy Laurel Freedman is concerned with the fundamental question”How old is the universe?”  She received her B.S., M.S., and Ph.D. from the University of Toronto in the 1970s and 80s. After earning her Ph.D. she joined Observatories of the Carnegie Institution in Pasadena, California as a postdoctoral fellow and became faculty a few years later, as the first woman to join the Observatory’s permanent scientific staff. She has received several awards and honors, among them the Gruber Cosmology Prize. Her current work is focusing on the Giant Magellan Telescope and the questions it will answer. 

Sandra Moore Faber researches the origin of the universe. Dr. Faber earned her B.A. from Swarthmore College and her Ph.D. from Harvard University in the 1960s and 70s. She joined the Lick Observatory at the University of California – Santa Cruz and moved through the Astronomer and Professorial rankings. Her achievements include being elected to the National Academy of Sciences, the Heineman Prize, a NASA Group Achievement Award, Harvard Centennial Medal, and the Bower Award. She continues to research the formation and evolution of galaxies and the evolution ofstructure in the universe.


Dr. Heidi Hammel

Heidi Hammel is known as an excellent science communicator, researcher, andleader. She earned her B.S. from Massachusetts Institute of Technology and Ph.D. from the University of Hawaii in the 1980s. At NASA she led the imaging team of the Voyager 2’s encounter with Neptune and became known for her science communication for it.  She returned to MIT as a scientist for nearly a decade. Among her honors, she has received Vladimir Karpetoff Award , Klumpke-Roberts Award, and the Carl Sagan Medal.  She is currently at the Space Science Institute with a research focused on ground- and space-based studies of Uranus and Neptune.


Judith Sharn Young was inspired by black holes. She earned her B.A. from Harvard University and her M.S. and Ph.D. from the University of Minnesota in the 1970s. She began her academic career at the University of Massachusetts – Amherst, proceeding through the professorial ranks. She has earned several honors, including the Annie Jump Cannon Prize, the Maria Goeppert-Mayer Award, and a Sloan Research Fellowship. She is currently teaching and researching galaxies and imaging at the University of Massachusetts. 


Jocelyn Bell Burnell is the discoverer of pulsars. She earned her B.Sc. from the University of Glasgow and her Ph.D. from Cambridge University in the 1960s. After her graduation, she worked at the University of Southampton in research and teaching, and continued to work in research positions at several institutions. She is well known for her discovery of pulsars, which earned her research advisor a Nobel Prize. Among her awards are the Albert A. Michelson Prize, Beatrice Tinsley Prize, Herschel Medal, Magellanic Premium, and Grote Reber Metal. She has received honorary doctorates from Williams College, Harvard University, and the University of Durham. She is currently Professor of Physics and Department Chair at the Open University, England. 



Awards Mentioned:
The National Academy of Sciences is composed of select scientists who are leaders in their fields.
The National Medal of Science is a presidential award given to physical, biological, mathematical, or engineering scientists who have contributed outstanding knowledge to their field. 
The Gold Medal of the Royal Astronomical Society is the society’s highest honor given in astronomy
American Astronautical Society’s William Randolf Lovelace II Award recognizes outstanding contributions to space science.
The Women in Aerospace’s Lifetime Achievement Award is given for contributions to aerospace science over a career spanning 25 years. 
The Annie Jump Cannon Award is given for outstanding research a doctoral student in astronomy with promise of future excellence. 
The Mademoiselle Merit Award was presented annually to young women showing the promise of great achievement.
The Benjamin Apthorp Gould Prize is given in recognition of scientific accomplishments by an American citizen. 
The NASA Special Award is given for exceptional work.
The MacArthur “Genius” Award is given to those who show exception merit and promise in creative work. 
The James Craig Watson Award is given for contributions in astronomy. 
The Gruber Cosmology Prize is given for fundamental advances in our understanding by a scientists. 
The Heineman Prize is given for outstanding work in the field of astrophysics. 
The NASA Group Achievement Award is given for accomplishment that advances NASA mission. 
The Harvard Centennial Medal is given to graduates of Harvard who have contributed to society upon graduation. 
The Bower Award is given for achievement in science. 
The Vladimir Karapetoff Award is given for outstanding technical achievement. 
The Klumpke-Roberts Award is given for enhancing public understanding and appreciation of astronomy. 
The Carl Sagan Medal is awarded for outstanding communication to the public about planetary science. 
The Maria Goeppert-Mayer Award is given to a female physicist for outstanding achievement in her early career. 
The Albert A. Michelson Prize is given for technical and professional achievement. 
The Beatrice Tinsley Prize is given for outstanding research contribution to astronomy or astrophysics. 
The Herschel Medal is given for investigations of outstanding merit in astrophysics.
The Magellanic Premium Medal is awarded for a discovery or invention advancing navigation or astronomy.


Much of the information for this post came from the book Notable Women in the Physical Sciences: A Biographical Dictionary edited by Benjamin F. Shearer and Barbara S. Shearer.

Adrienne M Roehrich, Double X Science Chemistry Editor

Anorexia nervosa, neurobiology, and family-based treatment

Via Wikimedia Commons
Photo credit: Sandra Mann
By Harriet Brown, DXS contributor

Back in 1978, psychoanalyst Hilde Bruch published the first popular book on anorexia nervosa. In The Golden Cage, she described anorexia as a psychological illness caused by environmental factors: sexual abuse, over-controlling parents, fears about growing up, and/or other psychodynamic factors. Bruch believed young patients needed to be separated from their families (a concept that became known as a “parentectomy”) so therapists could help them work through the root issues underlying the illness. Then, and only then, patients would choose to resume eating. If they were still alive.

Bruch’s observations dictated eating-disorders treatments for decades, treatments that led to spectacularly ineffective results. Only about 35% of people with anorexia recovered; another 20% died, of starvation or suicide; and the rest lived with some level of chronic illness for the rest of their lives.

Not a great track record, overall, and especially devastating for women, who suffer from anorexia at a rate of 10 times that of men. Luckily, we know a lot more about anorexia and other eating disorders now than we did in 1978.

“It’s Not About the Food”

In Bruch’s day, anorexia wasn’t the only illness attributed to faulty parenting and/or trauma. Therapists saw depression, anxiety, schizophrenia, eating disorders, and homosexuality (long considered a psychiatric “illness”) as ailments of the mind alone. Thanks to the rising field of behavioral neuroscience, we’ve begun to untangle the ways brain circuitry, neural architecture, and other biological processes contribute to these disorders. Most experts now agree that depression and anxiety can be caused by, say, neurotransmitter imbalances as much as unresolved emotional conflicts, and treat them accordingly. But the field of eating-disorders treatment has been slow to jump on the neurobiology bandwagon. When my daughter was diagnosed with anorexia in 2005, for instance, we were told to find her a therapist and try to get our daughter to eat “without being the food police,” because, as one therapist informed us, “It’s not about the food.”

Actually, it is about the food. Especially when you’re starving.

Ancel Keys’ 1950 Semi-Starvation Study tracked the effects of starvation and subsequent re-feeding on 36 healthy young men, all conscientious objectors who volunteered for the experiment. Keys was drawn to the subject during World War II, when millions in war-torn Europe – especially those in concentration camps – starved for years. One of Keys’ most interesting findings was that starvation itself, followed by re-feeding after a period of prolonged starvation, produced both physical and psychological symptoms, including depression, preoccupation with weight and body image, anxiety, and obsessions with food, eating, and cooking—all symptoms we now associate with anorexia. Re-feeding the volunteers eventuallyreversed most of the symptoms. However, this approach proved to be difficult on a psychological level, and in some ways more difficult than the starvation period. These results were a clear illustration of just how profound the effects of months of starvation were on the body and mind.

Alas, Keys’ findings were pretty much ignored by the field of eating-disorders treatment for 40-some years, until new technologies like functional magnetic resonance imaging (fMRI) and research gave new context to his work. We now know there is no single root cause for eating disorders. They’re what researchers call multi-factorial, triggered by a perfect storm of factors that probably differs for each person who develops an eating disorder. “Personality characteristics, the environment you live in, your genetic makeup—it’s like a cake recipe,” says Daniel le Grange, Ph.D., director of the Eating Disorders Program at the University of Chicago. “All the ingredients have to be there for that person to develop anorexia.”

One of those ingredients is genetics. Twenty years ago, the Price Foundation sponsored a project that collected DNA samples from thousands of people with eating disorders, their families, and control participants. That data, along with information from the 2006 Swedish Twin Study, suggests that anorexia is highly heritable. “Genes play a substantial role in liability to this illness,” says Cindy Bulik, Ph.D., a professor of psychiatry and director of the University of North Carolina’s Eating Disorders Program. And while no one has yet found a specific anorexia gene, researchers are focusing on an area of chromosome 1 that shows important gene linkages.

Certain personality traits associated with anorexia are probably heritable as well. “Anxiety, inhibition, obsessionality, and perfectionism seem to be present in families of people with an eating disorder,” explains Walter Kaye, M.D., who directs the Eating Disorders Treatment and Research Program at the University of California-San Diego. Another ingredient is neurobiology—literally, the way your brain is structured and how it works. Dr. Kaye’s team at UCSD uses fMRI technology to map blood flow in people’s brains as they think of or perform a task. In one study, Kaye and his colleagues looked at the brains of people with anorexia, people recovered from anorexia, and people who’d never had an eating disorder as they played a gambling game. Participants were asked to guess a number and were rewarded for correct guesses with money or “punished” for incorrect or no guesses by losing money.

Participants in the control group responded to wins and losses by “living in the moment,” wrote researchers: “That is, they made a guess and then moved on to the next task.” But people with anorexia, as well as people who’d recovered from anorexia, showed greater blood flow to the dorsal caudate, an area of the brain that helps link actions and their outcomes, as well as differences in their brains’ dopamine pathways. “People with anorexia nervosa do not live in the moment,” concluded Kaye. “They tend to have exaggerated and obsessive worry about the consequences of their behaviors, looking for rules when there are none, and they are overly concerned about making mistakes.” This study was the first to show altered pathways in the brain even in those recovered from anorexia, suggesting that inherent differences in the brain’s architecture and signaling systems help trigger the illness in the first place.

Food Is Medicine

Some of the best news to come out of research on anorexia is a new therapy aimed at kids and teens. Family-based treatment (FBT), also known as the Maudsley approach, was developed at the Maudsley Hospital in London by Ivan Eisler and Christopher Dare, family therapists who watched nurses on the inpatient eating-disorders unit get patients to eat by sitting with them, talking to them, rubbing their backs, and supporting them. Eisler and Dare wondered how that kind of effective encouragement could be used outside the hospital.

Their observations led them to develop family-based treatment, or FBT, a three-phase treatment for teens and young adults that sidesteps the debate on etiology and focuses instead on recovery. “FBT is agnostic on cause,” says Dr. Le Grange. During phase one, families (usually parents) take charge of a child’s eating, with a goal of fully restoring weight (rather than get to the “90 percent of ideal body weight” many programs use as a benchmark). In phase two, families gradually transfer responsibility for eating back to the teen. Phase three addresses other problems or issues related to normal adolescent development, if there are any.

FBT is a pragmatic approach that recognizes that while people with anorexia are in the throes of acute malnourishment, they can’t choose to eat. And that represents one of the biggest shifts in thinking about eating disorders. The DSM-IV, the most recent “bible” of psychiatric treatment, lists as the first symptom of anorexia “a refusal to maintain body weight at or above a minimally normal weight for age and height.” That notion of refusal is key to how anorexia has been seen, and treated, in the past: as a refusal to eat or gain weight. An acting out. A choice. Which makes sense within the psychodynamic model of cause.

But it doesn’t jibe with the research, which suggests that anorexia is more of an inability to eat than a refusal. Forty-five years ago, Aryeh Routtenberg, then (and still) a professor of psychology at Northwestern University, discovered that when he gave rats only brief daily access to food but let them run as much as they wanted on wheels, they would gradually eat less and less, and run more and more. In fact, they would run without eating until they died, a paradigm Routtenberg called activity-based anorexia (ABA). Rats with ABA seemed to be in the grip of a profound physiological imbalance, one that overrode the normal biological imperatives of hunger and self-preservation. ABA in rats suggests that however it starts, once the cycle of restricting and/or compulsive exercising passes a certain threshold, it takes on a life of its own. Self-starvation is no longer (if it ever was) a choice, but a compulsion to the death.

That’s part of the thinking in FBT. Food is the best medicine for people with anorexia, but they can’t choose to eat. They need someone else to make that choice for them. Therapists don’t sit at the table with patients, but parents do. And parents love and know their children. Like the nurses at the Maudsley Hospital, they find ways to get kids to eat. In a sense, what parents do is outshout the anorexia “voice” many sufferers report hearing, a voice in their heads that tells them not to eat and berates them when they do. Parents take the responsibility for making the choice to eat away from the sufferer, who may insist she’s choosing not to eat but who, underneath the illness, is terrified and hungry.

The best aspect of FBT is that it works. Not for everyone, but for the majority of kids and teens. Several randomized controlled studies of FBT and “treatment as usual” (talk therapy without pressure to eat) show recovery rates of 80 to 90 percent with FBT—a huge improvement over previous recovery rates. A study at the University of Chicago is looking at adapting the treatment for young adults; early results are promising.

The most challenging aspect of FBT is that it’s hard to find. Relatively few therapists in the U.S. are trained in the approach. When our daughter got sick, my husband and I couldn’t find a local FBT therapist. So we cobbled together a team that included our pediatrician, a therapist, and lots of friends who supported our family through the grueling work of re-feeding our daughter. Today she’s a healthy college student with friends, a boyfriend, career goals, and a good relationship with us.

A few years ago, Dr. Le Grange and his research partner, Dr. James Lock of Stanford, created a training institute that certifies a handful of FBT therapists each year. (For a list of FBT providers, visit the Maudsley Parents website.) It’s a start. But therapists are notoriously slow to adopt new treatments, and FBT is no exception. Some therapists find FBT controversial because it upends the conventional view of eating disorders and treatments. Some cling to the psychodynamic view of eating disorders despite the lack of evidence. Still, many in the field have at least heard of FBT and Kaye’s neurobiological findings, even if they don’t believe in them yet.

Change comes slowly. But it comes.

* * *

Harriet Brown teaches magazine journalism at the S.I. Newhouse School of Public Communications in Syracuse, New York. Her latest book is Brave Girl Eating: A Family’s Struggle with Anorexia (William Morrow, 2010).

be there for that person to develop anorexia.”

One of those ingredients is genetics. Twenty years ago, the Price Foundation sponsored a project that collected DNA samples from thousands of people with eating disorders, their families, and control participants. That data, along with information from the 2006 Swedish Twin Study, suggests that anorexia is highly heritable. “Genes play a substantial role in liability to this illness,” says Cindy Bulik, Ph.D., a professor of psychiatry and director of the University of North Carolina’s Eating Disorders Program. And while no one has yet found a specific anorexia gene, researchers are focusing on an area of chromosome 1 that shows important gene linkages.
Certain personality traits associated with anorexia are probably heritable as well. “Anxiety, inhibition, obsessionality, and perfectionism seem to be present in families of people with an eating disorder,” explains Walter Kaye, M.D., who directs the Eating Disorders Treatment and Research Program at the University of California-San Diego. Another ingredient is neurobiology—literally, the way your brain is structured and how it works. Dr. Kaye’s team at UCSD uses fMRI technology to map blood flow in people’s brains as they think of or perform a task. In one study, Kaye and his colleagues looked at the brains of people with anorexia, people recovered from anorexia, and people who’d never had an eating disorder as they played a gambling game. Participants were asked to guess a number and were rewarded for correct guesses with money or “punished” for incorrect or no guesses by losing money.
Participants in the control group responded to wins and losses by “living in the moment,” wrote researchers: “That is, they made a guess and then moved on to the next task.” But people with anorexia, as well as people who’d recovered from anorexia, showed greater blood flow to the dorsal caudate, an area of the brain that helps link actions and their outcomes, as well as differences in their brains’ dopamine pathways. “People with anorexia nervosa do not live in the moment,” concluded Kaye. “They tend to have exaggerated and obsessive worry about the consequences of their behaviors, looking for rules when there are none, and they are overly concerned about making mistakes.” This study was the first to show altered pathways in the brain even in those recovered from anorexia, suggesting that inherent differences in the brain’s architecture and signaling systems help trigger the illness in the first place.
Food Is Medicine
Some of the best news to come out of research on anorexia is a new therapy aimed at kids and teens. Family-based treatment (FBT), also known as the Maudsley approach, was developed at the Maudsley Hospital in London by Ivan Eisler and Christopher Dare, family therapists who watched nurses on the inpatient eating-disorders unit get patients to eat by sitting with them, talking to them, rubbing their backs, and supporting them. Eisler and Dare wondered how that kind of effective encouragement could be used outside the hospital.
Their observations led them to develop family-based treatment, or FBT, a three-phase treatment for teens and young adults that sidesteps the debate on etiology and focuses instead on recovery. “FBT is agnostic on cause,” says Dr. Le Grange. During phase one, families (usually parents) take charge of a child’s eating, with a goal of fully restoring weight (rather than get to the “90 percent of ideal body weight” many programs use as a benchmark). In phase two, families gradually transfer responsibility for eating back to the teen. Phase three addresses other problems or issues related to normal adolescent development, if there are any.
FBT is a pragmatic approach that recognizes that while people with anorexia are in the throes of acute malnourishment, they can’t choose to eat. And that represents one of the biggest shifts in thinking about eating disorders. The DSM-IV, the most recent “bible” of psychiatric treatment, lists as the first symptom of anorexia “a refusal to maintain body weight at or above a minimally normal weight for age and height.” That notion of refusal is key to how anorexia has been seen, and treated, in the past: as a refusal to eat or gain weight. An acting out. A choice. Which makes sense within the psychodynamic model of cause.
But it doesn’t jibe with the research, which suggests that anorexia is more of an inability to eat than a refusal. Forty-five years ago, Aryeh Routtenberg, then (and still) a professor of psychology at Northwestern University, discovered that when he gave rats only brief daily access to food but let them run as much as they wanted on wheels, they would gradually eat less and less, and run more and more. In fact, they would run without eating until they died, a paradigm Routtenberg called activity-based anorexia (ABA). Rats with ABA seemed to be in the grip of a profound physiological imbalance, one that overrode the normal biological imperatives of hunger and self-preservation. ABA in rats suggests that however it starts, once the cycle of restricting and/or compulsive exercising passes a certain threshold, it takes on a life of its own. Self-starvation is no longer (if it ever was) a choice, but a compulsion to the death.
That’s part of the thinking in FBT. Food is the best medicine for people with anorexia, but they can’t choose to eat. They need someone else to make that choice for them. Therapists don’t sit at the table with patients, but parents do. And parents love and know their children. Like the nurses at the Maudsley Hospital, they find ways to get kids to eat. In a sense, what parents do is outshout the anorexia “voice” many sufferers report hearing, a voice in their heads that tells them not to eat and berates them when they do. Parents take the responsibility for making the choice to eat away from the sufferer, who may insist she’s choosing not to eat but who, underneath the illness, is terrified and hungry.
The best aspect of FBT is that it works. Not for everyone, but for the majority of kids and teens. Several randomized controlled studies of FBT and “treatment as usual” (talk therapy without pressure to eat) show recovery rates of 80 to 90 percent with FBT—a huge improvement over previous recovery rates. A study at the University of Chicago is looking at adapting the treatment for young adults; early results are promising.
The most challenging aspect of FBT is that it’s hard to find. Relatively few therapists in the U.S. are trained in the approach. When our daughter got sick, my husband and I couldn’t find a local FBT therapist. So we cobbled together a team that included our pediatrician, a therapist, and lots of friends who supported our family through the grueling work of re-feeding our daughter. Today she’s a healthy college student with friends, a boyfriend, career goals, and a good relationship with us.
A few years ago, Dr. Le Grange and his research partner, Dr. James Lock of Stanford, created a training institute that certifies a handful of FBT therapists each year. (For a list of FBT providers, visit the Maudsley Parents website.) It’s a start. But therapists are notoriously slow to adopt new treatments, and FBT is no exception. Some therapists find FBT controversial because it upends the conventional view of eating disorders and treatments. Some cling to the psychodynamic view of eating disorders despite the lack of evidence. Still, many in the field have at least heard of FBT and Kaye’s neurobiological findings, even if they don’t believe in them yet.
Change comes slowly. But it comes.
* * *
Harriet Brown teaches magazine journalism at the S.I. Newhouse School of Public Communications in Syracuse, New York. Her latest book is Brave Girl Eating: A Family’s Struggle with Anorexia (William Morrow, 2010).

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

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.

Motherhood, war, and attachment: what does it all mean?


The antebellum tales
Scene 1: Two fathers encounter each other at a Boy Scout meeting. After a little conversation, one reveals that his son won’t be playing football because of concerns about head injuries. The other father reveals that he and his son love football, that they spoke with their pediatrician about it, and that their son will continue with football at least into middle school. There’s a bit of wary nodding, and then, back to the Pinewood Derby.

Scene 2: Two mothers meet on a playground. After a little conversation about their toddlers, one mother mentions that she still breastfeeds and practices “attachment parenting,” which is why she has a sling sitting next to her. The other mother mentions that she practiced “cry it out” with her children but that they seem to be doing well and are good sleepers. Then one of the toddlers begins to cry, obviously hurt in some way, and both mothers rush over together to offer assistance.

Scene 3: In the evening, one of these parents might say to a partner, “Can you believe that they’re going to let him play football?” or “I can’t believe they’re still breastfeeding when she’s three!” Sure. They might “judge” or think that’s something that they, as parents, would never do.

But which ones are actually involved in a war?

War. What is it good for?

I can’t answer that question, but I can tell you the definition of ‘war’: “a state of armed conflict between different nations or states or different groups within a nation or state.” Based on this definition and persistent headlines about “Mommy Wars,” you might conclude that a visit to your local playground or a mom’s group outing might require decking yourself out cap-á-pie in Kevlar. But the reality on the ground is different. There is no war. Calling disputes and criticisms and judgments about how other people live “war” is like calling a rowboat on a pond the Titanic. One involves lots of energy release just to navigate relatively placid waters while the other involved a tremendous loss of life in a rough and frigid sea. Big difference.

I’m sure many mothers can attest to the following: You have friends who also are mothers. I bet that for most of us, those friends represent a spectrum of attitudes about parenting, education, religion, Fifty Shades of Grey, recycling, diet, discipline, Oprah, and more. They also probably don’t all dress just like you, talk just like you, have the same level of education as you, same employment, same ambitions, same hair, or same toothpaste. And I bet that for many of us, in our interactions with our friends, we have found ourselves judging everything from why she insists on wearing those shoes to why she lets little Timmy eat Pop Tarts. Yet, despite all of this mental observation and, yes, judging, we still manage to get along, go out to dinner together, meet at one another’s homes, and gab our heads off during play dates.

That’s not a war. That’s life. It’s using our brains as shaped by our cultural understanding and education and rejection or acceptance of things from our own upbringing and talks with medical practitioners and books we’ve read and television shows we’ve watched and, for some of us, Oprah. Not one single friend I have is a cookie cutter representation of me or how I parent. Yet, we are not at war. We are friends. Just because people go online and lay out in black and white the critiques that are in their heads doesn’t mean “war” is afoot. It means expressing the natural human instinct to criticize others in a way that we think argues for Our Way of Doing Things. Online fighting is keeping up with the virtual Joneses. In real life, we are friends with the Joneses, and everyone tacitly understands what’s off limits within the boundaries of that friendship. That’s not war. It’s friendly détente.

The reality doesn’t stop the news media from trying to foment wars, rebellions, and full-on revolutions with provocative online “debates” and, lately, magazine covers. The most recent, from Time, features a slender mother, hand on cocked hip, challenging you with her eyes as she nurses her almost-four-year-old son while he stands on a chair. As Time likely intended, the cover caused an uproar. We’ve lampooned it ourselves (see above).

But the question the cover asks in all caps, “Are you mom enough?” is even more manipulative than the cover because it strikes at the heart of all those unspoken criticisms we think–we know–other women have in their heads about our parenting. What we may not consider is that we, too, are doing the same, and still… we are not actually at war. We’re just women, judging ourselves and other women, just like we’ve done since the dawn of time. It’s called “using your brain.” Inflating our interactions and fairly easily achieved parental philosophy détentes to “war” caricatures us all as shrieking harpies, incapable of backing off and being reasonable.

The real question to ask isn’t “Are you mom enough?” In fact, it’s an empty question because there is no answer. Your parenting may be the most perfect replica of motherhood since the Madonna (the first one), yet you have no idea how that will manifest down the road in terms of who your child is or what your child does. Whether you’re a Grizzly or a Tiger or a Kangaroo or a Panda mother, there is no “enough.”

So, instead of asking you “Are you mom enough?”, in keeping with our goal of bringing women evidence-based science, we’ve looked at some of the research describing what might make a successful parent–child relationship. Yes, the answer is about attachment, but not necessarily of the physical kind. So drop your guilt. Read this when you have time. Meanwhile, do your best to connect with your child, understand your child, and respond appropriately to your child.  

Why? Because that is what attachment is–the basic biological response to a child’s needs. If you’re not a nomad or someone constantly on the move, research suggests that the whole “physically attached to me” thing isn’t really a necessary manifestation of attachment. If you harken to it and your child enjoys it (mine did not) and it works for you without seeming like, well, an albatross around your neck, go for it.

What is attachment?

While attachment as a biological norm among primates has been around as long as primates themselves, humans are more complicated than most primates. We have theories. Attachment theory arose from the observations of a couple of human behaviorists or psychologists (depending on whom you ask), John Bowlby and Mary Ainsworth. Bowlby derived the concept of attachment theory, in which an infant homes in on an attachment figure as a “safe place.” The attachment figure, usually a parent, is the person who responds and is sensitive to the infant’s needs and social overtures. That parent is typically the mother, and disruption of this relationship can have, as most of us probably instinctively know, negative effects.

Bowlby’s early approach involved the mother’s having an understanding of the formational experiences of her own childhood and then translating that to an understanding of her child. He even found that when he talked with parents about their own childhoods in front of their children, the result would be clinical breakthroughs for his patients. As he wrote,

Having once been helped to recognize and recapture the feelings which she herself had as a child and to find that they are accepted tolerantly and understandingly, a mother will become increasingly sympathetic and tolerant toward the same things in her child.

Later studies seem to bear out this observation of a connection to one’s childhood experiences and more connected parenting. For example, mothers who are “insightful” about their children, who seek to understand the motivations of their children’s behavior, positively influence both their own sensitivity and the security of their infant’s attachment to them.  

While Bowlby’s research focused initially on the effects of absolute separation between mother and child, Mary Ainsworth, an eventual colleague of Bowlby, took these ideas of the need for maternal input a step further. Her work suggested to her that young children live in a world of dual and competing urges: to feel safe and to be independent. An attachment figure, a safe person, is for children an anchor that keeps them from become unmoored even as they explore the unknown waters of life. Without that security backing them up, a child can feel always unmoored and directionless, with no one to trust for security.

Although he was considered an anti-Freudian rebel, Bowlby had a penchant for Freudian language like “superego” and referred to the mother as the “psychic organizer.” Yet his conclusions about the mother–child bond resonate with their plain language:

The infant and young child should experience a warm, intimate, and continuous relationship with his mother (or permanent mother substitute) in which both find satisfaction and enjoyment.

You know, normal biological stuff. As a side note, he was intrigued by the fact that social bonds between mother and offspring in some species weren’t necessarily tied to feeding, an observation worth keeping in mind if you have concerns about not being able to breastfeed.

The big shift here in talking about the mother–child relationship was that Bowlby was proposing that this connection wasn’t some Freudian libidinous communion between mother and child but instead a healthy foundation of a trust relationship that could healthily continue into the child’s adulthood.

Ainsworth carried these ideas to specifics, noting in the course of her observations of various groups how valuable a mother’s sensitivity to her child’s behaviors were in establishing attachment. In her most famous study, the “Baltimore study” [PDF], she monitored 26 families with new babies. She found that “maternal responsiveness” in the context of crying, feeding, playing, and reciprocating seemed to have a powerful influence on how much a baby cried in later months, although some later studies dispute specific influences on crying frequencies.

Ainsworth also introduced the “Strange Situation” lab test, which seems to have freaked people out when it first entered the research scene. In this test, over the course of 20 minutes, a one-year-old baby is in a room full toys, first with its mother, then with mother and a strange woman, then with the stranger only (briefly), then with the mother, and then alone before the stranger and then the mother return. The most interesting findings of the study came from when the mother returned after her first absence, having left the baby alone in the room with a stranger. Some babies seemed quite angry, wanting to be with their mothers but expressing unhappiness with her at the same time and physically rejecting her.

From her observations during the Strange Situation, Ainsworth identified three types of attachment. The first was “Secure,” which, as its name implies, suggested an infant secure and comfortable with an attachment figure, a person with whom the infant actively seeks to interact. Then there’s the insecure–avoidant attachment type, in which an infant clearly is not interested in being near or interacting with the attachment figure. Most complex seems to be the insecure–resistant type, and the ambivalence of the term reflects the disconnected behavior the infant shows, seeming to want to be near the attachment figure but also resisting, as some of the unhappy infants described above behaved in the Strange Situation.

Within these types are now embedded various subtypes, including a disorganized–disoriented type in which the infant shows “odd” and chaotic behavior that seems to have no distinct pattern related to the attachment figure.

As you read this, you may be wondering, “What kind of attachment do my child and I have?” If you’re sciencey, you may fleetingly even have pondered conducting your own Strange Situation en famille to see what your child does. I understand the impulse. But let’s read on.

What are the benefits of attachment?

Mothers who are sensitive to their children’s cues and respond in ways that are mutually satisfactory to both parties may be doing their children a lifetime of favors, in addition to the parental benefit of a possibly less-likely-to-cry child. For example, a study of almost 1300 families looked at levels of cortisol, the “stress” hormone, in six-month-old infants and its association with maternal sensitivity to cues and found lower levels in infants who had “more sensitive” mothers.

Our understanding of attachment and its importance to infant development can help in other contexts. We can apply this understanding to, for example, help adolescent mothers establish the “secure” level of attachment with their infants. It’s also possibly useful in helping women who are battling substance abuse to still establish a secure attachment with their children.

On a more individual level, it might help in other ways. For example, if you want your child to show less resistance during “clean-up” activities, establishing “secure attachment” may be your ticket to a better-looking playroom.

More seriously, another study has found that even the way a mother applies sensitivity can be relevant. Using the beautiful-if-technical term ‘dyads’ to refer to the mother–child pair, this study included maternal reports of infant temperament and observations of maternal sensitivity to both infant distress and “non-distress.” Further, the authors assessed the children behaviorally at ages 24 and 36 months for social competence, behavioral problems, and typicality of emotional expression. They found that a mother’s sensitivity to an infant’s distress behaviors was linked to fewer behavioral problems and greater social competence in toddlerhood. Even more intriguing, the child’s temperament played a role: for “temperamentally reactive” infants, a mother’s sensitivity to distress was linked to less dysregulation of the child’s emotional expression in toddlerhood. 


And that takes me to the child, the partner in the “dyad”

You’re not the only person involved in attachment. As these studies frequently note, you are involved in a “dyad.” The other member of that dyad is the child. As much as we’d like to think that we can lock down various aspects of temperament or expression simply by forcing it with our totally excellent attachment skills, the child in your dyad is a person, too, who arrived with a bit of baggage of her own.

And like the study described above, the child’s temperament is a key player in the outcome of the attachment tango. Another study noted that multiple factors influence “attachment quality.” Yes, maternal sensitivity is one, but a child’s native coping behaviors and temperament also seem to be involved. So, there you have it. If you’re feeling like a parental failure, science suggests you can quietly lay at least some of the blame on the Other in your dyad–your child. Or, you could acknowledge that we’re all human and this is just part of our learning experience together.

What does attachment look like, anyway?

Dr. William Sears took the concept of attachment and its association with maternal sensitivity to a child’s cues and security and… wrote a book that literally translated attachment as a physical as well as emotional connection. This extension of attachment–which Sears appends to every aspect of parenting, from pregnancy to feeding to sleeping–has become in the minds of some parents a prescriptive way of doing things with benefits that exclude all other parenting approaches or “philosophies.” It also involves the concept of “baby wearing,” which always brings up strange images in my mind and certainly takes outré fashion to a whole new level. In reality, it’s just a way people have carried babies for a long time in the absence of other easy modes of transport.

When I was pregnant with our first child and still blissfully ignorant about how little control parents have over anything, I read Sears’ book about attachment parenting. Some of it is common-sense, broadly applicable parenting advice: respond to your child’s needs. Some of it is simply downright impossible for some parent–child dyads, and much of it is based on the presumption that human infants in general will benefit from a one-size-fits-all sling of attachment parenting, although interpretations of the starry-eyed faithful emphasize that more than Sears does.

Because much of what Sears wrote resonated with me, we did some chimeric version of attachment parenting–or, we tried. The thing is, as I noted above, the infant has some say in these things as well. Our oldest child, who is autistic, was highly resistant to being physically attached much of the time. He didn’t want to sleep with us past age four months, and he showed little interest in aspects of attachment parenting like “nurturing touch,” which to him was seemingly more akin to “taser touch.” We ultimately had three sons, and in the end, they all preferred to sleep alone, each at an earlier and earlier age. The first two self-weaned before age one because apparently, the distractions of the sensory world around them were far more interesting than the same boring old boob they kept seeing immediately in front of their faces. Our third was unable to breastfeed at all.

So, like all parents do, we punted, in spite of our best laid plans and intentions. Our hybrid of “attachment parenting” could better be translated into “sensitivity parenting,” because our primary focus, as we punted and punted and punted our way through the years, was shifting our responses based on what our children seemed to need and what motivated their behaviors. Thus, while our oldest declined to sleep with us according to the attachment parenting commandment, he got to sleep with a boiled egg because that’s what he wanted. Try to beat that, folks, and sure, bring on the judging.

The Double X Science
Sensitivity Parenting (TM) cheat sheet.

What does “sensitive” mean?

And finally, the nitty-gritty bullet list you’ve been waiting for. If attachment doesn’t mean slinging your child to your body until you’re lumbar gives out or the child receives a high-school diploma, and parenting is, indeed, one compromise after another based on the exigencies of the moment, what consistent tenets can you practice that meet the now 60-year-old concept of “secure” attachment between mother and child, father and child, or mother or father figure and child? We are Double X Science, here to bring you evidence-based information, and that means lists. The below list is an aggregate of various research findings we’ve identified that seem reasonable and reasonably supported. We’ve also provided our usual handy quick guide for parents in a hurry.
  • Plan ahead. We know that life is what happens while you’re planning things, but… life does happen, and plans can at least serve as a loose guide to navigation. So, plan that you will be a parent who is sensitive to your child’s needs and will work to recognize them.
  • Practice emotion detection. Work on that. It doesn’t come easily to everyone because the past is prologue to what we’re capable of in the present. Ask yourself deliberately what your child’s emotion is communicating because behavior is communication. Be the grownup, even if sometimes, the wailing makes you want your mommy. As one study I found notes, “Crying is an aversive behavior.” Yes, maybe it makes you want to cover your ears and run away screaming. But you’re the grownup with the analytical tools at hand to ask “Why” and seek the answer.
  • Have infant-oriented goals. If you tend to orient your goals in your parent–child dyad toward a child-related benefit (relieve distress) rather than toward a parent-oriented goal (fitting your schedule in some way), research suggests that your dyad will be a much calmer and better mutually adapted dyad.
  • Trust yourself and keep trying. If your efforts to read your child’s feelings or respond to your child’s needs don’t work right away, don’t give up, don’t read Time magazine covers, and don’t listen to that little voice in your head saying you’re a bad parent or the voice in other people’s heads screaming that at you. Just keep trying. It’s all any of us can do, and we’re all going to screw this up here and there.
  • Practice behaviors that are supportive of an infant’s sensory needs. For example, positive inputs like a warm voice and smiling are considered more effective than a harsh voice or being physically intrusive. Put yourself in your child’s place and ask, How would that feel? That’s called empathy. 
  • Engage in reciprocation. Imitating back your infant’s voice or faces, or showing joint attention–all forms of joint engagement–are ways of telling an infant or young child that yes, you are the anchor here, the one to trust, and really good time, to boot. Allowing this type of attention to persist as long as the infant chooses rather than shifting away from it quickly is associated with making the child comfortable with independence and learning to regulate behaviors.  
  • Talk to your child. We are generally a chatty species, but we also need to learn to chat. “Rich language input” is important in early child development beginning with that early imitation of your infant’s vocalizations.
Lather, rinse, repeat, adjusting dosage as necessary based on age, weight, developmental status, nanosecond-rate changes in family dynamics and emotional conditions, the teen years, and whether or not you have access to chocolate. See? This stuff is easy.

                                                          

Finally

As you read these lists and about research on attachment, you’ll see words like “secure” and “warm” and “intimate” and “safe.” Are you doing this for your child or doing your best to do it? Then you are, indeed, mom enough, whether you wear your baby or those shoes or both. That doesn’t mean that when you tell other women the specifics of your parenting tactics, they won’t secretly be criticizing you. Sure, we’ll all do that. And then a toddler will cry, we’ll drop it, and move on to mutually compatible things.

Yes, if we’re being honest, it makes most of us feel better to think that somehow, in some way, we’re kicking someone else’s ass in the parenting department. Unfortunately for that lowly human instinct, we’re all parenting unique individuals, and while we may indeed kick ass uniquely for them, our techniques simply won’t extend to all other children. It’s not a war. It’s human… humans raising other humans. Not one thing we do, one philosophy we follow, will guarantee the outcome we intend. We don’t even need science, for once, to tell us that.


By Emily Willingham, DXS managing editor

These views are the opinion of the author and do not necessarily either reflect or disagree with those of the
DXS editorial team.