Monday, July 30, 2012

Women in science ... on television?!? Evidently not

Really, TV people? Again with the "male only" science hosts?
Image via Wikimedia Commons, credit to Wonderlane
Emily Willingham, DXS managing editor

Today, I've seen yet another casting call for the "new Bill Nye the Science Guy" specifying a need for a male host for a science show. In fact, female science show hosts are so rare that even when a call seems to invite women as well as men, the people who write it can only think of men as examples. Ahem. Tiresome. So tiresome, in fact, that it's inspired me to make my very first video rant on behalf of women in science. [Apologies for the wobbly, underwater-like camera and my lack of a chin. I'm a writer, dammit, not a videographer. Obviously.]

Who are these women who could host shows about science? Several obvious candidates come to mind, including Carin Bondar and Joanne Manaster, who are degreed and experienced on camera and in talking about science. Another one who just eats a camera is Danielle Lee, although she's a tad busy in Tanzania right now doing, you know, science. It's possible that even television folk might consider any one of the Science Cheerleaders reasonably presentable and sufficiently educated to talk science to a television audience, or any one of our featured science communicators in our Double Xpression series profiling women into science. And that's just a starting list of the articulate, camera-friendly women out there with degrees in science and a happy capacity for communicating it to the masses. 

So... can we take the gonads out of it? Or, better yet, let's Title IX this puppy and level the playing field by making sure that for opportunities like this, gonads of all kinds are welcome. Testes don't do the talking when we communicate science, so why are they an important requirement?

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

Friday, July 27, 2012

Pregnancy 101: My placenta looked like meatloaf, but I wasn’t about to eat it.

By Jeanne Garbarino, Biology Editor
An historic view interpretation of the placenta (source). 

She gave me a few minutes to meet my daughter before she reeled me back into a state that was my new reality.  “You’re not finished Jeanne.  You still need to birth your placenta.”  What?!?! More pushing? But I was lucky and the efforts required to bring my placenta ex vivo were minimal. 
This is the second placenta my body helped make.  OK,
so it doesn't EXACTLY look like meatloaf...  
The idea of a placenta, which is the only human organ to completely and temporarily develop after birth, was fascinating.  That thing sitting in a rectangular periwinkle bucket was what allowed me to grow another human.. inside of my body!  There was no way I was not going to check it out, as well as create a permanent record of its relatively short-lived existence. 
My first impression was that it looked like “meatloaf.”  Not necessarily a well made meatloaf, but perhaps one that is made by my mother (sorry mom).  But, alas, chaos reigned and I wasn’t able to really take a good look.  However, for my second birth and hence second placenta, my midwife indulged me with a more detailed look and a mini-lesson.   

Baby's eye view:
Where geekling deux spent 39 weeks and 4 days. 
Her gloved hands, still wet with my blood and amniotic fluid, slid into the opening that was artificially created with a tool resembling a crocheting needle.  She opened the amniotic sac wide so I could get a baby's eye view of the crimson organ that served as a nutritional trading post between me and my new bundle of joy. 
She explained that the word “placenta” comes from from the Greek word plakoeis, which translates to “flat cake” (however, I’m sure if my mom’s meatloaf was more common in ancient Greece, the placenta would be named differently).   “It’s one of the defining features of being a mammal,” she explained as I was working on another mammalian trait – getting my baby to nurse for the first time.
That was about all I could mentally digest at the time, but still, more than three years later, the placenta continues to fascinate me, mostly due to the fact that it is responsible for growing new life.  It’s a natural topic for this long overdue Pregnancy101 post, so let’s dive in!
Development of the placenta
It all starts when a fertilized egg implants itself into the wall of the uterus.  But, in order to fully understand how it works, we should start with an overview of the newly formed embryo. 
The very early stages of us (and many other things that are alive).
The trophoblast invades the uterus,
leading to implantation of the blastocyst.
As soon as a male sperm cell fuses with a female egg cell, fertilization occurs and the cells begin to multiply.  But, they remain contained within a tiny sphere.  As the cells continue to divide, they are given precise instructions depending on their location within that sphere, and begin to transform into specific cell types.  This process, which is called cellular differentiation, actually seals the fate every cell in our body, sort of like how we all have different jobs – some of us are transport things, some of us are involved in policing the neighborhoods, some of us build structures, some of us communicate information, some of us deal with food, some of us get rid of waste, etc.  Every cell gets a job (it’s the only example of 100% employment rates!).
Now back to the cells in the fertilized egg.  As they start to learn what their specific job will be, the cells within the sphere will start to organize themselves.  After about 5 days after fertilization, the sphere of cells becomes something called a blastocyst, which readies itself for implantation into the wall of the uterus. 
The act of implantation is largely due to the cells found on the perimeter of the blastocyst sphere.  These cells, collectively known as the trophoblast, release a very important hormone – human chorionic gonadotropin (hCG) – that tells the uterus to prepare for it’s new tenant.  (If you recall, hCG is the hormone picked up by pregnancy tests.)  Around day 7, the trophoblast cells start to invade the lining of the uterus, and begin to form the placenta.  It is at this point that pregnancy officially begins.  (Here is a cool video, created by the UNSW Embryology Department, showing the process of implantation.)

Structure of the placenta
Eventually the trophoblast becomes the recognizable organ that is the placenta.  Consider the “flat cake” analogy, with the top of the cake being the fetal side (the side that is in contact with the baby), and the bottom of the cake being the maternal side (the side that is in contact with the mother).     
Cross section of the placenta: Blood vessels originating from the fetus sit in a pool
of maternal blood, which is constantly replenished my maternal arteries and veins.
The red represents oxygenated blood, and the blue represents de-oxygenated blood.
Projecting from the center of the fetal side of the placenta are two arteries and one vein, coiled together in a long, rubbery rope, often bluish-grey in color.   This umbilical cord serves as the tunnel through which nutrients and waste are shuttled, and essentially serves to plug the baby into the mother’s metabolic processes.  At the umbilical cord-placenta nexus, the umbilical cord arteries and vein branch out into a network of blood vessels, which further divide into a tree-like mass of vessels within the placenta. 
These tree-like masses originating from the umbilical cord (and thus fetus) sit in a cavity called the intervillous space, and are bathed in nutrient-rich maternal blood.  This maternal blood, which provides the fetus with a means for both nutrient delivery and waste elimination, is continually replenished via a network of maternal arteries and veins that feed into the intervillous space.  Furthermore, these arteries and veins help to anchor the placenta into the uterine wall.  One of the most interesting aspects about the mother-feus relationship is that the blood vessel connection is indirect.  This helps to prevent a detrimental immune response, which could lead to immunological rejection of the fetus (sort of like how a transplanted organ can become rejected by the recipient).  
Functions of the placenta
Just like a plant needs sunlight, oxygen, and water to grow, a baby needs all sorts of nutrients to develop.  And since a baby also produces waste, by nature of it being alive and all, there is an absolute requirement for waste removal.  However, because we can’t just give a developing fetus food or a bottle, nor are we able to change diapers in utero, the onus lies completely on the biological mother. 
This is where the placenta comes in. Because the fetus is plugged into the circulatory system of the mother via the umbilical cord and placenta, the fetus is provided with necessary nutrients and a mechanism to get rid of all the byproducts of metabolism.  Essentially, the placenta acts as a waitress of sorts – providing the food, and cleaning it all up when the fetus is done eating. 
But it’s not just about nutrition and waste.  The placenta also serves as a hormone factory, making and secreting biological chemicals to help sustain the pregnancy.  I mentioned above that the placenta produces hCG, which pretty much serves as a master regulator for pregnancy in that it helps control the production of maternally produced hormones, estrogen and progesterone.  It also helps to suppress the mother’s immunological response to the placenta (along with other factors), which cloaks the growing baby, thereby hiding it from being viewed as a “foreign” invader (like a virus or bacteria). 
Another hormone produced by the placenta is human placental lactogen (hPL), which tells the mother to increase her mammary tissue.  This helps mom prepare for nursing her baby once it’s born, and is the primary reason why our boobs tend to get bigger when we are pregnant.  (Yay for big boobies, but my question is, what the hell transforms our rear ends into giant double cheeseburgers, and what biological purpose does that serve??  But I digress…)

Despite the fact that the mother's circulatory system remains separate from the baby's circulatory system, there are a clear mixing of metabolic products (nutrients, waste, hormones, etc).  In essence, if it is in mom's blood stream, it will very likely pass into baby's blood stream.  This is the very reason that pregnant mothers are strongly advised to stay away from cigarettes, drugs, alcohol, and other toxic chemicals, all of which can easily pass through the placental barrier lying between mother and fetus.  When moms do not heed this warning, the consequences can be devastating to the developing fetus, potentially leading to birth defects or even miscarriage.        
There are also situations that could compromise the functions of the placenta – restriction of blood supply, loss of placental tissue, muted placental growth, just to name a few – reducing the chances of getting and/or staying pregnant.  This placental insufficiency is generally accompanied by slow growth of the uterus, low rate of weight gain, and most importantly, reduced fetal growth.     
And it’s not just the growth of the placenta that is important – where the placenta attaches to the uterus is also very important.  When the placenta grows on top of the opening of the birth canal, the chances for a normal, vaginal birth are obliterated.  This condition, known as placenta previa, is actually quite dangerous and can cuase severe bleeding in the third trimester.  0.5% of all women experience this, and it is one of the true medical conditions that absolutely requires a C-section. 
Then, there is the issue of attachment.  If the placenta doesn’t attach well to the uterus, it could end up peeling away from the uterine wall, which can cause vaginal bleeding, as well as deprive the baby from nutrient delivery and waste disposal.  This abruption of the placenta  is complicated by the use of drugs, smoking, blood clotting disorders, high blood pressure, or if the mother has diabetes or a history of placental abruption. 
Conversely, there are times when the blood vessels originating from the placenta implant too deeply into the uterus, which can lead to a placenta accreta.  If this occurs, the mother generally delivers via C-section, followed by a complete hysterectomy. 
Cultural norms and the placenta
There are many instances where the placenta plays a huge role in the culture of a society.  For instance, both the Maori people of New Zealand and the Navajo people of Southwestern US will bury the placenta.  There is also some folklore associated with the placenta, and several societies believe that it is alive, pehaps serving as a friend for the baby.   But the tradition that seems to be making it’s way into the granola culture of the US is one that can be traced back to traditional Chinese practices: eating the placenta. 
Placentophagy, or eating one’s own placenta, is very common among a variety of mammalian species.  Biologically speaking, it is thought that animals that eat their own placenta do so to hide fresh births from predators, thereby increasing the chances of their babies’ survival.  Others have suggested that eating the nutrient-rich placenta helps mothers to recover after giving birth.
However, these days, a growing number of new mothers are opting to ingest that which left their own body (likely) through their own vaginas.  And they are doing so though a very expensive process involving dehydrating and encapsulating placental tissue.  
Why would one go through this process?  The claims are that placentophagy will help ward of post partum depression, increase the supply of milk in a lactating mother, and even slow down the ageing process.  But, alas, these are some pretty bold claims that are substantiated only by anecdata, and not actual science (see this).
So, even though my placentas looked like meatloaf, there was no way I was eating them.  If you are considering this, I’d approach the issue with great skepticism.  There are many a people who will take advantage of maternal vulnerabilities in the name of cold hard cash.  And, always remember, if the claims sound to good to be true, they probably are!   

Thanks for tuning into this issue of Pregnancy101, and enjoy this hat, and a video!


Wednesday, July 25, 2012

Rest in peace, Sally Ride

Photo public domain image, via Wikimedia Commons.
By Matthew Francis, DXS Physics Editor

This week—on Monday, July 23—Sally Ride passed away after a battle with pancreatic cancer. She was 61.

Dr. Ride was a physicist and passionate advocate for STEM education for girls, a position she bolstered through her fame as a former Space Shuttle astronaut. In fact, she was the first American woman in space, and only the third woman worldwide to travel into space. She flew twice aboard the Challenger, first in 1983 and then again in 1984, when she controlled the Shuttle's robotic arm to deploy a satellite. Later, she served in the investigations after both the Challenger and Columbia disasters, the only person to sit on both committees. After retiring from NASA, she started Sally Ride Science, a company devoted to providing educational materials and classroom presentations to schools, specifically with an eye toward encouraging girls in the fields of science and engineering.

I remember her flights well, as I paid a lot of attention to the space program when I was young. (I also loved the robotic arm on the Shuttle, and wanted a chance to play with it. Now I understand that, while it might resemble a video game, it's a video game with millions of dollars in equipment at stake. However, I still haven't gotten over wanting to play with robotic arms. I can admit that, right?) I was the kid who wrote letters to NASA, asking for photos and information about their spacecraft. I have the pictures they sent me in a stack on my desk right now, in fact, and I'm looking at them as I write this post. While the photos themselves predated Dr. Ride's trips into space (the last group photo in the batch comes from the third flight, STS-3, while she first flew on STS-7), my greatest interest in the Shuttle peaked during her time as as an astronaut.

Much digital ink has been spilled over the revelation about her sexual orientation—her partner in business, writing, and life for the last 27 years was Tam O’Shaughnessy, which was no secret to her family and friends but not widely known beyond. I can't really blame Dr. Ride for keeping mostly quiet about it. After all, in the 1980s, it could have been grounds for dismissal from NASA; she faced enough sexism as it was. Her very existence as a woman astronaut was symbolic, and even today the default American astronaut is a white, (presumably) heterosexual male. Although the astronaut corps is a lot more diverse than it used to be, NASA's close ties with the military and its historical homophobia have no doubt made it difficult for any astronaut to acknowledge their sexual identity openly. For Dr. Ride and her primary mission in life to encourage girls in science, I can understand her reluctance to make herself into another symbol. However, that very fact is a sad comment, that being a woman in the public sphere is enough to be considered unusual that she didn't want to bring her sexual orientation into the picture. (I don't even presume to call her a lesbian, since human sexual identity is more fluid than many of us like to admit.)

Over the last two days, many people have written eulogies, reminiscences, tributes, and biographies; I'm not sure I can add much to those. Here are some of the best:
  • Nadia Drake's personal story from her childhood brought tears to my eyes. Similarly, I love astronomer Meg Urry's tribute.
  • Here's the big New York Times official obituary, which (as you might expect) is quite good and thorough.
  • While we rightfully celebrate Sally Ride's accomplishments, let's face it: the United States was really late in sending women into space. Institutional sexism delayed women astronauts far longer than should be acceptable in any civilized nation, and the locker-room culture at NASA during that era bears a lot of responsibility for the problem. Thirteen women trained to be part of the Mercury program, but were barred from ever flying. I lost a lot of respect for John Glenn when I found out he actively worked against allowing women to fly.
  • Natalie Wolchover at examines why there aren't openly gay astronauts in much more detail; here's another post on a similar personal note, from a lesbian astronomer.
  • An obituary from BuzzFeed, with comments from Ride's sister, Bear. (Seriously, isn't it also awesome to have a sister nicknamed "Bear"?)
Please leave your recollections of Sally Ride in the comments.

Monday, July 23, 2012

Mental illness, autism, and mass murder, and why Joe Scarborough needs to stop talking

Via Wikimedia Commons. Public domain. 
[Ed. note: Some of this information comes from a post that previously appeared at The Biology Files following the shooting massacre in Arizona targeting U.S. Rep. Gabrielle Giffords, among others.]
By Emily Willingham 

Today, Joe Scarborough at MSNBC warned viewers not to generalize about the horrific events in Aurora, CO, and then proceeded to opine that the killer in question was "on the autism scale." I'm not exactly sure what "on the autism scale" means, as I've never in all my years of involvement in the autism community come across such a device, but many of us in that community were waiting--nay, expecting--something like this almost from the minute we learned who had committed these murders. Too bad it came from a parent member of that community.

Hey, Joe, you've got a gun in your hand, and it's not like the one that the who-knows-what-his-disorder-is murderer in Aurora used. No. Your weapon is of a more subtle nature, and you wield it from a venue that reaches millions of people who don't know that the ammo you're firing is empty bullshit. But that bullshit ends up smearing the autistic community as violent criminals capable of all manner of psychotic behavior, including the taking of innocent lives and the well-planned rigging of an apartment building with dangerous explosives. And you must understand this on some level, as you have a son who is on the autism spectrum.

Here's the thing, Joe. You're conflating what can be very personal, nonfatal aggression of an overwhelmed autistic person with the wanton and willful and carefully planned destruction of total strangers in a crowded theater. Yes, some autistic people are aggressive, in the moment, in response to a moment, to being overwhelmed and not understood, to being mishandled and misused. That sort of aggression is a very, very different animal from the sort of cold, calculated malevolence that leads a young man to inflict tragedy across a large swath of humanity, total strangers to him, arriving with a measured burst of deadly force before calmly surrendering himself to authorities. You, Joe Scarborough, see that behavior as somehow "on the autism scale." Anyone who has even a mild grasp of autism knows how very far from reality that kind of behavior is for an autistic person. 

So let's talk about violence. 

A look at the violence literature reveals two rough categories of violent brain and genetics: the brain of the impulsively or hostilely violent and the brain of the proactive, or instrumentally violent--the one who carefully plans the violent act, rather than committing it in the heat of the moment. Impulsive violence, thanks to its unpredictability and relative ubiquity, seems to get the bulk of the attention. Proactive violence, which encompasses the planned violence of war, is a different animal altogether. And psychopathic instrumental violence may well be the most terrifying of them all. The two appear to have very different underlying mechanisms and origins, as well:
Biological models of violence have identified distinct neural patterns that characterize each type of violence. For example, the "low-arousal" aggressor more likely to commit instrumental violence is underreactive and responds sluggishly to stressors. In contrast, the "high-arousal" aggressor who is more prone to hostile violence tends to be hypervigiliant and easily frustrated 
In humans, instrumental aggression is roughly analogous to predatory aggression although it is limited to intraspecies behavior....Similarly, emotional or hostile aggression in humans could be considered the analogue of defensive aggression in response to a threat or perceived threat.
No one--and I mean, no one--has a clue what drove this man to commit his heinous crimes. What we do know is that he planned his hellish introduction into our psyches for months beforehand, carefully accumulating all the accouterments needed to generate a national and personal nightmare. What we also know is that he carefully planned his violent act; it was not, like an autistic meltdown, an act of the moment, an unplanned reaction

And you're wrong on some other counts as well, demonstrating the real dangers of a weapon like yours in the hands of the uninformed. You said that the minute you heard about the shooting, you knew it would be young white male, probably from "an affluent neighborhood." While being young, white, and male may fit the profile of many serial killers, mass murders are a different breed. They come from different backgrounds and ethnicities, but most share a single motivation: revenge. When they go beyond personal connections in their targets and kill total strangers, that revenge is usually against a society the killer thinks has wronged him. 

Other features in common are being male, being a "loner," and feeling alienated from the world. For the record, "autistic" does not equate with "loner" or "male," as much as you or the news media would like to distort it into that mold. Research, such as it is, suggests that the more a killer goes impersonal and targets strangers, the more likely a mental illness is to be involved. While that mental illness is usually paranoid schizophrenia, we must all remember that there are many, many more murderers in this world who are not schizophrenic than there are schizophrenics who commit this kind of violence. The coupling is not inevitable or even common. Indeed, better predictors of violence are unemployment, physical abuse, and recent divorce. The killer in the Aurora case had recently in effect become unemployed, having left graduate school and done poorly on spring exams. 

I'll close with this final observation: Autism is a disorder that is present from birth or very soon after. There are, however, other mental disorders and mental breaks that occur, particularly in young men and particularly at vulnerable developmental periods like adolescence and early adulthood. Not only does autism not fit here simply by virtue of its lifelong presence, but also, it's not something that just kinda shows up when a man turns 24 years old. 

The man who destroyed so many lives showed several signs of extreme stress prior to his murderous rampage. Were these stressors the trigger for him? That I cannot say. But I can say that stress does not bring on autism in one's 20s, and autism at any age doesn't lead to carefully calculated revenge killings of innocent strangers. So, Joe, why don't you just put down your weapon and back away... as quickly as you can.

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

Friday, July 20, 2012

Shmeat and Potatoes: The dinner of the future?

By Jeanne Garbarino, Biology Editor


“Meatloaf, beatloaf, double s[h]meatloaf…”  Was little Randy on to something?
Food engineering has been on an incredibly strange journey, but there is none stranger (at least to me) than the concept of in vitro meat.  Colloquially referred to as “shmeat,” a term born out of mashing up the phrase “sheets of meat,” in vitro meat may be available in our grocer’s refrigerator section in just a few years.  But how exactly is shmeat produced and how does it compare to, you know, that which is derived from actual animals?  Here, I hope to shed some light on this petri dish to kitchen dish phenomenon.
The shmeaty deets
When it comes to producing shmeat, scientists are taking advantage the extensive cell culture technologies that have been developed over the course of the 20th century (for a brief history of these developments, check this out).  Because of what we have learned, we can easily determine the conditions under which cells grow best, and swiftly turn a few cells into a few million cells.  However, things can get a little tricky when growing complex, three-dimensional tissues like steak or boneless chicken breast.
For instance, lets consider a living, breathing cow.  Most people seem to enjoy fancy cuts like beef tenderloin, which, before the butcher gets to it, is located near the back of the cow.  In order for that meat to be nice and juicy, it needs to have enough nutrients and oxygen to grow.  In addition, muscles (in this case, the tenderloin) need stimulation, and in the cow (and us too!) that is achieved by flexing and relaxing.
If shmeat is to be successfully engineered, scientists need to replicate all of the complexities that occur during the normal life of an actual animal.  While the technology for making shmeat is still being optimized, the components involved in this meat-making scheme successfully address many of the major issues with growing whole tissues in a laboratory. 
The first step in culturing meat is to get some muscle cells from an animal.  Because cells divide as they grow, a single animal could, in theory, provide enough cells to make meat for many, many people – and for a long period of time.  However, the major hurdle is creating a three-dimensional tissue, you know, something that would actually resemble a steak. 
Normally, cells will grow in a single layer on a petri dish, with a thickness that can only be measured by using a microscope.  Obviously that serving size would not be very satisfying.  In order to create that delicious three-dimensional look, feel, and taste, and be substantial enough to count as a meal, scientists have developed a way to grow the muscle cells on scaffold made of natural and edible material.  As sheets of cells grow on these scaffolds, they are laid on top of each other to bulk up the shmeat (hence “sheets of meat”).  But, in order for the cells on the inside of this 3D mass to grow as well as the cells on the outside, there has to be an sufficient way to deliver nutrients and oxygen to all cells. 
Back to the tenderloin – when it is still in the cow, the cells that make up this piece of meat are in close contact to a series of veins, arteries, and capillaries.  Termed vasculature, this system allows for the cells to obtain nutrients and oxygen, while simultaneously allowing cells to dump any waste into the blood stream.  There are some suggestions that the shmeat can be vascularized (grown such that a network of blood vessels are formed); however, the nutrient delivery system most widely used at this point is something called a bioreactor
A Bioreactor (Source)
This contraption is designed to support biologically active materials and how it works is actually quite cool.  The cells are placed in the cylindrical bioreactor, which spins at a rate that balances multiple physical forces, which keep the entire cell mass fully submerged in liquid growth medium at all times.  This growth medium is constantly refreshed, ensuring that the cells are always supplied with a maximum level of growth factors.  In essence, the shmeat is kept in a perpetual free fall state while it grows.         
But there is one last piece to the meat-growing puzzle, and that is regular exercise.  If we look at meat on a purely biological level, we would see that it is just a series of cells arranged to form muscle tissue.  Without regular stimulation, muscles will waste away (atrophy).  Clearly, wasting shmeat would not be very efficient (or tasty).  So, shmeat engineers have reduced the basic biological process involved with muscle stimulation to the most basic components – mechanical contraction and electrical stimulation.  Though mechanical contraction (the controlled stretching and relaxing of the growing muscle fibers) has been shown to be effective, it is not exactly feasible on a large scale.  Electrical stimulation – the process of administering regular electrical pulses to the cells – is actually more effective than mechanical contraction and can be widely performed.  Therefore, it seems to be a more viable option for shmeat production.    
Why in the world would we grow meat in a petri dish?
Grill it, braise it, broil it, roast it – as long as it tastes good, most people don’t usually question the origins of their meat.  Doing so could easily make one think twice about what they are eating.  Traditionally speaking, every slab of meat begins with a live animal – cow, pig, lamb, poultry (yes, despite what my grandmother says, this vegetarian does consider chicken to be meat) – with each animal only being able to provide a finite number of servings.  While shmeat does ultimately begin with a live animal, only a few muscle, fat, and other cells are required.
Given the theoretical amount that can be produced with just a few cells, the efficiency of traditional meat-generating farms and slaughterhouses is becoming increasingly scrutinized.  There are obvious costs – economic, agricultural, environmental – that are associated with livestock, and it has been proposed (article behind dumb pay wall, grrrr….) that shmeat engineering would substantially cut these costs.  For instance, it has been projected that shmeat production could use up to 45% less energy, compared to traditional farming methods.  Furthermore, relative to the current meat production process, culturing shmeat would use 99% less land, 82-96% less water, and would significantly reduce the amount of greenhouse gases produced. 
The impact of shmeat compared to tradtional agricultural processes.
(Environ. Sci. Technol., 2011, 45 (14), pp 6117–6123)
But the potential benefits of making the shift toward shmeat (as opposed to meat) doesn’t stop with its positive environmental impact.  From a nutritional standpoint, it is possible to produce shmeat in a way that would significantly reduce the amount of saturated fat it contains.  Additionally, there are technologies that would allow shmeat to be enriched with heart-healthy omega-3 fats, as well as other types of polyunsaturated fats.  In essence, shmeat could possibly help combat our growing obesity epidemic, as well as the associated illnesses such as diabetes and heart disease.  That’s *if* it can be produced in a way that is both affordable and widely available (more on that in a bit). 
In terms of health, switching to shmeat would improve more than our waistlines.  Because shmeat would be produced in a sterile environment, the incidence of E. coli and other bacterial and/or viral contamination would be next to nothing relative to current meat production methods.  On a more superficial level, shmeat technology would allow for the introduction of some very exotic meats into the mainstream.  Because this technology does not require an animal to be slaughtered (another good reason that supports shmeat productions) and it is not limited to the more common sources of meat, it would be entirely possible to make things like panda sausage and crocodile burgers.  But, of course, getting people to actually eat meat grown in a test-tube is another issue…
The limitations of shmeat
Now that I’ve just spent a few paragraphs singing shmeat’s praises, it is probably best that I fill you in on some of the major roadblocks associated with shmeat production.  According to scientists, there are two main concerns: the first is that shmeat production will not be subjected to the normal regulatory (homeostatic) mechanisms that naturally occur in animals (scientists are having trouble figuring out how to replicate these processes); and the second is that shmeat engineering technology has not evolved enough so that it can occur on an industrial scale.  Because of these issues and others, the cost of culturing shmeat in the laboratory is very high.  But, there has always got to be a starting point.  As the technologies advance, the cost-production ratios will decrease and, eventually, shmeat will find its way to the dining table – our dining table. 
Interestingly, the folks at PETA are all for shmeat and offered a one million dollar prize to the first group who could come up with the technology to make shmeat commercially available by June, 2012.  Obviously, that did not happen, and the contest has been extended to January 2013 (this offer has been on the table since 2008).  But, the first tastes test for shmeat hamburgers is going down in October of this year. 
At the moment, the largest piece of shmeat to be created is about the size of a contact lens and my guess is that, barring unforeseen technological breakthroughs, this reward will go unclaimed for a long, long time.  But, many a miracle has been known to happen in about nine months time…   
A few final thoughts on shmeat
With the world population expected to hit 9 billion by 2050, which will be accompanied by a major increase in the need for the amount of food produced, perhaps shmeat technology will become one of the critical innovations required for our collective survival on this planet.  But, there is just one thing: the ick factor.  It is a little hard for me to weigh in on this issue because almost all meat seems gross to me (unless it is a pulled pork sandwich, lovingly made by my long-time pal and professional chef – Julie Hall).  While most of my peers have less of an aversion to meat, I can’t imagine that they would eagerly line up for a whopping serving of lab-grown shmeat. 
But, say scientists finally figure it out and shmeat production is scaled up for mass consumption – how will the agricultural sector react?  As of right now, the agricultural industry in the USA is worth over $70 billion, with a yearly beef consumption tipping over the 26 million pound mark (of which 8.7% is exported).  Shmeat probably has definitely gotten the attention of cattle farmers (and other meat farmers/production companies) and, given the size of this industry, I wonder how much muscle will be used to block shmeat from becoming a household phenomenon.
Over all, I think that shmeat is a revolutionary idea as it could have a significant impact on humanity.  However, there are many complex questions that need to be both asked and answered.  As excited as I am at the thought of not having to kill an animal to eat a steak, I still remain skeptical (though this sentiment may not have been fully present for the majority of this post).  Will shmeat be produced in such a way that it will be indistinguishable from traditional meat?  Additionally, will shmeat live up to all of these expectations?  I am going to try and keep a positive outlook with this one.  Perhaps the next time I actually step foot in a kitchen to prepare a meal, I’ll follow Randy’s lead by making a shmeatloaf, served alongside a heaping side of mashed potatoes.  Now that’s some pretty cool kitchen science.

And now, an oldie but a goodie (let it be known that I am in love with Stephen Colbert):

The Colbert ReportMon - Thurs 11:30pm / 10:30c
World of Nahlej - Shmeat
Colbert Report Full EpisodesPolitical Humor & Satire BlogVideo Archive

For more information:
The Brian Lehrer Show, Shmeat: It’s whats for dinner
New Harvest, Cultured Meat FAQs
Environmental Science and Technology, Environmental Impacts of Cultured Meat Production
The Telegraph, First artificial burger to cost 250K

**This was a post that made it's first appearance on my old blog, The Mother Geek.  Long may it live on Joe Bonner's Google Reader - that's the only place it exists now! (at least that I know).  Update: wait, I just found it on Science Seeker!

Tuesday, July 17, 2012

Dinosaur Aunts, Bacterial Stowaways, & Insect Milk

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

Dinosaur Aunts, Bacterial Stowaways, & Insect Milk

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

Evolutionary Origins of Lactation

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


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

Ophiacodon by Dmitri Bogdanov

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

Illustration by Carl Buell

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

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

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

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

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

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

Vertical Transmission of Bacteria via Milk

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


A number of insects have evolved the ability to rely on nutritionally incomplete food sources. They are able to do so because bacteria that live inside their cells provide what the food does not. These bacteria are known as endosymbionts and the specialized cells the host provides for them to live in are called bacteriocytes. For example, the tsetse fly has a bacterium, Wigglesworthia glossinidia,* that provides B vitamins not available from blood meals. Um, if you are squeamish, don’t read the previous sentence.     

 *I submit the tsetse fly and its bacterial symbiont (Wigglesworthia glossinidia
for consideration as the number one mutualism in which the common name of the host 
and the Latin name of the bacteria are awesome to say out loud! 
Bring on your challenger teams.

Hosokawa and colleagues recently revealed the Russian nesting dolls that are bats (Miniopterus fuliginosus), bat flies (Nycteribiidae), and endosymbiotic bacteria (proposed name Aschnera chenzii)(2012). Bat flies are the obligate ectoparasites of bats (Peterson et al. 2007). They feed on the blood of their bat hosts, and for nearly their entire lifespan, bat flies live in the fur of their bat hosts. Females briefly leave their host to deposit pupae on stationary surfaces within the bat roost. 
Bat flies are even more crazy amazing because they have a uterus and provide MILK internally through the uterus to larva! Male and female bat flies have endosymbiotic bacteria living in bacteriocytes along the sides of their abdominal segments (revealed by 16S rRNA). Additionally, females host bacteria inside the milk gland tubules, “indicating the presence of endosymbiont cells in milk gland secretion”. 

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


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


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