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Are These Crime Drama Clues Fact or Fiction?

Steven Avery, featured in the Netflix documentary Making a Murderer, served 18 years in prison for rape, then was exonerated by DNA. He was convicted of murder in 2007, based partly on DNA evidence.
Steven Avery, featured in the Netflix documentary Making a Murderer, served 18 years in prison for rape before being exonerated by DNA in 2003. In 2007, he was convicted of murder, based partly on DNA evidence.

I’m often just as surprised by what forensic scientists can’t do as by what they can. In the Netflix documentary Making a Murderer, for instance, the question of whether police planted the main character’s blood at a crime scene comes down to whether or not the FBI can detect a common laboratory chemical called EDTA in a bloodstain.

On a TV crime show, this would be a snap. The test would take about five minutes and would involve inserting a swab into a magic detector box that beeps and spits out an analysis of every substance known to humankind.

In real life, there’s no common and accepted test in forensic labs for EDTA even today, nine years after the FBI tested blood for the Steven Avery trial featured in Making a Murderer. In that case, the FBI resurrected a test they had last used in the 1995 O.J. Simpson trial, and testified that the blood in question did not contain EDTA and therefore was not planted using EDTA-preserved blood from an evidence vial. (Avery was convicted.)

Questions about the test’s power and reliability have dogged the case ever since. There’s even an in-depth Reddit thread where fans of the Netflix show are trying to sort out the science.

Having worked in chemistry labs, it surprised me at first that this analysis would be difficult or controversial. After all, a quick search of the scientific literature turns up methods for detecting low levels of EDTA in everything from natural waters to beverages.

Steven Averys
Steven Avery’s attorneys Jerome Buting (shown) and Dean Strang struggled to dispute chemical evidence introduced mid-trial that undermined the idea that police had planted blood evidence.

But the key here is that we’re talking about forensic science, not beverage chemistry. Beverage chemistry, in this case, is much more exacting. Was there really no EDTA in the blood swabbed from victim Teresa Halbach’s vehicle, or was the chemical simply too diluted or degraded to be detected with the FBI’s method? Could the test have missed a small amount of EDTA? It would be hard to say without further experiments that replicate crime scene conditions, experiments that essentially put the test to the test.

The reality is that forensic science today is a strange mix of the high-tech and the outdated, so questions about evidence like those in Avery’s case are not uncommon. Methods that we take for granted, like measuring a particular chemical, or lifting a fingerprint off a gun and matching it to a suspect, can be difficult—and far from foolproof. On the other hand, some of the real science happening now sounds like something dreamed up by Hollywood script writers, such as new methods aiming to reconstruct what a person’s face looks like using only their DNA.

Making a Murderer, whether it sways your opinion on Steven Avery or not, has done a service by getting people interested in something as arcane as EDTA tests, and by showing why real-life crimes are not solved nearly so neatly as fictional ones.

I see the messiness of forensic science all the time, because I scan its journals and often come across new studies that make me think either “you mean we couldn’t already do that?” or “I had no idea that was possible.” I’ve gathered a few recent examples for a quiz.

How well can you separate CSI fact from fiction? Here are a few crime-solving scenarios I’ve cooked up; see if you can tell which use real methods based on new forensic research. You’ll find the answers below.

  1. A skeleton is found buried in a shallow grave. The body’s soft tissues have completely decomposed, so only the teeth and bones remain. A forensic anthropologist examines the bones and reports that they come from a female who was five foot six inches tall, and obese. Could she really tell the person was overweight?
  2. The body of a white male in his 50s turns up on a nature trail, scavenged by animals. The victim’s bones show a number of puncture wounds consistent with animal bites, but x-rays reveal fine lines of different density in the bone around some of the punctures. An expert says these lines show that the wounds were made about 10 years before death. Is it possible to tell the approximate age of these wounds from x-rays?
  3. A woman is found dead in her home, bludgeoned to death. A bloody frying pan lies on the floor next to her. Her husband is the main suspect. Fingerprints on the pan’s handle are too smudged to make a definitive ID, but an analyst says she can still rule out the husband: All of the fingerprints on the pan came from a woman, the expert says. Is it possible to tell if the fingerprints were from a male or female?
  4. A woman is sexually assaulted and identifies her male attacker in a lineup. The suspect’s DNA matches DNA found on her body. It looks like an easy case for the prosecutor—until the suspect reveals that he has an identical twin. Neither twin admits to the crime. Is it possible to tell which twin’s DNA was found at the crime scene?
  5. A witness sees a man in a stocking mask rob and shoot a man outside his home. A stocking is found near the house, and a hair-analysis expert testifies that 13 hairs in the mask are all human head hairs from an African-American. A microscopic analysis matches the characteristics of one hair to a particular African-American suspect. The prosecutor tells the jury that the chances are one in ten million that this could be someone else’s hair. Can hairs be matched to an individual this accurately?


Answers Below


  1. Yes. Biologists have long known that greater body mass changes the weight-bearing bones of the legs and spine, and a new study shows that even bones that aren’t supporting most of the body’s weight, such as arm bones, have greater bone mass and are stronger in obese people. So even in a skeleton missing its legs, our forensic anthropologist might be able to tell that the person was obese.
  2. No. This one is from an actual episode of Bones (The Secret in the Siege, Season 8, Episode 24, reviewed here by real-life bioarchaeologist Kristina Killgrove). In the episode, Dr. Temperance Brennan uses Harris lines to determine the age of bone injuries in two victims. Harris lines are real, but they form only in growing bones, so are useful only in determining childhood injuries or illness.
  3. Yes. A study published in November showed that the level of amino acids in sweat is about twice as high in women’s fingerprints as in men’s. Of course, as with all the new methods, this one could face challenges as evidence in a U.S. court of law, where the Daubert standard allows judges to decide whether scientific evidence is admissible based on factors including its degree of acceptance by the scientific community.
  4. Yes, if you do it right. Standard DNA tests don’t distinguish between twins, who are born with nearly identical DNA, but it’s possible to do a more sophisticated test to catch post-birth mutations and epigenetic differences, which you can think of as genetic “add-ons” that don’t affect the DNA sequence itself. One new test distinguishes between twins by looking for small differences in the melting temperature of their DNA that are caused by such epigenetic modifications.
  5. No. The field of hair analysis has come under heavy scrutiny, especially after a review by the U.S. Justice Department revealed major flaws in 257 out of 268 hair analyses from the FBI. The case described here is the real-life case of Santae Tribble, convicted in 1978 of murder. In 2012, DNA tests showed that none of the hairs matched Tribble—and one was from a dog.
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Mice Inherit Specific Memories, Because Epigenetics?

Two weeks ago I wrote about some tantalizing research coming out of the Society for Neuroscience meeting in San Diego. Brian Dias, a postdoctoral fellow in Kerry Ressler’s lab at Emory University, had reported that mice inherit specific smell memories from their fathers — even when the offspring have never experienced that smell before, and even when they’ve never met their father. What’s more, their children are born with the same specific memory.

This was a big, surprising claim, causing many genetics experts to do a double-take, as I discovered from a subsequent flurry of Tweets. “Crazy Lamarkian shit,” quipped Laura Hercher (@laurahercher), referring to Lamarckian inheritance, the largely discredited theory that says an organism can pass down learned behaviors or traits to its offspring. “My instinct is deep skepticism, but will have to wait for paper to come out,” wrote Kevin Mitchell (@WiringTheBrain). “If true, would be revolutionary.”

The paper is out today in Nature Neuroscience, showing what I reported before as well as the beginnings of an epigenetic explanation. (Epigenetics usually refers to chemical changes that affect gene expression without altering the DNA code).

Having the data in hand allowed me to fill in the backstory of the research, as well as gather more informed reactions from experts in neuroscience and in genetics. I’ve gone into a lot of detail below, but here’s the bottom line: The behavioral results are surprising, solid, and will certainly inspire further studies by many other research groups. The epigenetic data seems gauzy by comparison, with some experts saying it’s thin-but-useful and others finding it full of holes.

So what is the surprising part, again? 

If you’ve followed science news over the past decade then you’ve probably heard about epigenetics, a field that’s caught fire in the minds of scientists and the public, and understandably so. Epigenetic studies have shown that changes in an organism’s external environment — its life experiences and even its choices, if you want to get hyperbolic — can influence the expression of its otherwise inflexible DNA code. Epigenetics, in other words, is enticing because it offers a resolution to the tedious, perennial debates of nurture versus nature.

But some scientists dispute the notion that epigenetic changes have much influence on behavior (see this Nature feature for a great overview of the debate). Even more controversial is the idea that epigenetic changes can be passed down from one generation to the next, effectively giving parents a way to prime their children for a specific environment. The key question isn’t whether this so-called ‘transgenerational epigenetic inheritance’ happens — it does — but rather how it happens (and how frequently, and in what contexts and species).

That’s what Dias and Ressler wanted to investigate. Trouble is, environmental influences such as stress are notoriously difficult to measure. So the researchers focused on the mouse olfactory system, the oft-studied and well-mapped brain circuits that process smell. “We thought it would give us a molecular foothold into how transgenerational inheritance might occur,” Dias says.

The researchers made mice afraid of a fruity odor, called acetophenone, by pairing it with a mild shock to the foot. In a study published a few years ago, Ressler had shown that this type of fear learning is specific: Mice trained to fear one particular smell show an increased startle to that odor but not others. What’s more, this fear learning changes the organization of neurons in the animal’s nose, leading to more cells that are sensitive to that particular smell.

Ten days after this fear training, Dias allowed the animals to mate. And that’s where the crazy begins. The offspring (known as the F1 generation) show an increased startle to the fruity smell even when they have never encountered the smell before, and thus have no obvious reason to be sensitive to it. And their reaction is specific: They do not startle to another odor called propanol. Craziest of all, their offspring (the F2 generation) show the same increased sensitivity to acetophenone.

The scientists then looked at the F1 and F2 animals’ brains. When the grandparent generation is trained to fear acetophenone, the F1 and F2 generations’ noses end up with more “M71 neurons,” which contain a receptor that detects acetophenone. Their brains also have larger “M71 glomeruli,” a region of the olfactory bulb that responds to this smell.

“When Brian came in with the first set of data, we both just couldn’t believe it,” Ressler recalls. “I was like, ‘Well, it must just be random, let’s do it again.’ And then it just kept working. We do a lot of behavior [experiments], but being able to see structural change that correlates with behavior is really pretty astounding.”

Still, those experiments couldn’t rule out some kind of social, rather than biological transmission. Perhaps fathers exposed to the fear training treated their children differently. Or maybe mothers, sensing something odd in their mate’s behavior, treated their children differently.

To control for these possibilities, the researchers performed an in vitro fertilization (IVF) experiment in which they trained male animals to fear acetophenone and then 10 days later harvested the animals’ sperm. They sent the sperm to another lab across campus where it was used to artificially inseminate female mice. Then the researchers looked at the brains of the offspring. They had larger M71 glomeruli, just as before. (The researchers couldn’t perform behavioral tests on these animals because of laboratory regulations about animal quarantine.)

“For me it clicked when we did the IVF,” Dias says. “When the brain anatomy persisted, that to me emphasized that it’s not really a social transmission. It’s inherited.”

Other researchers also seem convinced. “It is high time public health researchers took human transgenerational responses seriously,” says Marcus Pembrey, emeritus professor of paediatric genetics at University College London, who has been championing the idea of epigenetic inheritance for over a decade. “I suspect we will not understand the rise in neuropsychiatric disorders or obesity, diabetes and metabolic disruptions generally without taking a multigenerational approach,” he says.

In an interesting historical aside, Pembrey also notes that the new study echoes an experiment that Ivan Pavlov did* 90 years ago, in which he trained mice to associate food with the sound of a bell. Pavlov “reported that successive generations took fewer and fewer training sessions before they would search for food on hearing a bell even when food was absent,” Pembrey says. Nevertheless, the idea that experience could be biologically inherited fell out of favor in the 20th century. “If alive today, Pavlov would have been delighted by the Dias and Ressler paper, first as a vindication of his own experiment and results, and second by the amazing experimental tools available to the modern scientist.”

Neuroscientists, too, are enthusiastic about what these results might mean for understanding the brain.

“To my knowledge this is the first example, in any animal, of epigenetic transmission of a simple memory for a specific perceptual stimulus,” says Tomás Ryan, a research fellow at MIT who studies how memories form in the brain. “The broader implications for the neuroscience of memory and to evolutionary biology in general could be paradigm shifting and unprecedented.”

There are still some unanswered questions, Ryan notes. For example, the researchers didn’t do a control experiment where the F0 animals are exposed to the fruity odor without the shock. So it’s unclear whether the “memory” they’re transmitting to their offspring is a fear memory, per se, or rather an increased sensitivity to an odor. This is an important distinction, because the brain uses many brain circuits outside of the olfactory bulb to encode fear memories. It’s difficult to imagine how that kind of complicated brain imprint might get passed down to the next generation.

Ressler and Dias agree, and for that reason were careful not to refer to the transmitted information as a fear memory. “I don’t know if it’s a memory,” Dias says. “It’s a sensitivity, for now.”

What’s that got to do with epigenetics?

So let’s call it a sensitivity. How could a smell sensitivity, formed in an adult animal’s olfactory bulb in its brain, possibly be transmitted to its gonads and passed on to future generations?

The researchers are nowhere near being able to answer that question, but they have some data that points to epigenetics.

There are several types of epigenetic modifications. One of the best understood is DNA methylation. There are millions of spots along the mouse genome (and the human genome), called CpG sites, where methyl groups can attach and affect the expression of nearby genes. Typically, methylation dials down gene expression.

Dias and Ressler sent sperm samples of mice that had been fear-conditioned to either acetophenone or propanol to a private company, called Active Motif, which specializes in methylation analyses. The company’s researchers (who were blinded to which samples were which) mapped out the sperm methylation patterns near two olfactory genes: Olfr151, which codes for the M71 receptor that’s sensitive to acetophenone, and Olfr6, which codes for another odor receptor that is not sensitive to either odor.

It turns out that Olfr151, but not the other gene, is significantly less methylated in sperm from animals trained to fear acetophenone than in sperm from those trained to fear propanol. Because less methylation usually means a boost in gene expression, this could plausibly explain why these animals have more M71 receptors in their brains, the researchers say.

What’s more, the same under-methylation shows up in the sperm of F1 animals whose fathers had been trained to fear acetophenone.

“It’s a very precise signal,” Ressler says. “The convergence of this data, we think, shows that this is a really profound and robust phenomenon.”

Others, though, find a number of flaws in this epigenetic explanation.

Timothy Bestor, professor of genetics and development at Columbia University, points out that methylated CpG sites only affect gene expression when they are located in the so-called gene promoter, a region about 500 bases upstream of the gene. But the Olfr151 gene doesn’t have any CpG sites in its promoter.

That means the differences in methylation reported in the paper must have occurred within the body of the gene itself. “And methylation in the gene body is common to all genes whether they’re expressed or not,” Bestor says. “I don’t see any way by which that gene could be directly regulated by methylation.”

But what would explain the methylation differences between the trained animals and controls? They’re pretty subtle, he says, and “could easily be a statistical fluke.”

Bestor was skeptical from the outset, based on the mechanics of the reproductive system alone. “There’s a real problem in how the signal could reach the germ cells,” he says.

For one thing, the seminiferous tubules, where sperm is made inside of the testes, don’t have any nerves. “So there’s no way the central nervous system could affect germ cell development.” What’s more, he says it’s not likely that acetophenone would be able to cross the blood-testis barrier, the sheet of cells that separates the seminiferous tubules from the blood.

By this point in my conversation with Bestor, I was starting to feel a bit defensive on behalf of epigenetics and all of its wonder. “Are you saying you think epigenetic inheritance is a bunch of bologna?” I asked helplessly.

“No,” he said, laughing. “It’s just not as dynamic as people think.”

What’s next?

A good next step in resolving these pesky mechanistic questions would be to use chromatography to see whether odorant molecules like acetophenone actually get into the animals’ bloodstream, Dias says. “The technology is surely there, and I think we are going to go down those routes.”

First, though, Dias and Ressler are working on another behavioral experiment. They want to know: If the F0 mice un-learn the fear of acetophenone (which can be done by repeated exposures to the smell without a shock) and then reproduce, will their children still have an increased sensitivity to it?

“We have no idea yet,” says Ressler, a practicing psychiatrist who has long been interested in the effects of post-traumatic stress disorder (PTSD). “But we think this would have tremendous implications for the treatment of adults [with PTSD] before they have children.”

It will take a lot more work before scientists come close to understanding how these data relate to human anxiety disorders. So what, after all of these words, should we take away from this study now?

Hell if I know. Here’s the most rational and conservative appraisal I can muster: Our bodies are constantly adapting to a changing world. We have many ways of helping our children make that unpredictable world slightly more predictable, and some of those ways seem to be hidden in our genome.

Anne Ferguson-Smith, a geneticist at the University of Cambridge, put it more succinctly. The study, she says, “potentially adds to the growing list of compelling models telling us that something is going on that facilitates transmission of environmentally induced traits.”

Scientists, I have to assume, will be furiously working on what that something is for many decades to come. And I’ll be following along, or trying to, with awe.

*Update, 12/1/13, 2:35pm: It seems that that Pavlov experiment may have been retracted in 1927, though I don’t know anything about that beyond what is stated here.

Style note: A few paragraphs of this post were adapted from my earlier post on this research, published November 15.

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Mice Inherit the Fears of Their Fathers

UPDATE (12/1, 2:37pm): This study was just published in Nature Neuroscience; you can read all of the juicy details here.

UPDATE (11/17, 11:22 am): I just published a new post showing how scientists reacted to this study on Twitter, with comments ranging from “awe-inspiring biology” to “deep skepticism.”


There’s no question that trauma gets handed down from one generation to the next.

In one highly publicized example, researchers in New York studied several dozen women who were pregnant on September 11, 2001, and had been in the vicinity of the terrorist attacks. Some of these women developed post-traumatic stress disorder (PTSD), and this group shows lower levels of the stress hormone cortisol in their saliva than do those who did not develop PTSD. But here’s the rub: At 9 months old, the babies of the women with PTSD have significantly lower cortisol levels than babies of healthy mothers.

In earlier work, the same researchers had reported low cortisol levels in adult children of Holocaust survivors with PTSD. And in yet another study, Kerry Ressler’s group at Emory University showed that the so-called “startle response” to a sudden stimulus — a marker of anxiety — is more pronounced in kids whose mothers were physically abused as children then in those whose mothers were not abused. I could go on.

But how, exactly, does a parent’s stress leave such a deep impression on its progeny?

Part of it is nurture. A parent’s sadness and stress naturally affects how they interact with other people, including their children. The Holocaust study, in fact, found that the survivors with PTSD tended to emotionally abuse or neglect their children. And we know from some remarkable experiments in rats that parental care affects the offspring’s genes: Rat pups that get a lot of licking and grooming from their mothers show distinct changes in their epigenome, the chemical markers that attach to DNA and can turn genes on and off. Neglected pups, in contrast, don’t show these epigenetic tweaks.

Now a fascinating new study reveals that it’s not just nurture. Traumatic experiences can actually work themselves into the germ line. When a male mouse becomes afraid of a specific smell, this fear is somehow transmitted into his sperm, the study found. His pups will also be afraid of the odor, and will pass that fear down to their pups.

“Parents transfer information to their offspring, and they do so even before the offspring are conceived,” said Brian Dias, a postdoctoral fellow in Ressler’s lab, at an engaging talk about this unpublished data on Tuesday at the Society for Neuroscience meeting in San Diego.

And why, evolutionarily, would a parent pass down such specific information? “So that when the offspring, or descending generations, encounter that environment later in life, they’ll know how to behave appropriately,” Dias said.

The researchers made the mice afraid of certain odors by pairing them with a mild shock to the foot. In a study published a few years ago, Ressler had shown that this type of fear learning is specific: Mice trained to fear one particular smell show an increased startle to that odor but not others. What’s more, this fear learning changes the organization of neurons in the animal’s nose, leading to more cells that are sensitive to that particular smell.

Dias trained mice to fear acetophenone — which, according to this chemist, smells “like orange blossom with a bit of artificial cherry” — over three days, then waited 10 days and allowed the animals to mate. The offspring (known as the F1 generation) show an increased startle to acetophenone (with no shock) even though they have never encountered the smell before. And their reaction is specific: They do not startle to a different odor, propanol (which smells like alcohol). What’s more, the researchers found the same thing in the F1 generation’s offspring (known as F2).

The scientists also looked at the F1 and F2 animals’ brains. When the grandparent generation is trained to fear acetophenone, the F1 and F2 generations have more “M71 neurons” in their noses, Dias said. These cells contain a receptor that detects acetophenone. Their brains also have larger “M71 glomeruli,” a region of the olfactory bulb that responds to this smell. “Like father like son, we’re getting some ancestral information,” Dias said. “But how is that occurring?”

His team performed an in vitro fertilization (IVF) experiment in which they trained animals to fear acetophenone and then 10 days later harvested their sperm. They sent the sperm to another lab across campus where it was used to artificially inseminate female mice. Then the researchers looked at the brains of the offspring. “What is striking is that the neuroanatomical results still persist after IVF,” Dias said. “There’s something in the sperm.”

I’ve been to a lot of scientific talks. The excitement around this one was notable, with many scientists whispering about it in the room and more loudly buzzing in the hallways outside.

But I know what you’re wondering. It was the first question that Dias received from the audience after the talk: “Do you have any idea of how this information being stored in the brain is being transmitted to the gonads?” the questioner asked.

The short answer is that the researchers don’t have any idea, though they’ve thought about several possible explanations. Apparently a study in cats and pigeons showed that after smelling an odor, the odorant receptor molecules can get into the blood stream, and other studies have reported odorant receptors on sperm. So maybe the odor molecules get into the bloodstream and make their way to sperm. Another possibility is that microRNAs — tiny RNA molecules involved in gene expression — get into the bloodstream and deliver odor information to sperm.

For now, though, Dias said, “those are two science-fiction hypotheses.”


Read more about Ressler’s work in a feature on stress and resilience that I wrote for Nature last year.

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Reversible gene marks linked to reversible careers in bees

A different version of this story appears at The Scientist.

Honeybee workers spend their whole lives toiling for their hives, never ascending to the royal status of queens. But they can change careers. At first, they’re nurses, which stay in the hive and tend to their larval sisters. Later on, they transform into foragers, which venture into the outside world in search of flowers and food.

This isn’t just a case of flipping between tasks. Nurses and foragers are very distinct sub-castes that differ in their bodies, mental abilities, and behaviour – foragers, for example, are the ones that use the famous waggle dance. “[They’re] as different as being a scientist or journalist,” explains Gro Amdam, who studies bee behaviour. “It’s really amazing that they can sculpt themselves into those two roles that require very specialist skills.” The transformation between nurse and forager is significant, but it’s also reversible. If nurses go missing, foragers can revert back to their former selves to fill the employment gap.

Amdam likens them to the classic optical illusion (shown on the right) which depicts both a young debutante and an old crone. “The bee genome is like this drawing,” she says. “It has both ladies in it. How is the genome able to make one of them stand out and then the other?

The answer lies in ‘epigenetic’ changes that alter how some of the bees’ genes are used, without changing the underlying DNA. Amdam and her colleague Andrew Feinberg found that the shift from nurse to forager involves a set of chemical marks, added to the DNA of few dozen genes. These marks, known as methyl groups, are like Post-It notes that dictate how a piece of text should be read, without altering the actual words. And if the foragers change back into nurses, the methylation marks also revert.

Together, they form a toolkit for flexibility, a way of seeing both the crone and the debutante in the same picture, a way of eking out two very different and reversible skill-sets from the same genome.


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Reprogrammed stem cells carry a memory of their past identities


Imagine trying to rewind the clock and start your life anew, perhaps by moving to a new country or starting a new career. You would still be constrained by your past experiences and your existing biases, skills and knowledge. History is difficult to shake off, and lost potential is not easily regained. This is a lesson that applies not just to our life choices, but to stem cell research too.

Over the last four years, scientists have made great advances in reprogramming specialised adult cells into stem-like ones, giving them the potential to produce any of the various cells in the human body. It’s the equivalent of erasing a person’s past and having them start life again.

But a large group of American scientists led by Kitai Kim have found a big catch. Working in mice, they showed that these reprogrammed cells, formally known as “induced pluripotent stem cells” or iPSCs, still retain a memory of their past specialities. A blood cell, for example, can be reverted back into a stem cell, but it carries a record of its history that constrains its future. It would be easier to turn this converted stem cell back into a blood cell than, say, a brain cell.

The history of iPSCs is written in molecular marks that annotate its DNA. These ‘epigenetic’ changes can alter the way a gene behaves even though its DNA sequence is still the same. It’s the equivalent of sticking Post-It notes in a book to tell a reader which parts to read or ignore, without actually editing the underlying text. Epigenetic marks separate different types of cells from one another, influencing which genes are switched on and which are inactivated. And according to Kim, they’re not easy to remove, even when the cell has apparently been reprogrammed into a stem-like state.


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Alcohol tastes and smells better to those who get their first sips in the womb

Blogging on Peer-Reviewed ResearchPregnant women are generally advised to avoid drinking alcohol and for good reason – exposing an unborn baby to alcohol can lead to a range of physical and mental problems from hyperactivity and learning problems to stunted growth, abnormal development of the head, and mental retardation.

But alcohol also has much subtler effects on a foetus. Some scientists have suggested that people who get their first taste of alcohol through their mother’s placenta are more likely to develop a taste for it in later life. This sleeper effect is a long-lasting one – exposure to alcohol in the womb has been linked to a higher risk of alcohol abuse at the much later age of 21. In this way, mums could be inadvertently passing down a liking for booze to their children as a pre-birthday present.

Now, Steven Youngentob from SUNY Upstate Medical University and Jon Glendinning from Columbia University have found out why this happens. By looking at boozing rats, they have found that those first foetal sips of alcohol make the demon drink both taste and smell better.

The duo raised several pregnant rats on diets of either chow, liquids or liquids that had been spiked with alcohol. The third group eventually had a blood alcohol concentration of about 0.15%, a level that would cause a typical human to slur, stagger or become moody.

When the females eventually gave birth, month-old pups born to boozy mothers were more likely to lick an alcohol-coated feeding tube than those whose mothers were tee-total. These rats had been born with more of a taste for booze.


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Child abuse permanently modifies stress genes in brains of suicide victims

Blogging on Peer-Reviewed ResearchThe trauma of child abuse can last a lifetime, leading to a higher risk of anxiety, depression and suicide further down the line. This link seems obvious, but a group of Canadian scientists have found that it has a genetic basis.

By studying the brains of suicide victims, Patrick McGowan from the Douglas Mental Health University Institute, found that child abuse modifies a gene called NR3C1 that affects a person’s ability to deal with stress. The changes it wrought were “epigenetic”, meaning that the gene’s DNA sequence wasn’t altered but it’s structure was modified to make it less active. These types of changes are very long-lasting, which strongly suggests that the trauma of child abuse could be permanently inscribed onto a person’s genes.

Child abuse, from neglect to physical abuse, affects the workings of an important group of organs called the “hypothalamic-pituitary-adrenal axis” or HPA. This trinity consists of the hypothalamus, a funnel-shaped part of the brain; the pituitary gland, which sits beneath it; and the adrenal glands, which sit above the kidneys.  All three organs secrete hormones. Through these chemicals, the HPA axis controls our reactions to stressful situations, triggering a number of physiological changes that prime our bodies for action.

The NR3C1 gene is part of this system. It produces a protein called the glucocorticoid receptor, which sticks to cortisol, the so-called “stress hormone”. Cortisol is produced by the adrenal glands in response to stress, and when it latches on to its receptor,  it triggers a chain reaction that deactivates the HPA axis. In this way, our body automatically limits its own response to stressful situations.

Without enough glucocorticoid receptors, this self-control goes awry, which means that the HPA is active in normal situations, as well as stressful ones. No surprise then, that some scientists have found a link between low levels of this receptor and schizophrenia, mood disorders and suicide. So, childhood trauma alters the way the body reacts to stress, which affects a person’s risk of suicide or mental disorders later in life. Now, McGowan’s group have revealed part of the genetic (well, epigenetic) basis behind this link.


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Ask an IVF baby: does smoking while pregnant lead to antisocial behaviour?

Blogging on Peer-Reviewed ResearchOur health isn’t just affected by the things we do after we’re born – the conditions we face inside our mother’s womb can have a lasting impact on our wellbeing, much later in life. This message comes from a growing number of studies that compare a mother’s behaviour during pregnancy to the subsequent health of her child.

But all of these studies have a problem. Mothers also pass on half of their genes to their children, and it’s very difficult to say which aspects of the child’s health are affected by conditions in the womb, and which are influenced by mum’s genetic legacy.

Take the case of smoking. Doing it while pregnant is bad news for the foetus, and studies have suggested that children whose mothers smoke during pregnancy are more likely to be born prematurely, be born lighter, have poorer lung function, and be more likely to die suddenly before their first birthday. More controversially, they may even show higher levels of behavioural problems including autistic disorders and antisocial tendencies.

Biologically, these results make sense, but many of these risks can be inherited too. For example, genetic factors can strongly influence both a person’s susceptibility to nicotine addiction and their propensity for violent behaviour. A mother’s genes could also affect the birth weight of her child.

To untangle these influences, the ideal experiment would involve randomly implanting foetuses either in the wombs of their own mothers, or those of unrelated women.  That’s possible in animals but deliberately doing so in humans would be both unethical and impractical. Nonetheless, Frances Rice from Cardiff University realised that this experiment was actually well underway.

Since the advent of in vitro fertilisation (IVF) technology in the late 1970s, many mothers have nourished babies in their womb, who weren’t genetically related to them. Here was an ideal chance to study the effects of conditions in the womb, without any confusion caused by shared genes.


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Obesity amplifies across generations; can folate-rich diets stop it?

Blogging on Peer-Reviewed Research
Many measures to curb the obesity epidemic are aimed at young children. It’s a sensible strategy – we know that overweight children have a good chance of becoming overweight adults. Family homes and schools have accordingly become critical arenas where the battle against the nation’s growing waistlines is fought. But there is another equally important environment that can severely affect a person’s chances of becoming overweight, but is more often overlooked – the womb.

Overweight parents tend to raise overweight children but over the last few years, studies have confirmed that this tendency to transcend generations isn’t just the product of a shared home environment. Obesity-related genes are involved too, but even they aren’t the whole story. Research has shown that a mother’s bodyweight in the period during and just before pregnancy has a large influence on the future weight of her children.

For example, children born to mothers who have gone through drastic weight-loss surgery (where most of the stomach and intestine are bypassed) are half as likely to be obese themselves. On the other hand, mothers who put on weight between two pregnancies are more likely to have an obese second child. In this way, the obesity epidemic has the potential to trickle down through the generations, like a snowball rolling its way into an avalanche.

Now, Robert Waterland from the Baylor College of Medicine has demonstrated how the snowball gains momentum by studying three generations of mice that have a genetic tendency to overeat. And using a special diet that was high in folate and other nutrients, he found that he could stop the snowball’s descent and spare future generations of mice from a heightened risk of obesity.