The John Medina Interview Roundup

Just because Brain Rules and Brain Rules for Baby have been published doesn't mean that Dr. John Medina has stopped educating the public with his scientifically backed insights on how our brains work. Dr. Medina has kept busy by doing a variety of interviews for the wide audiences of readers who are interested in learning more about the Brain Rules. Here are the links to a few of them:

-At the Positive Business Blog, Dr. Medina discusses how using our brains better leads to doing better business--especially when it comes to Rule #8: stress.

-Stream or download Dr. Medina's interview with independent business radio station BFM 89.9.

-Business blogger Bob Morris sits down with Dr. Medina.

-Watch Dr. Medina's conversation with Microsoft's Mary Cullinane at the Innovative Education Forum.

-Listen to Dr. Medina's in-depth interview about a set of Brain Rules that are especially handy for teachers.

Brain Rules for Educators

As anybody who has read Brain Rules knows, Dr. John Medina has a few bones to pick with how the traditional classroom is structured. If Dr. Medina were in charge, a typical day at school would be transformed in a myriad of ways that would increase levels of efficiency, permanence, and, well, fun while learning. Fortunately, educators are listening to Dr. Medina as well, and they're starting to share their thoughts with the rest of us:

-At The Huffington Post, Tom Vander Ark hypothesizes what a Brain Rules-inspired classroom would look like.

-Watch Dr. Medina's interview about which "brain rules" are myths and which ones are backed by scientific evidence in his interview with Mary Cullinane at the Microsoft Innovative Education Forum.

-Listen to Dr. Medina's in-depth discussion of Brain Rules for Teachers from the "Leaps and Bounds for Teachers" series from Berklee Faculty Development.

-You don't need to transform the entire educational system from the bottom up in order for the message Brain Rules to take a positive effect in your classroom: watch high school wrestling coach Mike Hagerty give his unsolicited praise detailing how Brain Rules has influenced his teaching.

Have you figured out new ways to integrate Brain Rules in your classroom? Don't hesitate to share and start a discussion with other educators at the Brain Rules Facebook page.

The NFL's New Brain Rules

You can always find Dr. John Medina's latest writing on brain research and how it affects our daily lives over at Brainstorm. Recently, Dr. Medina has been writing about how new knowledge about the brain could start having a direct impact on America's most popular sport: the NFL.

Like many of us, Dr. Medina is a long-time football fan, but the sport's future looks grim. Since so many current and former football players suffer from the debilitating brain injury CTE, there has been a growing public debate as to whether or not football is a safe game for anybody to consistently play. Dr. Medina points out that there are still significant gaps in research on CTE and its correlation with playing football, but sports fans could be hearing about this darker side of brain research for years to come.

You can read the entire series of Dr. Medina's posts on the NFL here.

New Brain Rules for Baby Videos

We are excited for you to meet Brain Rules Baby, who shares parenting wisdom from Brain Rules for Baby in these 60-second videos.

Watch Out - Your Kids Are Watching You More Than You Think


That's right, kids are really good a imitation.  Even a 13-month-old child can remember an event a week after a single exposure.  Even when you don't realize it, your kids are watching the world around you.  What you allow into your child's brain influences their expectations about the world, which in turn influences not only what they are capable of perceiving, but their very behavior.

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Under 2? No TV for you!


Americans 2 years of age and older now spend an average of four hours and 49 minutes per day in front of the TV—20 percent more than 10 years ago. And we are getting this exposure at younger and younger ages, made all the more complex because of the wide variety of digital screen time now available. In 2003, 77 percent of kids under 6 watched television every day. And children younger than 2 got two hours and five minutes of “screen time” with TVs and computers per day. The average American is exposed to about 100,000 words per day outside of work. Fully 45 percent of those words come from television. The fact is, the amount of TV a child should watch before the age of 2 is zero.

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Raising a toast to the human brain

John Medina discusses Brain Rules with Warren Etheredge at The High Bar.

Brain Rules for Meetings

Molecular biologist John Medina, speaker and author of the best-selling book Brain Rules: 12 Principles for Surviving and Thriving at Work, Home, and School, didn't set out to become a media star. But he got so fed up with encountering myths about the brain - that you use only 10 percent of it, for example, or that there are right- and left- brain personalities - that he once threw a magazine across a seat on an airplane. (The flight, he notes, wasn't full.) "So I decided to write Brain Rules," Medina said, "as an attempt to say, ‘Look, here's what we do know, here's what we don't know, here are a few things you can try that might have an application in the business world - and the meetings world as well.'"

Not that Brain Rules will tell you how the brain operates. "We don't know squat about how the brain works," said Medina, who has focused on brain research for nearly three decades. He added: "I don't know how you know how to pick up a glass of water and drink it. But we do know the conditions that [the brain] operates best in, even if we don't know all the ins and outs of that operation."

Which of the 12 Brain Rules has the most impact on meetings?
Well, probably, the biggest one would have to be about attentional states. This rule is very simple: People don't pay attention to boring things. So if you really want to have a lousy meeting, make sure it's boring. If you want to have a lousy classroom, make sure it's boring. And if you want to vaccinate against the types of things that really do bore the mind, we have some understanding of that.

So how do you design a good meeting?
Here are the top three "brain gadgets" that probably have a bearing on the question. First, the human brain processes meaning before it processes detail. Many people, when they put meetings together, actually don't even think about the meaning of what it is they're saying. They just go right to the detail. If you go to the detail, you've got yourself a bored audience. Congratulations.
Second, in terms of attentional states, we're not sure if this is brain science or not, but certainly in the behavioral literature, you've got 10 minutes with an audience before you will absolutely bore them. And you've got 30 seconds before they start asking the question, "Am I going to pay attention to you or not?" The instant you open your mouth, you are on the verge of having your audience check out. And since most people have been in meetings - 90 percent of which have bored them silly - they already have an immune response against you, particularly if you've got a PowerPoint slide up there.

How do you then hold attention?
This is what you have to do in 10 minutes. You have to pulse what I just said - the meaning before detail - into it. I call it a hook. At nine minutes and 59 seconds, you've got to give your audience a break from what it is that you've been saying and pulse to them once again the meaning of what you're saying.

What is the third "brain gadget"?
The brain cycles through six questions very, very quickly. Question No. 1 is "Will it eat me?" We pay tons of attention to threat. The second question is "Can I eat it?" I don't know if you have ever watched a cooking show and have loved what they are cooking, but you pay tons of attention if you think there's going to be an energy resource. Question No. 3 is highly Darwinian. The whole reason why you want to live in the first place is to project your genes to the next generation - that means sex. So Question No. 3 is "Can I mate with it?" And Question No. 4 is "Will it mate with me?"

It turns out we pay tons of attention to - it actually isn't sex per se, it's reproductive opportunity. [It is also] hooked up to the pleasure centers of your brain - the exact same centers you use when you laugh at something. Oddly enough, I think that's one of the reasons why humor can work. If you can pop a joke or at least tell an interesting story, it's actually inciting those areas of the brain that are otherwise devoted to sex. You don't become aroused by listening to a joke. I'm saying those areas of the brain can be co-opted. You can utilize them, and a good speaker knows how to do that.

What are Questions 5 and 6?
"Have I seen it before?" and "Have I never seen it before?" We are terrific pattern matchers. There is an element of surprise that comes when patterns don't match, but the reason why that happens is because we are trying to match patterns all the time.

Is there a Brain Rule that addresses whether you should try to control the use of laptops and phones during a meeting session?
I have this rule response, based on data, and then I have a visceral response, also based on data. In other words, I'm about ready to tell you a contradiction. Are you ready?

Yes, I am.
Alrighty. I do believe what you can show is that there are attentional blinks. The brain actually is a beautiful multitasker, but the attentional spotlight, which you use to pay attention to things, [is not]. You can't listen to a speaker and type what they are saying at the same time.

What you can show in the laboratory is that you get staccato-like attentional blinks. Just like you come up for air: You look at the speaker, then when you're writing, you cannot hear what the speaker is saying. Then you come up for air and hear the speaker again. So you're flipping back and forth between those two, and your ability to be engaged to hear what a speaker is saying is necessarily fragmented.
At the same time, if your speaker is boring, you could have checked out anyway. So you see, in many ways it depends upon the speaker.

How so?
If the speaker is really compelling and is clear and is emotion- ally competent, and has gone through those six questions, letting you come up for air every 10 minutes, I've actually watched audiences put their laptops away just to pay attention.

I have a style that is purposely a little speedier. And the rea- son why is that it produces a tension that says, "I need to pay attention closely to him or I'm going to lose what he's saying." I don't make it so fast that it's unintelligible - at least I hope I don't. But I do make it fast, and occasionally I see comments that say, "Great speaker, but you know, you were too freaking fast."

This interview originally appeared in the Professional Convention Management Association (PCMA) magazine Convene.

What Humans Can Learn From Monkeys

We are exploring the sometimes creepy, always fascinating distance between genes and behaviors. In this entry, I wish to illustrate a dramatic example of how nature and nurture interact, not by examining humans, but by considering some genetic next-door neighbors: vervet monkeys. This is a great example of  “Learn from your parents — it’s good for you!” without a human parent in sight.

Vervet monkeys have interesting predator vocalizations, and even something of a vocabulary. The animals appear to be born with this ability — there’s our nature. As we shall see, however, the application requires some practice — and that’s our nurture. This is easily seen in vervet monkey foraging behaviors, whether the animals are searching for food on the ground or in the trees.

Vervet monkeys have a vocalization for the warning “Run, you idiot, there’s a snake on the ground!”, for example. When an adult vocalizes this warning, the whole tribe runs into the trees, and everyone is safe. They have another word for “Run, you idiot, there’s a predatory bird in the air!” When an adult vocalizes this warning, the whole tribe dives to the ground, and everyone is safe one again.

Note that I italicized the word “adult” throughout the previous paragraph. That’s because when the tribe hears a youngster vocalize either the snake or bird warning, the tribe doesn’t do anything. The members wait until they hear an adult say it. Why do they pause? Because the little ones often get the vocabulary mixed up. They have not yet learned the correct application of their handy early warning system.

The adults aren’t trying to be obnoxious. They are trying to avoid a disaster. Imagine the tragedy if the whole tribe responded to a juvenile’s call to hit the dirt when the little guy saw a snake. The funny cartoon version has him saying sheepishly, “Oops. I meant, trees” — but the deadly real world version is “no more tribe.” Little vervets may be born with the ability to warn others, but they have not yet been instructed on its proper use. They will eventually learn the correct behavior by persistent interactions with older members of the tribe, but the instruction set is not innate. They may have been born with pre-loaded vocalizing software. That doesn’t mean they know how to use it.

A very similar situation between biological ability and social experience is observed with humans, examples of which we will explore in the next few entries. We may come into this world with some pretty sophisticated DNA, but like our primate cousins, that is no guarantee we know how to use it.

How do you get a baby to sleep through the night? We have no idea.

I am often asked why Brain Rules for Baby doesn't include advice on how to get your child to sleep through the night. The omission is deliberate, and my recent answer to one reader's question via e-mail explains the reasoning. I thought you would like to see the answer, too. Thanks for all of your interest in the book. It means a great deal.
-- John

Dear Reader;

You raise an important issue regarding sleep, one of the most critical in the early months of child-rearing. Unfortunately, I cannot give a response equal to its criticality.

If you are having problems with getting your child to sleep through the night, you have probably read everything you could on the issue. In that journey, you might have noticed there are many different opinions about how to get kids to sleep through the night - often by experts in the field. You might further have noticed that these well-established researchers and clinicians often appear to say contradictory things. The advice can almost be put into a continuum. On one end, there are researchers like Dr. Richard Ferber, interpreted as saying draconian things like “let your kid tough it out at night” (that’s hardly a fair characterization, by the way). On the other end is pediatrician William Sears and family who is interpreted as saying “respond to every demand at night” (also hardly a fair characterization). Here are the two references from these seasoned medical professionals, which make great comparative reading for the views they hold:

“Solve Your Childs’ Sleep Problems”,

Richard Ferber, 2006

and

“The Baby Sleep Book”

William Sears et al, 2005

Why the contradiction? BECAUSE NOBODY REALLY KNOWS HOW TO ADDRESS THE SLEEP ISSUE. There does not appear to be a one-size-fits-all answer, which is why any advice which claims to be THE ANSWER does not pass my “grump factor”, as a scientist. My standard response, therefore, is to appeal to the wisdom of the real expert, the parent – YOU – and say something like “Every brain is wired differently from every other brain. Go out and buy both of these books and expose yourself to the various recommendations. Then determine which strategies (or combinations of strategies) your child – based on your knowledge – is most likely to respond. Try these strategies in a systematic fashion, and progressively design new ones until you find the strategy that does work.”

I have an example of this flexible, deliberate approach in my own child-rearing experience.

It was almost seven months before my eldest child slept successfully through the night. What worked for me was to give him a “modified” Ferber protocol – a gentler version of his recommendation, which took almost a week to execute successfully (I literally took off time from work to do it, relieving my poor exhausted wife).

My youngest child also had trouble getting to sleep. But when I tried my “modified” Ferber strategy, it did not work for him. What did the trick was a modified “Sears” strategy. And it also took about a week to become successful too. Living proof for the fact there is no over-arching strategy that will work for every child.

I wish you well. Solving this riddle is one of the toughest tasks in the early years of child-rearing.

John Medina

Why is it So Hard to Get Kids To Do the Right Thing? (VIDEO)

If children are born with a sense of right and wrong, as brain science shows, why don't they just do the right thing?

Part of the reason it's tough is that the moment children observe bad behavior, they have learned it. Even if the bad behavior is punished, it remains easily accessible in the child's brain. Psychologist Albert Bandura was able to show this with help from a clown.

In the 1960s, Bandura showed preschoolers a film involving a Bobo doll, one of those inflatable plastic clowns weighted on the bottom. In the film, an adult named Susan kicks and punches the doll, then repeatedly clobbers it with a hammer. After the film, the preschoolers are taken into another room filled with toys, including (surprise) a Bobo doll and a toy hammer.

What do the children do? It depends. If they saw a version of the film where Susan was praised for her violent actions, they hit the doll with great frequency. If they saw a version where Susan got punished, they hit Bobo with less frequency. But if Bandura then strides into the room and says, "I will give you a reward if you can repeat what you saw Susan do," the children will pick up a hammer and start swinging at Bobo.

Whether the children saw the violence as rewarded or punished, they learned the behavior. Bandura calls this "observational learning," and his finding is an extraordinary weapon of mass instruction. Observational learning plays a powerful role in moral reasoning.

How does moral reasoning develop? Slowly. Harvard psychologist Kohlberg believed that moral reasoning depended upon general cognitive maturity--another way of saying that these things take time. He outlined a progressive process:

1. Avoiding punishment. Moral reasoning starts out at a fairly primitive level, focused mostly on avoiding punishment. Kohlberg calls this stage pre-conventional moral reasoning.

2. Considering consequences. As a child's mind develops, she begins to consider the social consequences of her behaviors and starts to modify them accordingly. Kohlberg terms this conventional moral reasoning.

3. Acting on principle. Eventually, the child begins to base her behavioral choices on well-thought-out, objective moral principles, not just on avoidance of punishment or peer acceptance. Kohlberg calls this coveted stage post-conventional moral reasoning. One could argue that the goal of any parent is to land here.

This willingness to make the right choices--and to withstand pressure to make the wrong ones, even when the possibility of detection and punishment is zero--is the goal of moral development. We parents use rules and discipline, of course, to get our children to this stage.

In my book "Brain Rules for Baby: How to Raise a Smart and Happy Child from Zero to 5," I discuss the research-tested strategies that parents can use to aid moral development. At the end of the book, I gather practical tips, including these two:

CAP your rules

Discipline FIRST

Need one more? Read "A Magic Trick for Getting Kids to Follow Rules."

Watch more parenting videos or learn more about your baby's brain at brainrules.net.

Custom-Made Neural Stem Cells

It is ironic that an attempt to do a molecular end-run around a politically hot topic could result in an important breakthrough in the treatment of neurological disease with potentially strong implications for the psychiatric community. Ironic maybe, but true.

In this column, we explore how the judicious use of neural stem cells (NSCs) has led to a research Holy Grail: the creation of research-ready, patient-specific neurons. This technology did not use the famously controversial embryonic stem cells. These custom-made NSCs were created from politically neutral adult tissues (fibroblasts), which were originally isolated from an affected patient. With no embryo in sight, scientists genetically reprogrammed fibroblasts into stem cells, which were then induced to develop into NSCs. This is an extraordinary finding with many topics to be discussed here:

• The potential research utility for patient-specific neurons

• An explanation of how stem cells can be made from adult tissues

• A striking set of results that involve one of the most commonly inherited and lethal childhood neurological disorders: spinal muscular atrophy (SMA)

Research utility for NSCs

Of what possible utility could molecular investigations of a motor disorder have for the mental health community? Before getting into the specifics of the breakthrough, it might be useful to address a real-world psychiatric need, using depression and SSRIs as an example, to see where these data fit.

When we consider the molecular mechanisms of SSRI interactions, it is easy to resort to commonly taught ideas about interactions that involve a single synapse. Nothing could be further from the truth. The most comprehensive neurological view of SSRI interactions must take into account the participation of thousands of individual neurons strung together in coordinated, complex neural networks.

And not just serotonergic neurons. These cells are in contact with many other central nervous denizens, from adjacent glial cells to the extracellular matrix into which the cells are embedded. What do these circuits actually look like in patients who are vulnerable to depression? Is their architecture all that different from patients who do not exhibit this vulnerability? If there are differences, could they eventually predict drug efficacy? Could these differences only be detected by constructing parts of the circuit from scratch, or could they be observed at the level of a single cell?

The first step in answering these questions involves growing a custom-made batch of serotonergic neurons derived only from the affected patients, and then asking relevant structure/function questions. From attempting to understand molecular mechanisms of disease to testing the efficacy of potential medications, such patient-specific test beds would have a powerful research utility. Until recently, the creation of such tailor-made neural substrates had been an impossible goal.

While it will certainly be quite some time before we can grow entire parkinsonian dopaminergic pathways in a dish, it is now possible to create individual patient-specific neurons in culture. The technology comes from that end-run I mentioned earlier, through the use of a certain type of stem cell. It is to these interesting cellular substrates that we now turn.

Inducible stem cells

To say that embryonic stem cell research has been subject to heated political debate is an understatement. The bugaboo has been the source materials from which the stem cells would be isolated—human embryos—many left over from embryos generated in in vitro fertilization laboratories.

In 2006, researchers found a way to create stem cells that bypassed the need for human embryos. The original technique involved the introduction of 4 specific gene products into mature mouse fibroblasts. Surprisingly, this cocktail was found to reprogram adult stem cells and reverse-engineer them into pluripotent stem cells. Like embryonic stem cells, the altered stem cells had the ability to differentiate into any cell type. Eventually, a protocol was developed that did the same thing in human tissues. The cells were called iPSCs, short for induced pluripotent stem cells.

This was quite a breakthrough. No longer would researchers need to harvest cells from extant human embryos to do stem cell research. Skin cells would do. Scientists were soon able to regenerate—and then correct—molecular dysfunction in a mouse model of sickle cell anemia using this technology.

Could any of this work apply to humans, specifically to human neural tissue? Another successful round of experiments (with amyotrophic lateral sclerosis neurons) prompted researchers to study motor disease, ie, SMA.

Of those hereditary neurological disorders capable of causing death in pediatric populations, SMA is easily the most common. The disease is unique to humans and associated with 2 genes, SMN1 and SMN2. For reasons that are not well understood, the absence of the survival motor neuron (SMN) protein results in an alteration of the function of spinal motor neurons. The primary feature is muscle weakness and atrophy. Death occurs at infancy in the most severe forms of the disease, with symptoms generally presenting several weeks after birth. There are many other, nonlethal forms of the disorder, however, with a wide spectrum of symptoms that range from trivial motor effects to catastrophic impairment.

Why this variation? Both genes express in unaffected individuals, but the biological heavy lifting belongs to the SMN1 gene. Because of structural constraints, the expression pattern of the SMN2 gene normally results in only 10% of its protein being processed as a full-length (and functional) polypeptide; 90% of its protein output is truncated (and nonfunctional). That is okay, as long as the SMN1 gene is intact. But when SMN1 is mutated and silent, the disease condition results. Assuming there is a damaged SMN1, the severity of SMA varies according to the number of other SMN2 copies the infant may carry. The more copies of SMN2 gene, the greater the population of functional protein. This interaction explains in part why there can be so much varia-tion in the clinical presentation.

The great mystery is why SMN protein loss results in motor cell alterations that lead to the disease state in the first place. The protein is known to be essential for normal messenger RNA processing and is expressed throughout the body. Yet its absence most severely affects spinal motor neurons.

The most exacting way to attack this “black box” would be to isolate the motor neuron populations from the patient, then compare these populations with unaffected controls and look for differences, of which there are many. These include responses to various medications. It is well known that the application of valproic acid (an anticonvulsant and/or mood stabilizer) or tobramycin(Drug information on tobramycin) (an aminoglycoside) to cultured cells, for example, leads to changes in the expression patterns of both full-length SMN protein and truncated forms. What is the molecular basis of this unusual interaction? And could such differences be used as a “molecular flashlight” to ferret out other secrets regarding the SMN protein? Creating custom-made neurons—one population from an affected individual, another from an unaffected control—would certainly give a test bed capable of answering this question.

The data

Studying these 2 populations is precisely what a group of investigators did. The researchers isolated fibroblasts from an affected child and also from the child’s healthy unaffected mother.

The next step was to generate custom-made neurons. Several steps would be required (Figure). First, using the iPSC protocols I mentioned, the researchers would attempt to create stem cells from both child and parent sources. If that worked, the researchers would then try to induce these patient-derived stem cells into motor neurons—ones that would carry the same biological mechanisms observed in both the diseased and the healthy populations. If successful, the researchers would have their custom-made test beds. They could begin characterization studies; reactions to valproic acid and tobramycin would make obvious first choices to try.

The first step worked. The researchers were able to generate custom-made stem cells from both child and parent. The researchers then tackled the hard part: manufacturing spinal motor neurons from these stem cell populations. They certainly generated promising cellular populations. But the iPSC technolo-gies are new enough that a visual inspection of the generated cells might be necessary—but certainly not sufficient—to show the presence of motor neurons.

There are ways to gain greater reassurance. One way to assay the success of the protocol is to look for bona fide molecular markers of developing spinal neurons. It is known, for example, that extant motor neurons express the protein SMI032 and choline acetyltransferase. Did these induced cells express such proteins? The answer turned out to be yes, both for the affected child and for the unaffected parent. Developing cells in these populations possess transcription factors such as HOXB4, ISLET1, HB9, and OLIG2 as well. Did the induced populations express these markers? They did indeed. While not completely conclusive, it appeared that the researchers had generated patient-specific motor neurons from known affected and unaffected sources.

The next characterization experiments also yielded fruit. They were able to find that the child and parent neurons reacted very differently to the normally stimulating effects of valproic acid and tobramycin. The child’s cells showed elevated levels of SMN protein, both of the truncated form and full-length version. In addition, SMN-containing nuclear structures were altered. No such elevation occurred in the unaffected maternal line of cells.

These differences were significant for 2 reasons. First, it gave the investigators a toehold in their attempts to characterize at a more intimate level the differences between affected and unaffected cells. Second, the differences were discovered as reactions to known medications. The hope is that similar approaches could be used to test the efficacy of various medications before committing to human trials.

Conclusions

These data, full of promising implications as they are, need to be treated with some caution. First, the experimental cells are pure populations derived from stem cells. This hardly reflects the physical in vivo situation. The cells and matrix components that normally surround such cells in nature, including skeletal muscle tissues and even other neurons, are not present in these studies.

Another objection concerns the fidelity of the conversion process itself. The differentiation pattern seen in various molecular markers hinted that the investigators generated real live spinal motor neurons; however, one cannot a priori say they have in every way created a motor neuron that precisely mimics the real-world situation. These cells may lack many subtle molecular processes—and a few extra, equally subtle interactions—that could easily escape detection, at least by current technologies. Because subtle differences can profoundly influence intracellular molecular interactions, especially when we think about reactions to medications, this is a true concern.

The most exciting aspect of these studies comes from what the future holds. A great deal of speculation has gone into thinking about how to tailor medications to individual patients. That certainly is a psychiatric issue . . . I need not talk to this audience about the variable effects of, say, fluoxetine(Drug information on fluoxetine) on clinical outcomes. We have visited this topic in past columns. The ability to create patient-specific cellular test beds may go a long way toward solving some of these problems. Indeed, clinics of the future might routinely screen to decide what medications their patients should receive—and in what concentrations.

There is much work to do. To date, none has been applied to neurological systems relevant to mental health professionals. Even given the cautions mentioned above, there is no reason why it couldn’t. That’s not bad for having to do with an end-run around a hostile, politically charged issue such as stem cell debates. Would that all ethical issues could be decided so cleanly, or with so much fruit.

This article first appeared in Psychiatric Times.