Coming sort of soon to a bookstore near you: The Orchid and the Dandelion


I’m happy to announce that Houghton Mifflin Harcourt, publisher of many a fine book over the decades, will be publishing “The Orchid and the Dandelion” (working title), in which I’ll explore further the emerging “orchid-dandelion hypothesis” I wrote about in my recent Atlantic story. (In brief, that hypothesis — a simple but deeply transformative amendment of current views — hoids that many ‘risk genes’ for behavior and mental problems magnify not just maladaptive responses to bad environments but advantageous responses to good environments. That is, these “risk genes” confer not just vulnerability, but greater responsiveness, sometimes to bad effect, sometimes to good.)

I’ll be working with editor Amanda Cook, whom I met at the sensible urging of my compadre Jonah Lehrer. No publication date yet set, and I’m not crazy enough to promise one here. It will, of course, take some time. But if the Atlantic story left you wanting to read more about this hypothesis, and about how genetics and environment constantly interact to create everything from murder and madness to benevolence and high art, ye shall be satsified — soon as I get a bit of work done. Okay, a lot of work. (I’m on it. Don’t rush me.)

Meanwhile, I’ll use Orchid Neuron Culture to share ruminations on research and reading; published studies old and new that relate to the bidirectional sensitivity emphasized by the hypothesis; outtakes, sidetracks, etc — in short, a parallel but non-duplicative exploration of this emerging hypothesis, its study, and its implications.

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Orchids and dandelions on the Brian Lehrer Show

Brian Lehrer
I’ll be talking with WNYC’s excellent Brian Lehrer on his show this morning, from 11:06 to about 11:25, discussing my Atlantic article about the “orchid gene” hypothesis, which holds that many of the genes that are known to make us vulnerable to problems such as depression, hyperaggression or antisocial behavior, or distractibility — can also make us less vulnerable to these same afflictions.
update: You can listen to the segment here:

You can tune in in the NYC area at FM 93.9 or AM 820; listen to a live internet stream; or go here afterwards for a podcast of the section.
There will be call-ins too (212 433 9692), so listen in and give a call if you wish.

Best blog post title of the day: “I will suck your gruyere”

I will suck your gruyere

Tyler Cowen on why people love vampire tales:

Vampire stories offer a platform for exploring the theme of pure, limitless, and eternal desire, yet without encountering the absurdities that might result from planting that theme in a realistic, real world setting, such as a man who loves cheese studded with raisins above all else.


Posted via web from David Dobbs’s Somatic Marker

Roz Chast’s “finite filing cabinet model” of memory confirmed

One of my favorite Roz Chast cartoons shows a woman dumping out the high-falutin’ contents of a filing cabinet drawer — 16th century art, or something like that — to make room for a new drawer full of information about new TV shows. This is the finite filing cabinet model of memory, in which you toss out one set of memory to make room for new information. It’s not one that has had much credence in neuroscience. Memories have been considered, the last decade or so, to be in there somewhere, but perhaps just inaccessible. The old “I haven’t forgotten it; I just can’t recall it right now” situation.

Science New, via Wired Science, covers a paper suggesting the finite filing cabinet model may have some application after all. I’d say this needs some replication before it overturns the store-it-all paradigm; file it under “Interesting if true,” and remember what I call Ioanidis’s Maxim, which is that most novel findings don’t prove out.

So let the testing begin. In the meantime, it’s intriguing to see Roz Chast’s hypothesis bolstered experimentally.

A new rodent study shows that newborn neurons destabilize established connections among existing brain cells in the hippocampus, a part of the brain involved in learning and memory. Clearing old memories from the hippocampus makes way for new learning, researchers from Japan suggest in the November 13 Cell.

sciencenewsOther researchers had proposed the idea that neurogenesis, the birth of new neurons, could disrupt existing memories, but the Cell paper is the first to show evidence supporting the idea, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto.

Scientists have known that memories first form in the hippocampus and are later transferred to long-term storage in other parts of the brain. For some amount of time the memory resides both in the hippocampus and elsewhere in the brain. What’s not been known is how, after a few months or years, the memory is gradually cleared from the hippocampus.

Researchers have also debated the role of neurogenesis in learning and memory. The hippocampus is one of only two places in the adult brain where scientists know that new neurons form. On the basis of previous studies, many researchers think new neurons stabilize memory circuits or are somehow otherwise necessary to form new memories.

The new study suggests the opposite: Newborn neurons weaken or disrupt connections that encode old memories in the hippocampus.

Posted via web from David Dobbs’s Somatic Marker

The Neurocritic: Genomarketing!

Is this the foreshadowing of a highly unethical marketing practice? Marketing based on MAO-A genotype, as determined from mailed-in credit card applications and payments? Credit card companies will have in-house labs to extract DNA from stamps and envelope flaps (Sinclair & McKechnie, 2000; Ng et al., 2007).1 Taking it one step further, entire marketing campaigns will be tailored to specific markers in an individual’s genome.2

Is this what it’s coming to? Not so fast. Are there any limitations in the findings of De Neve and Fowler (2009)? There are many!!


Vintage Neurocritic here. Gotta see it.

Posted via web from David Dobbs’s Somatic Marker

Senator Asks Pentagon To Review Antidepressants

us-soldiers-afghanBen Cardin, a Maryland Democrat, has asked the Pentagon for info on how many troops in war zones have been prescribed antidepressants while they were deployed. Cardin sent a letter Tuesday to US Department of Defense Secretary Robert Gates expressing concern about how antidepressants are being administered troops in Iraq and Afghanistan.

Cardin wants to determine if the Defense Department is prescribing antidepressants appropriately and is concerned about any connection between the meds and suicide rates among troops. In October, for instance, 16 active-duty US soldiers killed themselves, bringing the total number of active-duty suicides in 2009 to 134. At this rate, the number of 2009 suicides will eclipse last year’s total of 140 – the highest yearly number of suicides in Army history. Cardin also notes the rate of active-duty suicides is greater than that of the US population, although he doesn’t question the “long-term efficacy” of the drugs.


Most soldier/vet suicides get blamed on PTSD. This overlooks a couple important things:

1. Depression and drinking problems are both more common than PTSD is, even among combat vets, and have a more robustly established and higher suicide risk.

2. As the story above notes, antidepressant use among younger people, especially if not monitored closely, is shown to carry a significant suicide risk.

Cardin’s effort is an attempt to address the second problem. This is a good example of how reflexive diagnoses, as PTSD has become for any combat veteran (and sometimes even prospective combat veterans — i.e., troops preparing to deploy), can do harm. They can lead you to ignore other possible causes of the symptoms on display.

Posted via web from David Dobbs’s Somatic Marker

Raymond Tallis trashtalks some “Neurotrash”

Hardly a day passes without yet another breathless declaration in the popular press about the relevance of neuroscientific findings to everyday life. The articles are usually accompanied by a picture of a brain scan in pixel-busting Technicolor and are frequently connected to references to new disciplines with the prefix “neuro-“. Neuro-jurisprudence, neuro-economics, neuro-aesthetics, neuro-theology are encroaching on what was previously the preserve of the humanities. Even philosophers – who should know better, being trained one hopes, in scepticism – have entered the field with the discipline of “Exp-phi” or experimental philosophy. Starry-eyed sages have embraced “neuro-ethics”, in which ethical principles are examined by using brain scans to determine people’s moral intuitions when they are asked to deliberate on the classic dilemmas. Benjamin Libet’s experiments on decisions to act and the work on mirror neurons (observed directly in monkeys but only inferred, and still contested, in humans) have been ludicrously over-interpreted to demonstrate respectively that our brains call the shots (and we do not have free will) and to point to a neural basis for empathy.


Ray Tallis talks trash to neurotrash who talk too much neuro. Suggested read; good for all your neuromatter.

Posted via web from David Dobbs’s Somatic Marker

I’m not vulnerable, just especially plastic. Risk genes, environment, and evolution, in the Atlantic

The video interview above, with NIH primatologist Stephen Suomi, is embedded within a feature of mine that that appeared today at The Atlantic website — and is in the December 2009 issue now shipping — about a new hypothesis in behavioral genetics.

This emerging hypothesis, which draws on substantial data, much of which has gone simply unnoticed or unremarked, I call the “orchid-gene hypothesis,” for lack of a better name. Some of the researchers have other offerings. It’s been around for several years but is now blooming as evidence accumulates. When I came across it at a conference this spring — gaggles of scientists talking excitedly in the halls — it immediately struck me as a deeply transformative and powerful idea. It recasts the genes we now see simply as ‘risk alleles’ for things such as depression or ADHD as ‘sensitivity’ genes that create greater responsiveness not just to bad environments (creating the well-documented risk) but good environments — creating an upside to these genes that has gone largely unnoticed.

It is thus

a new interpretation of one of the most important and influential ideas in recent psychiatric and personality research: that certain variants of key behavioral genes (most of which affect either brain development or the processing of the brain’s chemical messengers) make people more vulnerable to certain mood, psychiatric, or personality disorders. Bolstered over the past 15 years by numerous studies, this hypothesis, often called the “stress diathesis” or “genetic vulnerability” model, has come to saturate psychiatry and behavioral science. During that time, researchers have identified a dozen-odd gene variants that can increase a person’s susceptibility to depression, anxiety, attention-deficit hyperactivity disorder, heightened risk-taking, and antisocial, sociopathic, or violent behaviors, and other problems–if, and only if, the person carrying the variant suffers a traumatic or stressful childhood or faces particularly trying experiences later in life.

This vulnerability hypothesis, as we can call it, has already changed our conception of many psychic and behavioral problems. It casts them as products not of nature or nurture but of complex “gene-environment interactions.” Your genes don’t doom you to these disorders. But if you have “bad” versions of certain genes and life treats you ill, you’re more prone to them.

Recently, however, an alternate hypothesis has emerged from this one and is turning it inside out. This new model suggests that it’s a mistake to understand these “risk” genes only as liabilities. Yes, this new thinking goes, these bad genes can create dysfunction in unfavorable contexts–but they can also enhance function in favorable contexts. The genetic sensitivities to negative experience that the vulnerability hypothesis has identified, it follows, are just the downside of a bigger phenomenon: a heightened genetic sensitivity to all experience.

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Fallows on the Fort Hood shootings: “Don’t mean nothing.”

James Fallows gets the shootings right, as he does so much else:

In the saturation coverage right after the events, the “expert” talking heads are compelled to offer theories about the causes and consequences. In the following days and weeks, newspapers and magazine will have their theories too. Looking back, we can see that all such efforts are futile. The shootings never mean anything. Forty years later, what did the Charles Whitman massacre “mean”? A decade later, do we “know” anything about Columbine? There is chaos and evil in life. Some people go crazy. In America, they do so with guns; in many countries, with knives; in Japan, sometimes poison.

We know the emptiness of these events in retrospect, though we suppress that knowledge when the violence erupts as it is doing now. The cable-news platoons tonight are offering all their theories and thought-drops. They’ve got to fill time. I wish they could stop. As the Vietnam-era saying went, Don’t mean nothing.


Posted via web from David Dobbs’s Somatic Marker

Gorgeous thing of the day: Sky’s-eye view of the Maldives & other islands