The Ash Twins Blog

Immigrant Elephants Stick Together:

[S]cientists in California got to wondering how elephants, which are highly social creatures, handle making themselves at home when they get to a new neighborhood.

It turns out they form enclaves that are the elephant equivalent of a ghetto, where the new pachyderms in the park associate with one another and with other immigrant elephants. Then, once the transplants have been around for a year, they get friendly with the locals.

The Amnesia Gene:

In healthy subjects events that are emotionally charged—and it doesn’t matter if the emotions are positive or traumatic—tend to be much better remembered than emotionally neutral events. This psychological tendency comes with a glaring exception, however: in some individuals, extremely stressful or traumatic events can induce amnesia, so that they lose the ability to remember what happened. In some instances this loss can lead to the erasure of a vast amount of memory, so that people even forget basic facts about their identity, such as where they live or what their name is.

Amnesia induced by negative emotions is considered a psychological defense mechanism that protects the organism from the consequences of extreme trauma and catastrophic fear…

This new study, by the neuroscientist Bryan Strange and colleagues at the Wellcome Trust Center for Neuroimaging in London, examined the role of serotonin transporter genes (5-HTTLPR) in the development of emotion induced amnesia. (Such transporter genes influence the availability of the serotonin transporter, a key regulator of serotonin transmission between brain cells.) Serotonin transporter genes have been extensively investigated for their role in stress induced psychiatric disorders, such as post-traumatic stress disorder (PTSD). In recent years, scientists have found that subjects with 5-HTTLPR short variant genotype are more likely to get depressed after stressful life events and are also at increased risk for PTSD. Furthermore, this short variant genotype is associated with anxiety related traits that have also been implicated in the susceptibility to anxiety and depression.

In the experiment, the authors demonstrate that subjects with the 5-HTTLPR short variant genotype had difficulty remembering a series of neutral words (harvest, kid, thought, and so on) that were presented prior to the presentation of emotionally charged words (such as rape, abortion, tumor), at least when compared with subjects who have the 5-HTTLPR long variant genotype. It’s important to note, however, that these genes did not affect memory for emotional words. Thus, the data suggest that the contribution of 5-HTTLPR to disturbances in emotional memory may be specific to emotion-induced retrograde amnesia, which occurs when subjects are unable to remember what happened before the traumatic event. In contrast, other serotonergic genes, or genes linked with other neurotransmitter systems, might influence memory for emotional words…

At a modest level of activation, the amygdala seems to augment the function of the hippocampus, a brain region involved in the formation of long-term memory. When the amygdala is greatly excited, as during traumatic events, however, hippocampal function is inhibited and memory impairment is triggered.  Other studies have demonstrated that subjects with the 5-HTTLPR short variant genotype have enhanced amygdala reactivity to emotional stimuli. The hyperactive amygdala in these individuals may, at least in part, explain why they are more susceptible to emotion-induced memory loss.

E-prescribing leads to more generics:

Massachusetts physicians who used an e-prescribing system increased their use of generics by 6 percent—from 55 percent to 61 percent of all prescriptions they filled—compared with when they wrote them out by hand the old-fashioned way, according to a study in this week’s Archives of Internal Medicine.

Some verse courtesy T.S. Eliot. I recommend the whole poem – it’s simultaneously beautiful, mournful, and meditative. Here are a couple of excerpts:

LET us go then, you and I,
When the evening is spread out against the sky
Like a patient etherised upon a table;
Let us go, through certain half-deserted streets,
The muttering retreats
Of restless nights in one-night cheap hotels
And sawdust restaurants with oyster-shells:
Streets that follow like a tedious argument
Of insidious intent
To lead you to an overwhelming question …
Oh, do not ask, “What is it?”
Let us go and make our visit.

In the room the women come and go
Talking of Michelangelo.

[...]

I should have been a pair of ragged claws
Scuttling across the floors of silent seas.
.      .      .      .      .
And the afternoon, the evening, sleeps so peacefully!
Smoothed by long fingers,
Asleep … tired … or it malingers,
Stretched on the floor, here beside you and me.
Should I, after tea and cakes and ices,
Have the strength to force the moment to its crisis?
But though I have wept and fasted, wept and prayed,
Though I have seen my head [grown slightly bald] brought in upon a platter,
I am no prophet—and here’s no great matter;
I have seen the moment of my greatness flicker,
And I have seen the eternal Footman hold my coat, and snicker,
And in short, I was afraid.

A new article in the Journal of Neuroscience links the placebo effect to a specific gene.

In the study, summarized here, researchers measured amygdala activity by PET scan in individuals with Social Anxiety Disorder while they recited speeches in front of an audience. Subjects gave the speech both before and after an eight week trial of SSRI or sugar pill.  A subset of the subject population demonstrated reduced anxiety and attenuated amygdala activity after the eight-week treatment period, even if they received the placebo. Notably, eight of the ten subjects who responded to the placebo had a unique allele at the tryptophan hydroxylase-2 promoter (TPH2), a gene involved in serotonin metabolism that has been ” linked to heightened amygdala activity in healthy people.”

The authors note that TPH2 is “the first genetic marker tied to any placebo response.”

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Anthropologist Nicholas Humphrey has written a book chapter about the evolution of the placebo effect in Psychology at the Turn of the Millennium, Vol. 2: Social, Developmental, and Clinical Perspectives, and it’s available online.

Humphrey reviews the power of the placebo effect here:

Indeed experimental studies have shown that placebos, as well as being particularly effective for the relief of pain and inflammation, can for example speed wound healing, boost immune responses to infection, cure angina, prevent asthma, lift depression, and even help fight cancer. Robert Buckman, a clinical oncologist and professor of medicine, concludes that “Placebos are extraordinary drugs. They seem to have some effect on almost every symptom known to mankind, and work in at least a third of patients and sometimes in up to 60%. They have no serious side-effects and cannot be given in overdose. In short they hold the prize for the most adaptable, protean, effective, safe and cheap drugs in the world’s pharmacopoeia.” Likewise, another medical authority, quoted in a recent review in the British Medical Journal, dubs placebos “the most effective medication known to science, subjected to more clinical trials than any other medicament yet nearly always doing better than anticipated. The range of susceptible conditions appears to be limitless.”

He continues:

And there’s the puzzle: the puzzle that I’ll try to address in this paper from the perspective of  evolutionary biology. If placebos can make such a contribution to human health, then what are e waiting for? Why should it be that we so often need what amounts to outside permission before taking charge of healing our own bodies? I can illustrate the paradox with one of Weil’s case histories. He describes the case of a woman with a metastatic cancer in her abdomen who refused chemotherapy and relied instead on dieting, exercise and a regime of “positive thinking” including “regular meditation incorporating visualization of tumour shrinkage” – following which, to the physicians’ astonishment, the tumour completely disappeared.

Weil asks: “What happened in this woman’s abdomen that eliminated widely disseminated cancer and restored her internal organs to good health? Her healing system, probably making use of immune mechanisms, was surely responsible; but why did it not act before?” Precisely. Why? Why should her bodily immune system be prepared, apparently, to let her die unless and until her mind decided otherwise? Weil asks the question as a doctor, and his “why?” is the why of physiological mechanism: “what happened?”. But I myself, as I said, want to take the perspective of an evolutionist, and my “why?” is the why of biological function: “why are we designed this way?”
There are two reasons for thinking that evolutionary theory may in fact have something important to say here. One reason is that the human capacity to respond to placebos must in the past have had a major impact on people’s chances of survival and reproduction (as indeed it does today), which means that it must have been subject to strong pressure from natural selection. The other reason is that this capacity apparently involves dedicated pathways linking the brain and the healing systems, which certainly look is if they have been designed to play this very role. I’d say therefore it is altogether likely that we are dealing with a trait that in one way or another has been shaped up as a Darwinian adaptation – an evolved solution to a problem that faced our ancestors. In which case, the questions are: what was the problem? and what is the solution?

After reviewing the significant evidence for evolutionary pressures that could select for the placebo effect, Humphrey concludes:

To start with, given that there are certain universals in how people fare in different situations, there are presumably general rules to be found linking global features of the physical and psychological environment to changes in the costs and benefits of health-care – features such as where you live, what the weather is like, the season of the year, what you can see out the window, how much you feel at home here, and, especially important, what social support you’ve got.

Generally speaking any such features that make you feel happy and secure – success, good company, sunshine, regular meals, comforting rituals – are going to be associated with lower benefits to having the symptoms of illness (e.g. feeling pain) and lower costs to self-cure (e.g. mounting a full scale immune response). By the same token any of them that make you feel worried and alone – failure, winter darkness, losing a job, moving house – are going to be associated with higher benefits to continuing to show the symptoms and higher costs to  elfcure.

Now, appreciating these cost/benefit changes, and switching health-care strategy accordingly, would bring clear advantages in the competition for biological survival. So it’s a fair bet that natural selection will have discovered these general rules and that humans will now be genetically designed to make good use of them – with the appropriate environmentally-activated switches being wired into the brain. And indeed there is lots of evidence that this is actually the case. People’s health does respond quite predictably to global environmental factors of the sort just listed. Much of the science of “health psychology” is now concerned with charting just how important these global effects are.

http://open.salon.com/content.php?cid=58361

http://www.nytimes.com/2008/12/07/fashion/07clubs.html?partner=permalink&exprod=permalink

Sometimes there is a rambler in the group, whose opinion far outlasts the natural interest of others, or a pedant, who never met a literary reference she did not yearn to sling. The most common cause of dissatisfaction and departures?

“It’s because there’s an ayatollah,” said Esther Bushell, a professional book-group facilitator who leads a dozen suburban New York groups and charges $250 to $300 a member annually for her services. “This person expects to choose all the books and to take over all the discussions. And when I come on board, the ayatollah is threatened and doesn’t say anything.” Like other facilitators, she is hired for the express purpose of bringing long-winded types in line.

For Doreen Orion, a psychiatrist in Boulder, Colo., the spoiler in her book group was a drama queen who turned every meeting into her own personal therapy session. Dr. Orion was used to such people in her practice, but in her personal life — well, no thanks. “There were always things going on in her life with relationships, and she’d want to talk about it,” she said. “There’d be some weird thing in a book and she’d relate it to her life no matter what. Everything came back to her. It was really exhausting after a while.”

http://www.nytimes.com/2008/12/05/health/05happy-web.html?partner=permalink&exprod=permalink

The researchers analyzed information on the happiness of 4,739 people and their connections with several thousand others — spouses, relatives, close friends, neighbors and co-workers — from 1983 to 2003…

How happy you are may depend on how happy your friends’ friends’ friends are, even if you don’t know them at all.

And a cheery next-door neighbor has more effect on your happiness than your spouse’s mood…

[T]heir research found that “if your friend’s friend’s friend becomes happy, that has a bigger impact on you being happy than putting an extra $5,000 in your pocket”…

In a separate study of 1,700 Facebook profiles, they found that people smiling in their photographs had more Facebook friends and that more of those friends were smiling…

[W]hen people changed from unhappy to happy in self-reported responses on a widely used measure of well-being, other people in their social network became happy too. Sadness was transmitted the same way, but not as reliably as happiness. Professor Cacioppo believes that reflects an evolutionary tendency to “select into circumstances that allow us to stay in a good mood.”

From John Tierney’s TierneyLab blog on NYT:

One of these restaurants was called “Good Karma Healthy Foods” and its menu included healthy choices such as cream of carrot soup (90 calories). The other restaurant was called “Jim’s Hearty Sandwiches” and its menu included high-calorie foods such as “Beef on a Wick” (800 calories).

We found that, just as in the other studies, people underestimated the number of calories of the same meal (a sandwich and a soda) when it was on the menu of the healthy restaurant compared to when it was on the menu of the unhealthy restaurant, and consequently were more likely to order chips in the healthy restaurant condition.

In another experiment, Dr. Wansink and Dr. Chandon showed people cups of granola and cups of M&Ms, two snacks containing about the same amount of calories per ounce. Some of the cups were labeled “Regular” and some were labeled “Low Fat” (even though there’s no such thing as low-fat M&Ms). As predicted, people significantly underestimated the calories in the “low-fat” varieties, and they compensated by raising their estimates of the “appropriate” serving size of each snack.

The low-fat labels also lessened the guilt associated with eating either snack — particularly the granola, which had a healthier (and less tasty, or “hedonic”) image in people’s minds even though it was just as caloric. Both normal-weight and overweight people said they’d feel little guilt about eating the “low-fat” granola. And while normal-weight people expressed guilt at eating even the “low-fat” M&Ms, overweight people “viewed the low-fat M&Ms as basically guilt-free,” according to Dr. Wansink and Dr. Chandon.

The researchers drew three conclusions from their series of experiments with snacks and foods in restaurants:

– Labeling snacks as low fat increases food intake during a single consumption occasion by up to 50 percent. This is robust across hedonic and utilitarian snacks, across young and old consumers, across self-reported nutrition experts and novices, in public and private consumption settings, and regardless of whether people serve themselves or not.

– For overweight people, low-fat labeling increases their consumption of all foods.

– Objective serving-size information prevents normal-weight people from overeating foods labeled as low fat. It does not influence overweight people.

Scientists in Sweden have demonstrated in a recent series of experiments that the self is a story that the brain tells itself:

At the annual meeting of the Society for Neuroscience last month, Swedish researchers presented evidence that the brain, when tricked by optical and sensory illusions, can quickly adopt any other human form, no matter how different, as its own…

The technique is simple. A subject stands or sits opposite the scientist, as if engaged in an interview.. Both are wearing headsets, with special goggles, the scientist’s containing small film cameras. The goggles are rigged so the subject sees what the scientist sees: to the right and left are the scientist’s arms, and below is the scientist’s body.

To add a physical element, the researchers have each person squeeze the other’s hand, as if in a handshake. Now the subject can see and “feel” the new body. In a matter of seconds, the illusion is complete. In a series of studies, using mannequins and stroking both bodies’ bellies simultaneously, the Karolinska researchers have found that men and women say they not only feel they have taken on the new body, but also unconsciously cringe when it is poked or threatened.

In previous work, neuroscientists have induced various kinds of out-of-body experiences using similar techniques. The brain is so easily tricked, they say, precisely because it has spent a lifetime in its own body. It builds models of the world instantaneously, based on lived experience and using split-second assumptions — namely, that the eyes are attached to the skull.

The fear of death and the evils of monopoly are in full bloom in the NYTimes article published today about Britain’s polices for buying proprietary prescription medications:

When Bruce Hardy’s kidney cancer spread to his lung, his doctor recommended an expensive new pill from Pfizer… A clinical trial showed that the pill, called Sutent, delays cancer progression for six months at an estimated treatment cost of $54,000.

But at that price, Mr. Hardy’s life is not worth prolonging, according to a British government agency, the National Institute for Health and Clinical Excellence. The institute, known as NICE, has decided that Britain, except in rare cases, can afford only £15,000, or about $22,750, to save six months of a citizen’s life…

Even in the United States, rising costs have led some in Congress to propose an institute that would compare the effectiveness of new medical technologies, although the proposals so far would not allow for price considerations. At the present rate of growth, medical costs will increase to 25 percent of the nation’s gross domestic product in 2025 from 16 percent, with half of the increase coming from new drugs and devices, according to the Congressional Budget Office…

The British government created NICE a decade ago to ensure that every pound spent buys as many years of good-quality life as possible, but the agency is increasingly rejecting expensive treatments. The denials have led to debate over what is to blame: company prices or the health institute’s math.

Dr. Michael Rawlins, chairman of NICE, blames the industry, saying that some companies raise prices “to get profits up so their executives can get better bonuses.”…

Robert Goldberg, vice president of the Center for Medicine in the Public Interest, an advocacy group financed by drug makers, likened Dr. Rawlins and his institute to terrorists and said their decisionswere morally indefensible…

Dr. Rawlins said he was frustrated that his institute had been censured instead of the drug company executives who set sky-high prices. Take the case of Celgene, the maker of Revlimid, a drug for multiple myeloma, a bone-marrow cancer, that in a preliminary ruling on Oct. 28 the institute said was too costly.

Celgene’s first big seller was thalidomide, a decades-old medicine now used as a cancer treatment, which is so cheap to manufacture that a company in Brazil sells it for pennies a pill.

Celgene initially spent very little on research and priced each pill in 1998 at $6. As the drug’s popularity against cancer grew, the company raised the price 30-fold to about $180 per pill, or $66,000 per year. The price increases reflected the medicine’s value, company executives said.

In 2005, the company introduced Revlimid, a derivative of thalidomide that is supposed to be less toxic, but may be no more effective. Celgene priced it at about $260 per pill, or $94,000 per year…

Private and public insurers in the United States must pay whatever Celgene and other makers of unique cancer medicines decide to charge, so prices are soaring. Spending on cancer drugs and other such specialty medicines rose 9 percent last year and now represents 24 percent of the nation’s drug bill…

But the most pressing question for the industry is what influence the British institute will have in the United States. The United States already spends more than twice as much per capita on health care as the average of other industrialized nations, while getting generally poorer health outcomes.