More fun from the NYT in the spirit of Why Zebras Don’t Get Ulcers (but in this crappy economy, a hopeful tagline: Chronic stress changes the brain, but relaxation can change it back.)

http://www.nytimes.com/2009/08/18/science/18angier.html

Since this website is supposed to be about sound as well as science, I’m excited to announce that most of the slides and podcasts for the Neuroimaging Training Program Summer Course at UCLA are up on the web!  Enjoy the sound and slides of experts from around the world as they discuss methods relevant to neuroimaging research.

The itunes link is here.  Note, slides and podcasts from last year’s course are available at the iTunes link as well.

I recently posted a summary of an article that I found interesting and likely to bring out some healthy controversy at PsychInAction. The article was about differences in the ways that liberals and conservatives process information (in the brain). The basic finding was that people who identified as conservative (compared to those who identified as liberal) showed less activity in a brain area that has previously been related to cognitive control during a task that requires one to inhibit a certain prepotent response (basically, you need to switch gears and restrain yourself from the habitual response). In concluding, the authors suggest that while liberals performed better on the laboratory task that required response inhibition, the conservatives in their sample would likely perform better on a task where a fixed response style is optimal.

As with many brain studies, there are several caveats and logical fallacies that are easy to fall into (see here for a discussion of what we can and can’t say with brain data), but in an informal lecture, even scientifically-conservative Russ lamented recently that in order to get papers in places like Nature, we, as scientists need to argue for why our findings are cool and worth the space they take to print in the absence of space to list all of the constraints, assumptions, and other details that might help people fully understand all of the limitations of a given dataset. So, while we should stick closely to our data and not make wild claims about what the brain has to tell us about social scientific questions, using brain data to generate new hypotheses (that are later tested) is how science can move forward.

The study described above is not perfect (would be interesting to see with a larger sample and to know more about third variable personality factors), and it is interesting to consider counter examples (as one colleague pointed out, it would be easy to argue that some religious conservatives show incredible flexibility in taking from the Bible), but I think as scientists, in addition to poking holes in the methods of others (a necessary set of checks and balances), we should also be considering how different methods can inform one another and how to test alternative hypotheses if we don’t believe the findings of published work.

Three separate teams of researchers have discovered the same set of genes that increase risk of addiction and lung cancer in smokers.  This is an exciting discovery.  When explained at the New York Times, the conclusion was:

“The genetic variations, which encode nicotine receptors on cells, could eventually help explain some of the mysteries of chain smoking, nicotine addiction and lung cancer that cannot be chalked up to environmental factors, brain biology and statistics, experts said. ”

Similarly, one researcher commenting on the finding suggested: “This is really telling us that the vulnerability to smoking and how much you smoke is clearly biologically based” (psychiatry professor Dr. Laura Bierut of Washington University in St. Louis, a genetics and smoking expert who did not take part in the studies).

However, what both of these sources do not comment on is the fact that more and more evidence suggests that biology AND the environment interact to create health, disease, dispositions.  Certain genetic variations may lead to riskier profiles, given a stressful environment, but in some cases, the same genes that are riskiest under threatening conditions can also be most protective under nurturing conditions.   Following this type of exciting discovery, in my view, what will be even more exciting is to understand the way(s) that the genes identified interact with both the physical and social environment to allow some people with those genes to avoid smoking all together, some to become addicted immediately, and some to fall in between.  To say that genes will explain the “mysteries of chain smoking, nicotine addiction and lung cancer that cannot be chalked up to environmental factors, brain biology and statistics” is to miss the most exciting part of the story– the interactions between all of these factors.

I have recently read a bunch of articles about placebo effects and pain. In the case of pain, placebo effects can be remarkable. In fact, pain-sensitive brain regions are less active when people receive pain and a placebo, compared to the equivalent pain without a placebo. Furthermore, in anticipating pain with a placebo, pre-frontal control regions are more active, which may serve to regulate the experience of pain and/ or to trigger the body’s own anti-pain medication (opioids).

Interestingly, placebo effects can be both positive (as in you feel better after taking a non-active pill, receiving an irrelevant intervention), or negative (you feel side effects from taking the pill, just as with regular meds). Also, placebo effects are often dose-response, and can have time-effect curves, and carryover effects, just like active medications.

This brings me to the topic of mind body interaction. Many people in my department study these types of effects, and certainly don’t think of them as placebo. So, where is the line between placebo and mind-body treatments? Is it just the way we label them?

As a really cool example of mind-body interaction, check out Mike Irwin’s study (press release) of immune response to the virus that causes shingles. In this study, older adults who did tai chi (meditation through movement), had higher levels of immune functioning and quality of life scores than people in a wait-list control group. Interestingly, the effects of the tai chi intervention were additive with the shingles vaccine, such that older adults who received both the tai chi intervention and the vaccine had cell-mediated immune levels comparable to those of younger adults (who are at much lower risk for getting shingles as a result).

Some other articles about pain and placebo:

Turner et al. (1994): The Importance of placebo effects in pain treatment and research.

Hrobjartsson & Gotzsche (2001): Is the placebo powerless? An analysis of clinical trials comparing placebo with no treatment.

Stewart-Williams (2004): The placebo puzzle: Putting together the pieces.

Some other articles about Mind-Body stuff:

Cruess, D. G., Antoni, M. H., McGregor, B. A., Kilbourn, K. M., Boyers, A.E., Alferi, S.M., Carver, C. S., & Kumar, M. (2000). Cognitive-behavioral stress management reduces serum cortisol by enhancing benefit finding about women being treated for early stage breast cancer. Psychosomatic Medicine, 62(3), 304-308. (4 pages)

Davidson, R.J., Kabat-Zinn, J., Schumacher, J. Rosenkranz, M., Muller, D., Santorelli, S.F., Urganowski, R., Harrington, A., Bonus, K. & Sheridan, J. F. (2003). Alterations in brain and immune function produced by mindfulness meditation. Psychosomatic Medicine, 65(4), 564-570. (6 pages)

Storch, M., Gaab, J., Kuttel, Y., Stussi, A, & Fend, H. (2007). Psychoneuroendocrine effects of resource-activating stress management training. Health Psychology, 26(4), 456-463. (7 pages)

I just got back from the Society for Personality and Social Psychology’s Annual Conference, this year in Albuquerque, NM.  Some of the highlights in my book included talks on SCN and neuro-endocrine interactions:

Symposium on Social Cognitive Neuroscience Perspectives on Intragroup and Intergroup Relations.  Of particular interest here, Jay Van Bavel discussed his work with Dominic Packer and Will Cunningham, using a minimal group paradigm (with mixed race teams).  As in previous work, participants showed ingroup bias (they favored people on their own team over people on the other team).  Using fMRI, the group found that viewing photos of ingroup members (compared to viewing photos of outgroup members) was associated with increased activity in regions of the brain that are associated with affective processing (amygdala, striatum).  This is especially interesting considering the fact that the amygdala is usually thought of as a “fear” region.  This work adds to the mounting evidence that the amygdala may be more broadly associated with motivationally relevant affective processes.  The work is also interesting because it adds to the literature suggesting that there is something special about the idea of an ingroup, regardless of familiarity/ race.

Jenn Pfeifer also presented results (from an impressive longitudinal fMRI study of children and adolescents) demonstrating increased amygdala activity in imitating facial expressions of ingroup compared to outgroup members (in this case, ingroup = gender).  Furthermore, across several areas of the brain that are typically associated with shared representations of the self and others, “children who were more biased in favor of their own gender showed greater activity in response to gender ingroup members, while in other preliminary data, girls with higher levels of estradiol [female sex hormone] showed greater activity in response to boys.”  In fact, in young girls who did not consciously show interest in boys, levels of sex hormones were associated with the ways that they responded to photos of the opposite sex in the scanner.  Hormones are powerful things…

Continuing on the topic of hormones, at a symposium on Social Endocrinology: How Hormones Can Contribute to Research in Social and Personality Psychology, Pranjal Mehta presented data suggesting the importance of considering the role of multiple hormone systems in concert.  Pranjal’s data demonstrated an interaction between cortisol and testosterone levels in predicting a response to defeat in a competition.  From Pranjal’s absract: “After facing social defeat, high testosterone- low cortisol individuals were more likely to choose to compete again than high testosterone, high cortisol individuals.  Hormones were unrelated to the decision to compete again after victory.  These data support the hypothesis that when social status is threatened, testosterone increases the motivation to gain status, whereas cortiso influences behavioral approach and avoidance.”   Given how much we have come to rely on hormonal measures to link psychology and health outcomes, I was especially interested to see how important the interaction of multiple hormones was in predicting the “dominance behavior” outcomes discussed.  This is potentially of interest to people interested in health as well, because dominance hierarchies seem to play such a key role in health outcomes.

Other talks at this symposium addressed the role of testosterone in decision making (e.g. testosterone made people more likely to maximize their gains in an ultimatum game, but placebo effects/ thinking you had received testosterone made people more likely to behave in aggressive ways).   I am not sure what to make of the data since the manipulations typically involved administering testosterone exogenously, and who knows whether giving someone testosterone is the same thing as having the body produce it in response to outside influences.  I actually thought one of the most interesting points here related to the placebo effects– despite the fact that actually receiving testosterone made people behave in one way, the belief that one had received testosterone made them behave in the opposite (aggressive) way that is typically depicted in the media.  Does testosterone as an excuse make men think that they can behave in aggressive ways?

More updates on SPSP soon.

Socioeconomic status (SES) is linked to health outcomes across a range of diseases, with increasing health at *every* level of the SES gradient (so it’s not just that being super poor is a risk factor, it’s that with every incremental increase in wealth, we see improved health).  Data suggests that in addition to the obvious culprits (access to health care, access to good food, health behaviors, etc.), stress is a major factor in SES/health disparities.

A recent article in SCAN reported one possible pathway linking SES and stress:

“after accounting for potential demographic confounds, subclinical depressive symptoms, dispositional forms of negative emotionality and conventional indicators of SES, self-reports of low subjective social status uniquely covaried with reduced gray matter volume in the perigenual area of the anterior cingulate cortex (pACC)—a brain region involved in experiencing emotions and regulating behavioral and physiological reactivity to psychosocial stress.^“

Reduced ability to regulate stress and emotion may have major health implications.

^{See also: why zebras don’t get ulcers and Naomi Eisenberger’s commentary on the article above.}

Baldwin Way wrote a really awesome primer on genetics for those of us who didn’t major in genetics or microbiology, but still want to capitalize on the power of the many new “-omics” technologies. Check it out.

I have been working on a script that will read in MacStim like code (tab delimited with same column concepts), and will play in MatLab.  I am so sick of only being able to use .sfil to play audio, and having to specify the length of each audio and video piece.  The default here (if you don’t specify a stimulus length) is to play for the length of the audio or video file.