Regular readers of this blog will be aware of my conception of positive emotions  in terms of promotion focus and negative emotions in terms of prevention focus. Today I will try to relate this to the specific action-tendency theory of negative emotions and broaden-and-build theory of positive emotions (as proposed by Barbara Fredrickson).

First its instructive to distinguish between negative and positive emotions. Negative emotions, like Fear, Anger, Disgust, traditionally have been conceptualized as specific action tendencies that get triggered or activated by particular type of threatening situations/stimuli. I view them as sensory driven. A stimuli impinges and is either presumed to be attacking/trespassing (thus arousing anger) or dangerous and threatening survival (thus arousing fear) or intimidating and overbearing (thus arousing sadness and disengagement)  or sickening and to be avoided (thus arousing disgust) ; in all cases a stimuli or situation acts as an immediate trigger for a specific action tendency – that of defending, fighting or fleeing, disengaging and surrendering or vomiting and keeping away.

In contrast consider positive emotions like Joy, Interest, Contentment and Love. They all happen when the environment is safe and bodily needs are met- they are not need driven, but growth oriented. They are not based around survival, but around growth.  they are non -specific thought action repertoire that is a broadened set and is not narrowly focused- rather one of the prime effects of positive emotions is to broaden attention, thought/cognition,  actions and interactions. I consider them as motor driven. they are not a response to a stimulus. Rather they are specific patterns of spontaneous action tendencies and opportunities to practice giving outlet to ones spontaneous action tendencies in a safe environmental. That is why every sort of play- be it physical rough-and-tumble or intellectual play of creativity or social play of flirting – is associated with the positive emotions.

To make my analogy more clear consider the fact that actions can be classically conditioned (and thus response to US/CS stimulus) or operant conditioned (and thus not reactive or reflexive but intrinsically driven and proactive) and while former may be more or less determined by  the external stimulus and internal associations and is deterministic in nature, the latter has spontaneous behavioral variability and initiation as its premise and has room for free will.  What I claim today is that negative emotions are reactive and thus keep you stuck in deterministic rut, while positive emotions are expansive and provide opportunities for exercise of free will in safe and playful environments by encouraging spontaneous behavioral fluctuations and felkxibility.

It has been found time and again that positive emotions are associated with a broadening and resource-building effect. Consider Joy. It encourages one to engage in acts for acts sake or encourages rough and tumble play- it builds physical resources.  Consider Interest . It encourages one to engage in exploration of a domain- be it actual physical domain or conceptual domain – it builds cognitive maps and cognitive or intellectual resources. Consider contentment. It encourages one to engage in reflection and self assessment and self integration – it builds psychological resources. consider Love (care-giving variety not romantic which is pathological and more of a negative emotion). It encourages one to engage in reciprocal interactions and to explore, act on and reflect on the other- it builds social resources.

Thus it is evident that positive emotions do help to broaden and build. That much has been proved by Barbara’s research program .  My additional claim is that negative emotions are sensory oriented and reactive while positive emotions are motor oriented, spontaneous and proactive. By signalling safe environments in which behavioral flexibility can be played around with they push us to relate to life more intrinsically.

Perhaps another analogy will be relevant.  there is a sympathetic nervous system and there is parasympathetic system. the sympathetic system helps us respond to stressful situations and readies the body. the parasympathetic restores the body and helps in regeneration of the body. So do negative emotions help us react to outside threats and make the mental-illness dimension while positive emotions help match intrinsic activity to opportunities in the environment and makes the mental health dimension.

The former (mental illness continuum)  is a zero sum game- if I win someone looses. For eg if a dominance hierarchy is there and I am on top I may feel manic while the person at bottom may feel depressed..but as long as dominance and survival and predation and germs are there the negative emotions would be there …the latter (mental health continuum)  is a win-win game.  There are more opportunities for everyone to fare better if everyone is positioned high on mental health spectrum as then doors to creativity and productivity open right then and there for all concerned. thus, I have become an advocate of the positive psychology movement and would like more efforts devoted to study of positive emotions.

Fredrickson, B. (1998). What good are positive emotions? Review of General Psychology, 2 (3), 300-319 DOI: 10.1037//1089-2680.2.3.300

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There is a letter published in the advance online edition of Nature Genetics, that reports that microduplication of genes in the region 16p11.2 are associated with the risk of schizophrenia in a large cohort. It has been earlier shown that microdeletions in the same region confer the risk of Autism.Thus, it seems that the region codes for genes too much of which causes schizophrenia and too little autism.  Here is the abstract of the study:

Recurrent microdeletions and microduplications of a 600-kb genomic region of chromosome 16p11.2 have been implicated in childhood-onset developmental disorders. We report the association of 16p11.2 microduplications with schizophrenia in two large cohorts. The microduplication was detected in 12/1,906 (0.63%) cases and 1/3,971 (0.03%) controls (P = 1.2 times 10-5, OR = 25.8) from the initial cohort, and in 9/2,645 (0.34%) cases and 1/2,420 (0.04%) controls (P = 0.022, OR = 8.3) of the replication cohort. The 16p11.2 microduplication was associated with a 14.5-fold increased risk of schizophrenia (95% CI (3.3, 62)) in the combined sample. A meta-analysis of datasets for multiple psychiatric disorders showed a significant association of the microduplication with schizophrenia (P = 4.8 times 10-7), bipolar disorder (P = 0.017) and autism (P = 1.9 times 10-7). In contrast, the reciprocal microdeletion was associated only with autism and developmental disorders (P = 2.3 times 10-13). Head circumference was larger in patients with the microdeletion than in patients with the microduplication (P = 0.0007).

Here is what medical news today (via which I found this article) has to say about the findings:

An international team of researchers led by geneticist Jonathan Sebat, Ph.D., of Cold Spring Harbor Laboratory (CSHL), has identified a mutation on human chromosome 16 that substantially increases risk for schizophrenia.

The mutation in question is what scientists call a copy number variant (CNV). CNVs are areas of the genome where the number of copies of genes differs between individuals. The CNV is located in a region referred to by scientists as 16p11.2. By studying the genomes of 4,551 patients and 6,391 healthy individuals, Sebat’s team has shown that having one extra copy of this region is associated with schizophrenia. The study appears online today ahead of print in the journal Nature Genetics.
Schizophrenia and autism: two sides of the same coin?

“This is not the first time that the 16p11.2 region has caught our eye,” says Sebat. It was previously spotted in a 2007 study with Professor Michael Wigler at CSHL — a deletion of the identical region was identified in a girl with autism. Studies by several other groups have shown that losing one copy of 16p11.2 confers high risk of autism and other developmental disorders in children.

Taken together these studies suggest that some genes are shared between schizophrenia and autism, according to Sebat and colleagues. “In some ways, we might consider the two disorders to be at opposite ends of the same neurobiological process” says Shane McCarthy, Ph.D., the lead author of the study, “and this process is influenced by the copy number of genes on chromosome 16.” One hypothesis is that the loss of 16p11.2 leads to the deprivation of key genes involved in brain development, while an extra copy of this region might have the opposite effect.

A correlation between 16p11.2 mutations and head size

It is not known what biological processes are affected by the copy number of 16p11.2, Sebat notes. He believes, however, that the team may have stumbled on to an important clue. By studying the clinical records of patients, they discovered that patients with deletions of the region differ significantly in head size from those with duplications of the same region. Sebat reports, “Head circumference of patients with the deletion were larger than average by more than one standard deviation. Head circumference was slightly below average in patients with the duplication.” These findings, he notes, are consistent with some previous studies that have observed a trend towards larger brain size in autism and an opposite trend toward smaller brain size in schizophrenia.

All this nicely fits in with what I have been proclaiming from the rooftops from the early days of this blog: that autism and Schizophrenia are opposites on the same continuum and the genes involved should also be the same. More copy numbers leading to propensity towards psychosis while lesser number or deletions associated with autistic traits. One more puzzle piece fits in and now we know why the brain size differences exist in autistic and schizophrenic persons and what the poetntial function (mentalizing) of region 16p11.2 may be.

McCarthy, S., Makarov, V., Kirov, G., Addington, A., McClellan, J., Yoon, S., Perkins, D., Dickel, D., Kusenda, M., Krastoshevsky, O., Krause, V., Kumar, R., Grozeva, D., Malhotra, D., Walsh, T., Zackai, E., Kaplan, P., Ganesh, J., Krantz, I., Spinner, N., Roccanova, P., Bhandari, A., Pavon, K., Lakshmi, B., Leotta, A., Kendall, J., Lee, Y., Vacic, V., Gary, S., Iakoucheva, L., Crow, T., Christian, S., Lieberman, J., Stroup, T., Lehtimäki, T., Puura, K., Haldeman-Englert, C., Pearl, J., Goodell, M., Willour, V., DeRosse, P., Steele, J., Kassem, L., Wolff, J., Chitkara, N., McMahon, F., Malhotra, A., Potash, J., Schulze, T., Nöthen, M., Cichon, S., Rietschel, M., Leibenluft, E., Kustanovich, V., Lajonchere, C., Sutcliffe, J., Skuse, D., Gill, M., Gallagher, L., Mendell, N., Craddock, N., Owen, M., O’Donovan, M., Shaikh, T., Susser, E., DeLisi, L., Sullivan, P., Deutsch, C., Rapoport, J., Levy, D., King, M., & Sebat, J. (2009). Microduplications of 16p11.2 are associated with schizophrenia Nature Genetics DOI: 10.1038/ng.474

UPDATE: I just revisited my 20th may 2008 post on the matter and realized how prophetic my musings were. Reproducing part of it below the fold for the benefit of newbies to this blog:

CNVs on the other hand present a different model of disease. One can have one or more types of CNVs (deletions, duplications, multiple duplications etc) associated with the same genetic code sequence and this in my view would lead to spectrum like diseases where one may find variations along a continuum on a particular trait- based on how many copies of the genetic sequence one has. One would remember that I adhere to a spectrum based view of schizophrenia/psychosis and also a spectrum based view of Autism. Moreover I believe that Schizophrenia and Autism are the opposite ends of the spectrum, whose middle is normalcy and that the appropriate traits may have to do with social brain, creativity etc.

now as it happen previous research has also found that CNVs are also found to a higher extent in autistics. Moreover, research has indicated that the same chromosomal regions have CNVs in both Autism and Schizophrenia. To me this is exciting news. Probably the chromosomal region (neurexin related is one such region) commonly involved in both schizophrenia and autism is related to cognitive style, creativity and social thinking. Qualitatively (deletions as opposed to duplications) and quantitatively (more duplications) different type of CNVs may lead to differential eruption of either Schizophrenia or Autism as the same underlying neural circuit gets affected due to CNVs, though in a different qualitative and quantitative way.

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