Aristotelianism
trag·ic
[ˈtrajik]
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causing or characterized by extreme distress or sorrow.“the shooting was a tragic accident”
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suffering extreme distress or sorrow.“the tragic parents reached the end of their tether”
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It is generally understood that Aristotle’s theory of mimesis and catharsis are responses to Plato‘s negative view of artistic mimesis on an audience. Plato argued that the most common forms of artistic mimesis were designed to evoke from an audience powerful emotions such as pity, fear, and ridicule which override the rational control that defines the highest level of our humanity and lead us to wallow unacceptably in the overindulgence of emotion and passion. Aristotle’s concept of catharsis, in all of the major senses attributed to it, contradicts Plato’s view by providing a mechanism that generates the rational control of irrational emotions.All of the commonly held interpretations of catharsis, purgation, purification, and clarification are considered by most scholars to represent a homeopathic process in which pity and fear accomplish the catharsis of emotions like themselves. For an alternate view of catharsis as an allopathic process in which pity and fear produce a catharsis of emotions unlike pity and fear, see E. Belfiore, “Tragic Pleasures: Aristotle on Plot and Emotion.” Princeton, 1992, 260 ff.
Disclosing and Sharing Emotion: Psychological, Social and Health Consequences
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Lessing sidesteps the medical attribution. He translates catharsis as a purification, an experience that brings pity and fear into their proper balance: “In real life,” he explained, “men are sometimes too much addicted to pity or fear, sometimes too little; tragedy brings them back to a virtuous and happy mean.”] Tragedy is then a corrective; through watching tragedy, the audience learns how to feel these emotions at proper levels.
D. W. Lucas, in an authoritative edition of the Poetics, comprehensively covers the various nuances inherent in the meaning of the term in an Appendix devoted to “Pity, Fear, and Katharsis”. Lucas also recognizes the possibility of catharsis bearing some aspect of the meaning “purification, purgation, and ‘intellectual clarification” although his discussion of these terms is not always, or perhaps often, in the precise form with which other influential scholars have treated them.
Lucas himself does not accept any one of these interpretations as his own but adopts a rather different one based on “the Greek doctrine of Humours” which has not received wide subsequent acceptance. Purgation and purification, used in previous centuries, as the common interpretations of catharsis are still in wide use today. More recently, in the twentieth century, the interpretation of catharsis as “intellectual clarification” has arisen as a rival to the older views in describing the effect of catharsis on members of the audience.
Effect on emotional recovery
This cathartic release of emotions is often believed to be therapeutic for affected individuals. Many therapeutic mechanisms have been seen to aid in emotional recovery. One example is “interpersonal emotion regulation,” in which listeners help to modify the affected individual’s affective state by using certain strategies. Expressive writing is also another common mechanism for catharsis. Joanne Frattaroli published a meta-analysis suggesting that written disclosure of information, thoughts, and feelings enhances mental health.
Emotional situations can elicit physiological, behavioral, cognitive, expressive, and subjective changes in individuals. Affected individuals often use social sharing as a cathartic release of emotions. Bernard Rimé also studies the patterns of social sharing after emotional experiences. His works suggests that individuals also seek social outlets in an attempt to modify the situation and restore personal homeostatic balance.
Rimé found that 80–95% of emotional episodes are shared. The affected individuals talk about the emotional experience recurrently to people around them throughout the following hours, days, or weeks. These results indicate that this response is irrespective of emotional valence, gender, education, and culture. His studies also found that social sharing of emotion increases as the intensity of the emotion increases.
However, other studies question the benefits of social catharsis. Finkenauer and colleagues found that non-shared memories were no more emotionally triggering than shared ones. Other studies have also failed to prove that social catharsis leads to any degree of emotional recovery. Zech and Rimé asked participants to recall and share a negative experience with an experimenter. When compared with the control group that only discussed unemotional topics, there was no correlation between emotional sharing and emotional recovery.
Some studies even found adverse effects of social catharsis. Contrary to the Frattaroli study, Sbarra and colleagues found expressive writing to greatly impede emotional recovery following a marital separation. Similar findings have been published regarding trauma recovery. A group intervention technique is often used on disaster victims to prevent trauma-related disorders. However, meta-analysis showed negative effects of this cathartic “therapy”.
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The term catharsis has also been adopted by modern psychotherapy, particularly Freudian psychoanalysis, to describe the act of expressing, or more accurately, experiencing the deep emotions often associated with events in the individual’s past which had originally been repressed or ignored, and had never been adequately addressed or experienced.
There has been much debate about the use of catharsis in the reduction of anger. Some scholars believe that “blowing off steam” may reduce physiological stress in the short term, but this reduction may act as a reward mechanism, reinforcing the behavior and promoting future outbursts. However, other studies also have suggested that using violent media may decrease hostility under periods of stress. Legal scholars have linked “catharsis” to “closure” (an individual’s desire for a firm answer to a question and also an aversion toward ambiguity) and “satisfaction” which can be applied to affective strategies as diverse as retribution, on one hand, and forgiveness on the other. Interestingly, there’s no “one size fits all” definition of “catharsis”, therefore this does not allow a clear definition of its use in therapeutic terms. http://everything.explained.to
Motives
Affect scientists have found differences in motives for social sharing of positive and negative emotions.
(1) Positive emotion
A study by Langston found: that individuals share positive events to capitalize on the positive emotions they elicit. Reminiscing about the positive experience augments positive affects like temporary mood and longer-term well-being. A study by Gable et al. confirmed Langston’s “capitalization” theory by demonstrating that relationship quality is enhanced when partners are responsive to positive recollections. The responsiveness increased levels of intimacy and satisfaction within the relationship. In general, the motives behind social sharing of positive events are to recall the positive emotions, inform others, and gain attention from others. All three motives are representatives of capitalization.
(2) Negative emotion
Rimé studies suggest that the motives behind social sharing of negative emotions are to vent, understand, bond, and gain social support. Negatively affected individuals often seek life meaning and emotional support to combat feelings of loneliness after a tragic event.
The grapevine effect
If emotions are shared socially and elicits emotion in the listener then the listener will likely share what they heard with other people. Rimé calls this process “secondary social sharing.” If this repeats, it is then called “tertiary social sharing.” https://www.theguard
Expert opinion: why are some cancers so difficult to treat?
Pancreatic cancer is a relatively rare cancer, but it remains one of the most lethal. “It’s a very complex disease; these people are hard to take care of, they have complicated medical issues,” says Dr. Margaret Tempero, research director at UC San Francisco’s Helen Diller Family Comprehensive Cancer Center. The field needs more trained practitioners and more funding for research, she says.
However, because early disease lacks obvious symptoms, only a minority of patients are candidates for surgery. And unfortunately, even after surgery the cancer often comes back. “About 20% of patients are candidates for surgery and, of those, about 20% are cured,” says Dr. Edward Garon, an oncologist at UCLA’s Jonsson Comprehensive Cancer Center.
Sometimes radiation therapy is also prescribed, although doctors disagree on its usefulness. “It’s discouraging that even basic issues like this — chemotherapy alone versus radiation and chemotherapy after surgery — have not been entirely worked out in this disease,” Garon says.
Physical symptoms of pancreatic cancer are not very specific to the disease. They include fatigue, weight loss and loss of appetite. Sometimes, jaundice and abdominal pain occur. Diagnosis depends on imaging procedures, such as CT or PET scans or also endoscopic ultrasound, but these tests cannot detect small, early-stage cancers.
As with other cancers, it’s becoming increasingly clear that pancreatic cancer is not a single disease but a group of diseases that look the same under the microscope but are molecularly different, says Dr. David Dawson, a pathologist at UCLA’s Jonsson center.
He and other pancreatic cancer researchers are heartened by the success of individualized treatment in breast cancer, which is becoming categorized and increasingly treated based on molecular differences in the tumors.
“I really think we’re on the cusp of doing that kind of work in pancreatic cancer,” Dawson says.
Can we chase tumours down evolutionary dead ends?
Professor Gerard Evan is Head of the Department of Biochemistry at the University of Cambridge. Earlier in the week, we wrote about his work on a crucial cancer-associated gene called Myc. In this thought-provoking article, Professor Evan explains how cancer is an evolving and adapting enemy, and talks about strategies to combat the disease.
Biology has undergone an unprecedented technical revolution in the past two decades. Despite its complexity, biological systems can now be mapped and catalogued in minute detail – we can monitor the activity of every one of our approximately 25,000 genes; identify almost every protein present in a cell; and even sequence the entire genomes of animals, plants, bacteria or cancer cells.
For cancer researchers, these technologies can appear a Godsend: cancers are extremely diverse diseases that arise through the build-up of mutations (errors) in the genes that regulate and restrain the growth, division, and movement of the cells that make up our bodies. The process is ‘Darwinian’ – in other words, the mutations occur at random over our lifetimes, and the faulty cells then either die out or survive and multiply as a result of the complex, changing and still largely mysterious selective pressures in the body.
The technical revolution of recent years has undoubtedly advanced our understanding of cancer, and is helping sustain impressive improvements in cancer survival rates, but why don’t we hear the word ‘cure’ very often when it comes to this disease? And what needs to be done so that we do?
Mapping complexity
Not surprisingly, given the haphazard and random way in which they evolve, every patient’s cancer is unique. Indeed, mapping and understanding the complexity within just one person’s cancer could occupy an entire research institute. In some ways, cancer research has reached an existential impasse – we can map and catalogue and annotate forever, but what is it about cancer that we really want to know?
For most of us, I suspect the answer is simple and pragmatic: we want to know how to cure patients. Simple questions have the habit of exposing others that are more fundamental: in this case, “Why are cancers so difficult to cure?” Here, there are two general schools of thought.
Personalised medicine
Many would point to the disconcerting genetic diversity of cancers – an inevitable consequence of the haphazard way that they evolve. In the past, cancer therapies were applied fairly indiscriminately, but now many believe that effective therapies need to be specific and tailored to the particular genetic faults in each individual’s cancer – in other words cancer therapy needs to be ‘personalised’. With the advent of new targeted drugs (such as Herceptin for some breast cancers, Glivec for certain leukaemias, and brand new drugs like vemurafenib for some skin cancers), many hope that this may, at least one day soon, be feasible.
But simply personalising treatment so that it targets the genetic faults present in a tumour at the point of diagnosis, disregards the most fundamental reason for why cancers are difficult to eradicate forever: cancer cells adapt and evolve in response to treatment. Because of this, even drugs that are initially very effective often have a progressively dwindling effect over time, as the biological systems that are blocked by the treatment spontaneously compensate by re-routing the cancer cells’ internal wiring, thereby restoring the cancer’s ability to grow and spread. To use an analogy, traffic hot spots in towns can cause major traffic jams, but cunning drivers will quickly find short cuts to get round the congestion.
Then, in those rare situations where cancer cells cannot take such ‘short cuts’, evolution takes over: in response to drug treatment, spontaneously arising mutant cancer cells that are resistant to the targeted drug rapidly outgrow their incapacitated siblings and the cancer comes back. Although some patients can be successfully cured and their cancers don’t return – such as is often the case for testicular cancer and some childhood cancers – for other cancers the situation is different, as so many patients and their families are all too aware. It doesn’t matter how effective or specific a therapy is – if the system the treatment is targeting can be bypassed by compensation or evolution, that therapy will become less effective over time and eventually fail, and the cancer will return.
Evolutionary dead end
Against two such formidable adversaries as compensation and evolution what are we to do? A solution is to identify targets that are essential for the survival of cancer cells but whose inhibition cannot be bypassed by compensation or evolution. Rather than causing localized traffic jams within the city that can be circumvented by short cuts, we identify the bridge that is the only way out of town and then block that.
But do such fundamental targets exist? Can we make drugs that inhibit them? How bad might the side effects of such therapies be, given that such essential and non-redundant engines of biology are likely to serve important functions in ‘normal’ bodily processes? We don’t yet know.
A second idea is to chase each cancer down an evolutionary valley and into a dead end from which it cannot escape. We accept that localized traffic jams can be bypassed but, each time that happens, we identify the back route and then target that – and we keep doing it until there are no short cuts left. In practice, this would mean treating a patient with one targeted drug and, if their cancer returns with newly-developed resistance to this treatment, we then identify how that resistance evolved and hit the tumour with another drug directed at that resistance mechanism. The process is repeated until the cancer runs out of evolutionary headroom.
Both of these strategies will need a significant re-tooling and refocusing of our cancer research enterprise. We need to pay more attention to the inherent robustness and evolutionary ability of the targets against which our drugs are directed, and see if we can identify the essential engines of tumour maintenance.
One potential benefit of finding such fundamental engines is that they might be a common requirement of many, perhaps all, cancers: in which case a therapy targeted against them might usher in an exciting and far more affordable era of ‘impersonalised’ cancer treatment.
On the other hand, if we are going to chase tumours into extinction, we need to track the evolutionary trajectories of cancers in patients through sequential episodes of treatment and relapse. To do this, we must establish what information we need and how to get it without putting patients through repeated and onerous biopsies and procedures.
Common goal
All cancer researchers share the common goal of wanting cancer therapies that are effective and durable. But to do this we must never lose sight of the fact that cancers are just another example of evolution at work. Cancers are blind. They are neither clever nor cunning – but humans are.
We can – and will – beat them. 🙂
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