MITPressLog

The Invention of Heterosexual Culture

October is LGBT History Month. We'll be posting about a few of our related titles each Friday in October. Today's post is an excerpt from The Invention of Heterosexual Culture by Louis-Georges Tin.

 

 

 

The belief that heterosexual love was the most natural thing in the world was accorded widespread acceptance and approval as the twentieth century progressed. Even so, the nascent discipline of psychoanalysis soon called the notion into question.

In his Three Essays on the Theory of Sexuality published in 1905, Sigmund Freud argued the probability that heterosexuality was not a given:

Thus from the point of view of psycho-analysis the exclusive sexual interest felt by men for women is also a problem that needs elucidating and is not a self-evident fact based upon an attraction that is ultimately of a chemical nature.

Far from being natural in biological or biochemical terms, therefore, heterosexuality and homosexuality were, in Freud’s submission, functions of an individual’s personal psychic makeup.

In his discussion of “polymorphously perverse” infantile bisexuality, Freud argued that heterosexuality was the result of a long and arduous psychic apprenticeship extending far back into earliest childhood. This assertion subsequently appeared elsewhere in his work, where he argued that “normal sexuality too depends upon a restriction in the choice of object.” In other words, although never going to the lengths that psychiatry once had and dismissing heterosexuality as a pathological condition, psychoanalysis was at pains to show that it was not an inborn characteristic. Analysis of every single complex—not least the Oedipus variety—tended to confirm this. Despite broad dissemination and awareness of psychoanalytical theory, however, the vast majority of the public (and most psychoanalysts) remained unaware of the notion that heterosexuality or, indeed, homosexuality was an acquired condition.

Understanding Pain

Pain is a biological enigma. It is protective, but not always. Its effects are not only sensory but also emotional. There is no way to measure it objectively, no test that comes back positive for pain; the only way a medical professional can gauge pain is by listening to the patient’s description of it. The idea of pain as a test of character or a punishment to be borne is changing; prevention and treatment of pain are increasingly important to researchers, clinicians, and patients. In honor of  Pain Awareness Month, here's an excerpt from Understanding Pain by Fernando Cervero. In Understanding Pain, Cervero explores the nature of pain: why it hurts and why some pain is good and some pain is bad.

Think about the simple act of buying a new pair of shoes. You try them on in the shop, think they fit quite well, and walk a few steps to make sure they are reasonably comfortable. After that simple test, you decide to buy them. You know from experience that the first few times you wear them they are going to hurt a bit. If you are unlucky they may hurt a lot. A minor rub that in the shop was almost imperceptible may develop into an unpleasant pain. It may take a while for your feet to get used to the shoes. Only after they stop rubbing the annoying sore spots will the pain go away.

The problem with your new shoes is the consequence of a unique property of pain sensation: its inability to adapt. Every other sensory experience, after a prolonged and constant stimulus, adapts to a lower level or even stops being perceived altogether. If you walk into a room and there is an intense odor, it doesn’t take long for you to stop perceiving the odor. You don’t hear the rumbling sound of your washing machine after a few minutes. Interestingly, you can tell when the washing machine stops, because you detect that the noise has ended even though by then you weren’t really hearing it. We have a powerful mechanism of sensory adaptation that eliminates a continuous noise or a persistent odor from our perceptual world and helps us to see in very bright or very dark conditions. Our senses are dampened by persistent and constant stimulation and are awakened by sudden changes and by contrasts. The alternating black and white stripes of pedestrian crossings and the two-tone sirens of fire engines and ambulances keep our senses alert to these important signals by preventing sensory adaptation. Nothing blunts our senses more than constant and uniform stimulation.

Pain is the only exception to the adaptation rule. In fact, pain not only doesn’t adapt; it produces the opposite effect: it amplifies as it persists. Hence the problem with your new shoes. In the shop you may not even have noticed the slight rubbing, and you would hardly have called it a pain sensation. Yet as this very small source of minor pain bombards your brain continuously, the tiny pain becomes progressively larger and larger. It amplifies to a point where wearing your new shoes may became torture. The amount of pain that you feel once the amplification process has set in is out of proportion to the minor rubbing. You are suffering the consequences of a process known as sensitization.

Using the tools of psychophysics (the science that studies the relationship between physical stimuli and the sensations they produce), sensory adaptation is revealed by a shift toward the right of the curve that relates stimulus intensity to sensory perception. This rightward shift means that after your senses adapt it will take a greater intensity of the stimulus to produce the same amount of sensation, and that your sensory threshold (the intensity at which you begin to perceive a stimulus) will be higher. However, when we use the same techniques to measure pain perception after a continuous painful stimulus, we note that the pain-perception curve has shifted in the opposite direction, toward the left, showing sensory amplification rather than sensory adaptation. Now, less intense stimuli produce more intense pain. We call this process hyperalgesia, meaning increased pain sensitivity. And because the pain threshold has also moved toward lower stimulus intensities, we may now feel pain at intensities of stimulation that hadn’t been painful before. We have a special word—allodynia—for the feeling of pain caused by stimulations that don’t normally produce pain. Allodynia and hyperalgesia are consequences of pain amplification, the properties that make pain unique among sensory perceptions and that demonstrate that pain doesn’t adapt to prolonged and continuous stimulation.

The pain caused by your new pair of shoes is trivial when compared to the pain of patients who suffer from chronic pain. A pain that doesn’t go away is a pain that increases and increases until eventually it dominates all aspects of a person’s life. The lack of adaptation to pain is what drives many chronic-pain patients to anxiety and then to depression. The pain is always there. You may learn to live with it, but it will never go away. Pain amplification can be helpful under normal circumstances because it helps you to take care of an injured body part. This is essential for the healing process, and it is a consequence of the protective nature of pain. For people with chronic pain, however, the amplification of pain sensitivity expressed as allodynia and hyperalgesia becomes the dominant symptom of their diseases and ruins the quality of their lives. Pain amplification adds suffering to the unpleasantness of chronic pain.

Alzheimer's disease and amyloid

According to The New York Times, "A study of a rare gene mutation that protects people against Alzheimer’s disease provides the strongest evidence yet that excessive levels of a normal brain substance, beta amyloid, are a driving force in the disease — bolstering hopes that anti-amyloid drugs already under development might alter the disease’s course or even prevent it." In Genetic Twists of Fate, Stanley Fields and Mark Johnston's discussion of the history of Alzheimer’s research includes mention of Martin Roth, Bernard Tomlinson, and Gary Blessed's 1970s demonstration that the degree of dementia in a person correlated with the number of amyloid deposits in the brain. Here's an excerpt from the book:

In late 1906, Dr. Alois Alzheimer presented his paper on “profound dementia in a young adult.” He concluded, “I have just presented a clearly defined and hitherto unrecognized disorder.” By all accounts, Alzheimer’s presentation had no impact on the audience of psychiatrists who heard it.

Because Auguste [Deter] displayed symptoms at only fifty-one years of age, her disease—dubbed Alzheimer’s disease a few years later by Alzheimer’s mentor, Emil Kraepelin, the father of modern psychiatry—was classified as a presenile dementia, defined then as occurring before sixty years of age. This disorder stood in contrast to the much more common senile dementia displayed by older patients. This distinction between dementia in a younger person and dementia in the aged would confound the field for half a century, during which time Alzheimer’s disease attracted hardly any attention from researchers.

Whereas presenile dementia showed characteristics that caused it to be considered a disease, senile dementia was thought to be the result of the normal deterioration of old age. Instead of giving credence to the idea of a physical illness, psychiatrists fostered a model of dementia in the aged that pinned the cause on some combination of personality, emotional trauma, mandatory retirement, social isolation, and the breakup of the family. In the 1940s and 1950s they linked social pathology to brain pathology, viewing the former as the cause of the latter. To psychiatrists of that era, it was all nurture, and no nature.

By the 1970s, however, society had come to appreciate that people should not be discriminated against on the basis of their advanced age any more than because of their race or sex. As a consequence, the stereotype of aging individuals as inevitably succumbing to dementia began to fade. Meanwhile, on the scientific front, Martin Roth, Bernard Tomlinson, and Gary Blessed at Newcastle University, in the U.K., demonstrated that the degree of dementia in a person correlated best not with age but with the number of deposits of amyloid and neurofibrillary tangles observed in the brain, suggesting that specific pathological changes, and not the general aging process, were the culprit. Because the clinical and pathological manifestations of the early-onset (presenile) and late-onset (senile) dementias were the same, both disorders were classified as Alzheimer’s disease.

These findings led to a much greater realization of the burden of Alzheimer’s disease, which until then had been thought to be relatively small. In 1976, Robert Katzman of the University of California in San Diego made the bold estimate that Alzheimer’s disease afflicted 1.2 million Americans and accounted for sixty thousand to ninety thousand deaths each year. Those numbers startled the public and galvanized the research community, stimulating big increases in funding for research into the causes of the disease and the development of therapies. The numbers from thirty years ago pale compared to those of today: about 5 million Americans currently suffer from this horrible disease; by 2050 it is expected to be between 11 million and 16 million.

 

Anatomical Alternatives

On March 23, 1983, Barney Clark, the world's first recipient of a permanent artificial heart, died only 112 days after his surgery. In Case Studies in Biomedical Research Ethics, Timothy Murphy examines this controversial case and raises questions about the ethics surrounding new medical interventions.

 

Barney Clark was born in 1921 and, after a lifetime of smoking, was diagnosed in 1978 with emphysema, congestive heart failure, and cardiomyopathy (degeneration of heart tissue). Heart transplantation was relatively new at that time, and Clark at 57 was considered too old to be eligible for the surgery.

A medical committee at the University of Utah was interested in finding a candidate to be the first person to receive an artificial heart, the Jarvik-7 (named after its designer). This committee thought that the candidate should be so ill that death was imminent and the prognosis offered no more than a year of life. Clark met these conditions.

Clark signed an eleven-page consent form, he was interviewed by members of the IRB about his choice, and a team of physicians tried to test his determination by urging him to change his mind. He did not.

Dr. William DeVries led the medical team that supervised the implantation of the artificial heart in a complicated surgery that began at 11 P.M. December 1, 1982. The Jarvik-7 was a mechanical device that was hooked by tubes to an external air compressor to move blood. The external compressor weighed 375 pounds, and Clark could never be without it. After the operation, Clark was in poor state and experienced considerable confusion, delirium, memory loss, periods of semiconsciousness, and seizures. He required surgical intervention to replace one of the heart valves which broke two weeks after the initial operation.

Clark’s health was never especially good, but he did appear before videocameras, and selectively edited videos were released to the media. This public visibility gave the impression that he was glad to be alive. In fact, Clark’s overall condition could only be called burdensome, and he died on March 23, 1983, of multiple organ failure. It was not long before scientists were split in their opinion about the value of the artificial heart. Some called it one of the boldest experiments ever attempted. Others said it more than failed. Still others called in unacceptably expensive. DeVries defended the artificial heart noting that, without it, Clark would have been dead by midnight on December 1, 1982.

The FDA, which oversees medical devices, allowed DeVries three more tries with the Jarvik-7. The first of these patients died after surviving for twenty-one months; the second survived for ten months and two days; the third survived ten days. In the last case, DeVries admitted that the surgery had probably shortened the patient’s life. In 1990 the FDA withdrew approval for use of the Jarvik-7 as a permanent device, or even as a bridge for a patient awaiting a human heart transplant. Patient referrals to DeVries dropped, because other physicians were concerned that he had too many conflicts of interest rooted in his desire for success and financial gain. They worried that he was putting technical success ahead of patient care.

Murphy closes this examination by leaving readers with the following three questions:

1. To what extent is it ethical for a health care team to offer a patient an intervention that might possibly extend his life and then try and persuade him to not accept it?
   
   
2. What information do you think would be crucial in explaining the risks and benefits of an artificial heart transplant?
   
   
3. It is reasonable to expect some failure with new medical interventions. In your view, do the survival times of the patients in this case amount to a reason to shut down the use of a mechanical heart, or should more attempts be allowed?

 

Watson and Crick and Genetic Twists of Fate

On February 28, 1953, James D. Watson and Frances Crick announced their discovery of DNA's chemical structure. To celebrate the anniversary of this breakthrough, here's an excerpt from Genetic Twists of Fate by Stanley Fields and Mark Johnston. The book explains how tiny variations in our personal DNA can determine how we look, how we behave, how we get sick, and how we get well.

 

More than half a century ago, on February 28, 1953, James D. Watson and his colleague, Francis Crick, launched an age of genetic discovery with their announcement to the lunchtime patrons of the Eagle Pub in Cambridge, England, that they had “found the secret of life.” Their discovery of the structure of DNA—the most important molecule of life, which specifies the form and function of every living thing—made clear how traits are passed down through the generations. Watson and Crick’s breakthrough paved the way for an age of discovery that culminated in the announcement on June 25, 2000—not in a pub but at the White House—that the human DNA code had been determined. A few years later, Watson himself became one of the first two people to read his own personal DNA code.

After 1953, Watson went on to a celebrated career, directing a laboratory at Harvard University, then a storied scientific institution at Cold Spring  Harbor on Long Island, and ultimately the Human Genome Project, which deciphered the DNA code. But shortly before his own DNA code was determined, Watson’s professional life ended amid charges of racism. He was quoted in the October 14, 2007 edition of The Sunday Times that he was “inherently gloomy about the prospect of Africa” because “all our social policies are based on the fact that their intelligence is the same as ours—whereas all the testing says not really.” He also said, “There is no firm reason to anticipate that the intellectual capacities of peoples geographically separated in their evolution should prove to have evolved identically. Our wanting to reserve equal powers of reason as some universal heritage of humanity will not be enough to make it so.”

As his comments rapidly circled the globe, drawing condemnation from his fellow scientists, the 1962 Nobel Laureate quickly apologized for them. Speaking at a meeting of the Royal Society in London on October 18, 2007, he said, “To all those who have drawn the inference from my words that Africa, as a continent, is somehow genetically inferior, I can only apologize unreservedly…That is not what I meant. More importantly, there is no scientific basis for such a belief.”...

Watson had steered into the always-dangerous shoals of the genetics of race, and he should not have been surprised that his words sank him. In our penultimate chapter we, too, venture into these treacherous waters. We will show you that there are many more genetic differences within racially defined populations such as Africans and Caucasians than between these populations. You can see the close resemblance of the DNA codes of these races if you compare the few available sequences. Or, you can wait a few years and see it when you read your entire DNA code.

 

Fish-Inspired Vehicles?

Happy Monday! Here's an excerpt from How to Catch a Robot Rat by Agnès Guillot and Jean-Arcady Meyer to kick off the week.

Forms

Forms present in nature have mathematical properties that have inspired inventors.

In 1420, appearing before the eminent committee that questioned his competence to construct the cupola of Santa Maria del Fiore in Florence, Filippo Brunelleschi rapped an egg on the table and crushed the shell lightly at the base. Everyone could see that the egg remained vertical and immobile, whereas if the architect had tried to explain in words the planned construction, to do it would have seemed impossible. This egg presented in Florentine style (later used by Christopher Columbus) must have been convincing because Brunelleschi obtained carte blanche, and the gigantic dome that he built is still in place. He conceived it (by coincidence?) according to a principle that recalls the eggshell, so that bricks laid fishbone style mutually block each other and thus totally bypass the need for classic supports such as wooden arches. An ingenious encasing of two cupolas likewise ensures a good distribution of pressure.

An egg obviously does not contain arches, which would obstruct the embryo in development, yet its structure is capable of resisting considerable force: the shell of a hen's egg is 0.3 millimeters thick and can withstand up to 3.0 kilograms of pressure, and that of an ostrich egg is ten times thicker and can withstand a pressure twenty times stronger! The shells expoloit a "trick": the crystals of the mineral salts that constitute them are oriented toward the center of the egg and are self-blocking, like the bricks in the dome of Florence. Various architects--including the Germans Frei Otto, Carl Zeiss, and Heinz Isler--have recently adopted these characteristics to calculate the exact thickness needed to cover various domes or to establish force lines for immense stretched structures.

The oblong form is known to move rapidly in the air and in water without too much effort. Bizarrely, marine animals are also the best models for terrestrial or aerial mobiles! For example, the engineers of Daimler AG are currently trying out the form of the tropical boxfish to save precious liters of fuel in future automobiles. This research has resulted in a prototype presented in Washington in 2005. Although the animal presents an almost cubic belly, this characteristic makes it paradoxically very hydrodynamic and even, according to measurements undertaken by engineers, more aerodynamic than current cars, with a coefficient of air penetration of 0.06 instead of 0.30!  The "Mercedes-Benz bionic car" would boast a coefficient of 0.19 and could save 20 percent in fuel and 80 percent in nitrous oxide emissions. Its body, like the rigid carapace of the fish, is conceived as if it were composed of numerous hexagonal panels supported by a metallic vertebral column. Such a car would thus be very competitive in both lightness and robustness, the two great principles of both nature and the automobile industry.

Even an airplane of the future might be shaped like a fish, too. The Smartfish, being developed by several international companies and research laboratories at the initiative of Swiss engineer Koni Schafroth, is inspired by the form of several fish, especially the tuna, the fastest and most agile animal in the sea. A meterwide miniprototype has already successfully achieved first flight, in April 2007...

Two Nobels Among Us

Elizabeth H. Blackburn, University of California at San Francisco, Carol W. Greider of Johns Hopkins and Jack W. Szostak, Howard Hughes Medical Institute won the 2009 Nobel Prize in physiology or medicine for discovering a key mechanism in the genetic operations of cells, an insight that has inspired new lines of research into cancer.

MIT Press boasts the recent paperback reissue of the compelling biography, Elizabeth Blackburn and the Story of Telomeres.  University of San Francisco author Catherine Brady tells the story of Elizabeth Blackburn's life and work and the emergence of a new field of scientific research on the specialized ends of chromosomes and the telomerase enzyme that extends them.  In honor of the occasion, here's a brief excerpt from the book looking at the young and highly motivated Blackburn: 

Like many other seventeen-year-old girls in 1965, Elizabeth Blackburn listened to the records of the Beatles and Peter, Paul, and Mary and wore the miniskirts that were just coming into fashion, but she felt so shy in the presence of boys that she could not look them in the eye. Rigorously schooled by her mother in polite manners that sidestepped confrontation, Elizabeth was a model student who seemed readily guided by her teachers. But her delight in books exceeded the bounds of obedient studiousness—in particular, she was thrilled by her recent discovery of a biology text complete with detailed illustrations of amino acids, strung together in long chains and then folded up into complex three-dimensional shapes to form enzymes and other proteins. For Liz, these elegant structures had a teasing beauty, promising tantalizing clues to the processes of life and yet also enfolding that mystery. Even the names of the amino acids—phenylalanine, leucine—struck her as poetic. Though she confessed her fascination to no one, she traced drawings of amino acids on large, thin sheets of white paper and then tacked them up on her bedroom wall.

From the start she carefully protected the passion that would shape her life as a scientist, her fierce determination often masked by a polite, acquiescent demeanor. The nice girl who remained silent when confronted or thwarted purchased the freedom of a secret, willful, essential self. Blackburn’s first clear memory dates to when she was about three years old. Playing in the yard behind her family’s house, she had found a bull ant and was handling it gently, talking to it as it crisscrossed her palm and the back of her hand. When her mother came on the scene, she brushed the insect from Liz’s hand and vehemently warned her never to touch these insects, whose bite could result in a painful welt. Surprised by her mother’s concern, Liz obeyed. But she remained stubbornly and silently certain that the ant could not hurt her.

We'd also like to tip our hat to Jack Szostak, who is a contributor to Protocells: Bridging Nonliving and Living Matter, and Carol Greider. 

Ashley’s Rights

Norman Cantor, author of Making Medical Decisions for the Profoundly Mentally Disabled, comments on the recent debate over the medical treatment of a 9-year-old girl named Ashley who is severely mentally and physically disabled:

Some disability rights advocates say that Ashley’s medical intervention violates “basic human  rights.”   I disagree.  I argue (in Making Medical Decisions for the Profoundly Mentally Disabled, MIT Press, 2005) that every profoundly mentally incapacitated person has a right to have decisions about potentially beneficial medical interventions made by a conscientious surrogate acting with careful attention to the incapacitated person’s interests, well being, and dignity.  Bodily integrity is normally part of human dignity, but there are circumstances when bodily invasions are justified by the patient’s own interests.  For example, a therapeutic sterilization can be appropriate for a person whose bodily condition means that pregnancy and/or child birth would be torturous.  The surrogate’s decision must be free of negative stereotypes and must include consideration of alternative ways, other than bodily intervention, to promote the person’s well being.

Ashley’s case seems to fulfill the criteria for humane treatment.   Her parents have always been devoted to Ashley’s well being.  They have consulted with medical experts and with a 40 person ethics committee.  They have had considerable input from parents of similar children indicating that normal bodily development will result in a significantly diminished quality of life for Ashley.  If, as claimed, Ashley could not enjoy the normal benefits of physical maturation, and if there are no less intrusive alternatives, her parents’ decisions about medical intervention do not violate Ashley’s rights.

Read the New York Times article about Ashley.
Read about the debate that Ashley’s case has generated.

Scholarpedia

Wikipedia is useful for finding quick information, answering trivia questions, and for getting up to speed on things you think you should know.  But whether Wikipedia ought to be used for an academic citation is another story. 
One scholar, Eugene M. Izhikevich (author of Dynamical Systems in Neuroscience), has decided to harness the concept of Wikipedia into a format that is more likely to please academics:  he has founded Scholarpedia, a peer-reviewed version of Wikipedia.  Each article in Scholarpedia has a "curator", usually a leading researcher or scholar in that field.  The initial version of an article is submitted for a peer review process, and each successive version is permanently saved for purposes of citation.  While (in the spirit of a Wiki) anyone can propose changes to an article, the curator is responsible for approving these changes. 
Scholarpedia's current content focuses on Computational Neuroscience, Dynamical Systems and Computational Intelligence, but it plans to move in other directions if all goes well. 
An exciting aspect of Scholarpedia is that some articles are written and curated by the very people who discovered the concept - as in the case of Lotfi Zadeh, who has written about Fuzzy Logic, or Mandlebrot, who is slated to write the article on Mandelbrot sets.   And who can argue with that kind of citation?

What are you waiting for?

If you've ever wondered what keeps you listening to music, you may have the answers in the book Sweet Anticipation by David Huron.  Huron proposes that your sense of expectation plays a large role in music, and he outlines a range of aesthetic responses that are created by expectation.  If you'd like to hear a bit more about this interesting theory, it is discusssed in a podcast on a new website devoted to music cognition (Sound and Mind).  To listen, click here.  You can also read more new ideas about our brain's appreciation for music in this Boston Globe article.