Barbara Natterson-Horowitz

Barbara Natterson-Horowitz

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Adı:
Barbara Natterson-Horowitz
Unvan:
Profesör, Kardiyolog
Barbara Natterson-Horowitz, Harvard Üniversitesi'nde İnsanın Evrimi Biyolojisi Bölümünde Misafir Profesör. California, Los Angeles Üniversitesi Kardiyoloji Anabilim Dalı'nda Kardiyoloji Uzmanı ve Tıp Profesörüdür.
As we know, the heart-slowing reflex triggered by states of high arousal, such as fear, pain, or distress, is a core feature of vasovagal fainting in human beings. Alarm bradycardia has protected animals across all classes of vertebrates, and persists in us today precisely because its protective power is so deeply embedded into the autonomic nervous system, which has been passed down from our ancient water-dwelling ancestors. This hypothesis connects the acutely slowing heart of a hunted fish in the water to a human fainter in the ER.
If you are an ER doc in São Paulo, you are most likely aware that erections can arise from another surprising source: the venomous bite of the Brazilian spider Phoneutria nigriventer. While potentially toxic and possibly fatal, the venom can also induce an erection lasting many hours. Not surprisingly the venom has been marketed to males for whom more conventional pharmaceuticals have not provided success.
A leading physician of that era named Rudolf Virchow, still renowned today as the father of modern pathology, put it this way: “Between animal and human medicine there is no dividing line—nor should there be. The object is different but the experience obtained constitutes the basis of all medicine.”*
Fainting episodes often begin in the same way and in the same situations as the well-known fight-or-flight response. When animals, including human animals, sense a possibly mortal threat, adrenaline and other hormones (called catecholamines) flood into our bloodstreams. Our hearts race. Our blood pressures soar. We breathe faster. Crucially, we get a burst of energy, allowing us to either escape from the threat or battle it off.
But as you’ll soon see, the old duality of “fight or flight” needs an update. Many animals have at their disposal an additional trick to boost their odds of living through a dangerous encounter. It’s not just fight or flight. It’s fight, flight, or faint.
Remarkably, fainting begins the same way as the other two fear responses—with a high-emotion stressor and a surge of adrenaline. But from there fainting follows a different route. Instead of the heart beating faster (tachycardia), it plummets (bradycardia). Instead of blood pressure surging, it plunges. Detecting low-pressure, slow-moving blood, sensors throughout the body signal to the brain that something is terribly wrong: a failing heart or a catastrophic loss of blood. In a protective response, the brain shuts the system down by fainting.
On the night of January 18, 1991, during the Gulf War, Scud missiles launched by Iraqi troops began exploding in Israeli communities. Citizens were alerted by howling air-raid sirens that blared from outdoor speakers and on the radio and TV. Since there was a terrifying possibility that the bombs were carrying chemical payloads in addition to their explosive power, the frightened populations had been instructed to don gas masks and seek shelter when they heard the wail of a siren.
In the maternity ward of a Tel Aviv-area hospital that night, three women were in labor. As is standard practice, they had been fitted with fetal heart monitors that strapped around their bellies to keep track of their babies’ heartbeats. At three a.m., a sudden, terrifying shriek of a Scud alert siren penetrated the walls of the maternity ward—and, apparently, the wombs of the expectant mothers. As hospital staff scrambled to put gas masks on themselves and their patients, the nurses noticed something highly unusual on the fetal monitors. The heart rates of all three of the about-to-be-born infants suddenly and unexpectedly.… plummeted. From a healthy and brisk 100 to 120 beats per minute they slowed by half, to a frightening 40 to 60. The tiny hearts “lay low” like this for two minutes and then returned to normal.
All three babies, who hadn’t yet even heard their parents’ voices outside the womb, responded physiologically, with bradycardia, to the sound of danger. Some of the slowing may have resulted from the sounds of the siren itself and some from maternal stress hormones entering the fetus’s body in response to the siren. Either way, these obstetrical observations strongly suggest that even prior to birth itself, we’re equipped with unconscious anti-predator defenses, including a potent alarm bradycardia response. All three babies were ultimately born healthy, as well as apparently armed with the full complement of survival instincts we all possess but rarely think about.
Another common side effect of near fainting while conscious is both disgusting and tactically brilliant. A vagal state can make an animal lose control of its bodily functions. Some animals urinate or defecate under extreme emotion or fear. Many predators find urine or feces repugnant and will leave. Dogs are known to retreat at the smell of skunk; frightened shrews produce such foul odors from their anal pockets that even ravenous badgers keep their distance. Vomiting by the would-be prey can have the same conveniently repellant effect on the predator.
This potentially embarrassing loss of bodily control in response to fear is one vestige we humans probably wish we’d evolved out of. But in fact it may occasionally serve a protective function for us as well. Rape-prevention educators sometimes instruct women to urinate or vomit if rape is imminent. In some cases, the attacker will be repulsed and withdraw. A more common phenomenon is seen in women who successfully avoid sexual assault by fainting or by entering a “near fainting while conscious” state. Psychologists have studied cases of this and compared them to immobility reactions in animals. They suggest that when fighting back isn’t an option, not struggling may defuse the situation and reduce the likelihood of rape.† While far from foolproof, fainting succeeds enough of the time to warrant a serious consideration of its evolutionary roots.
Perhaps one of the most promising places to look for cancer clues among our fellow species is the disease that ranks among the top killers of female humans: breast cancer. Breast cancer strikes mammals from cougars, kangaroos, and llamas to sea lions, beluga whales, and black-footed ferrets. Some breast cancer in women (and the occasional man) is connected to a mutation of a gene called BRCA1. All humans have a BRCA1 gene. It’s on our seventeenth chromosome. But some of us (about 1 in 800) are born with a mutated version. For Jewish women of Ashkenazi descent, it’s as high as 1 in 50.
BRCA1 appears to be an especially skilled molecular copy editor. When it’s working right, it catches mistakes in the DNA every time a cell divides. It corrects typos and restores deletions. Like a great editor, BRCA1 keeps the DNA elegant, supple, concise, and true to its original intentions. But when BRCA1 is or becomes mutated, the DNA codes can get garbled and confused. Over generations of division this can lead to cancerous cell replication.
Many organisms have vulnerable BRCA1 genes. And in some animals, its malfunction seems to result in breast cancer, just as it does in humans. In one Swedish study, the presence of a BRCA1 mutation made English springer spaniels four times more likely to develop breast cancer. Jaguars in zoos in the United States that were on progestin-based birth control showed patterns of breast cancer that were very similar to those of women with BRCA1 mutations.* Zoo veterinarians report high incidence in other big cats, too, including tigers, lions, and leopards.
And yet, having a BRCA1 mutation doesn’t automatically lead to breast cancer. BRCA1-related breast cancer results when genetic predisposition meets something that activates it—including hormonal and environmental exposures. Researchers call these triggers “second hits.” And studying a variety of animals could help pinpoint which combination of genes and triggers leads to cancer.
Our human tumors, it turns out, are remarkably similar to those of the animals with whom we live: our pet dogs. Dog cancer cells and human cancer cells are nearly indistinguishable. Dogs live longer than mice, so researchers can observe the cancer—and the treatments—over the long term. And, unlike most lab mice, pet dogs’ immune systems are intact, allowing oncologists to study how a cancer acts when challenged by natural defenses. Dogs are also simply much bigger than mice. This has implications, both practical—the tumors are physically easier to see—and philosophical (think of Peto’s paradox).
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Adı:
Barbara Natterson-Horowitz
Unvan:
Profesör, Kardiyolog
Barbara Natterson-Horowitz, Harvard Üniversitesi'nde İnsanın Evrimi Biyolojisi Bölümünde Misafir Profesör. California, Los Angeles Üniversitesi Kardiyoloji Anabilim Dalı'nda Kardiyoloji Uzmanı ve Tıp Profesörüdür.

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