Chapter 5. Hormones and the Brain
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By Gary Stix First off, this study on a molecule tied to social interaction was conducted in animals. So I’m supposed to turn on the siren and the flashing red light here to let you know that the headline you just read might not apply in humans. Still, the animals in question, prairie voles, are a special case, models of faithfulness that put humans to shame when it comes to the delicate topic of monogamy. Once hitched, the rodents stick with their mates for life—an example of moral pulchritude in the animal kingdom that many of us human sinners can never hope to emulate. It could easily become the state animal for whole regions of the U.S. For just that alone, the implications of the experiment in question are particularly intriguing. The new research shows that oxytocin, the bonding hormone, is sometimes capable of turning the upstanding rodent into an anti-social lout, making the study results more compelling in many ways than if they were reported in errant humans. So the man-bites-dog headline stays. This all came up when Karen Bales, a professor at University of California, Davis, wanted to know what would happen if oxytocin gets administered for lengthy intervals, not the short-term dosing that has occurred in the multitude of previous vole studies that linked the hormone to monogamous behavior. In their experiment, Bales and team gave either a low, medium or high dose through the nose to 29 voles, and a saline solution to 14 controls At first, the animals became all cuddly as in previous studies But after three weeks, an entire vole childhood (from weaning to sexual maturity), they started breaking bad. Males did not engage in the normal behavior of “pair bonding,” that drives them to look for the girl of their dreams. And female voles’ natural mothering instinct seemed to disappear: when placed nearby young pups that were not their own, they didn’t dote, as they are wont to do. The cuddle hormone had turned the rodents into meanies. © 2012 Scientific American
(Relaxnews)—In a study of more than 90 men, scientists from the University of Bonn, Germany, found that subjects treated with a dose of testosterone before the study told fewer lies than those who received a placebo. "Testosterone has always been said to promote aggressive and risky behavior and posturing," says researcher and neuroscientist Bernard Weber. However, more recent studies indicate that it also fosters social behavior. Prior research has suggested that the hormone may actually cause people to be more "prosocial" in that they voluntarily act in the interest of others, writes the Atlantic magazine, but exactly how the hormone influences behaviors isn't understood. For this latest study, 46 subjects were treated with testosterone by applying it to the skin in gel form, while 45 subjects received a placebo. The next day, the subjects played a dice game in which it was easy for the men to lie to earn more money, with no possibility of being caught. The study was designed so that it was impossible even for the researchers to detect whether a subject was lying or not. Rather, they used statistics to analyze reported earnings that were higher than probability would allow, inferring from these how honest the subjects were being. While many people in the study lied about the game, there was a noticeable difference between the men boosted with testosterone and those who weren't—the testosterone group avoided the temptation to cheat more often. Blood tests confirmed the results that high testosterone levels were linked with more honest game playing. "Test subjects with the higher testosterone levels had clearly lied less frequently than untreated test subjects," says co-author Armin Falk. "This result clearly contradicts the one-dimensional approach that testosterone results in anti-social behavior." The study was published last week in the journal PLoS One . http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0046774 © 2012 NY Times Co.
Keyword: Hormones & Behavior
Link ID: 17378 - Posted: 10.17.2012
Cort Pedersen at the University of North Carolina at Chapel Hill and his team gave 11 alcohol-dependent volunteers two daily doses of an oxytocin nasal spray or a placebo, during the first three days of a detox programme. The volunteers also received lorazepam - a detox drug - when their withdrawal symptoms reached a specific level. The oxytocin group had fewer alcohol cravings and milder withdrawal symptoms than the placebo group, and used just one-fifth of the lorazepam (Alcoholism: Clinical and Experimental Research, doi.org/jgp). "Four [oxytocin] volunteers didn't need any lorazepam at all," says Pedersen. This is good news because lorazepam is highly addictive. While it reduces anxiety and seizures during alcohol withdrawal, users can experience insomnia and cravings when they come off the drug. Although it is unclear how oxytocin - famed for its role in social bondingMovie Camera - helps to aid withdrawal, it has no known side effects. Pedersen hopes that alcoholics who take the hormone will therefore be less likely to experience the unpleasant symptoms that can lead to relapse. © Copyright Reed Business Information Ltd.
by Gisela Telis In the industrialized world, women live at least 5 years longer, on average, than men. Scientists have attributed that difference to everything from healthier habits to hardier cells. Now, a new study that analyzes the longevity of eunuchs, or castrated men, suggests that testosterone may play a part in shortening men's lives. The idea that testosterone, the male sex hormone, affects lifespan isn't new. Neutered dogs and other animals that have had their sources of testosterone removed often live longer than their intact counterparts. But studies on the connection between castration and longevity in humans are harder to come by, and the results have been inconclusive. A 1969 study of institutionalized patients in Kansas found that castrated men lived an average of 14 years longer than other men in the same facility, but a 1993 study of Italian castrati (singers castrated as boys to preserve their high voices) found nothing unusual about their longevity. Almost 5 years ago, biologist Kyung-Jin Min of Inha University in Incheon, Korea, found himself considering this lack of data while watching a Korean TV drama about eunuchs. Min began to wonder if Korea's rich historical records could shed light on the link between castration and longevity in humans. Until the late 19th century, Korean rulers employed eunuchs to serve the royal court. These eunuchs were allowed to marry and adopt castrated boys as their sons. The Yang-Se-Gye-Bo, a genealogical record of the eunuch families, has survived, and it documents the birth and death dates and other personal details of 385 eunuchs who lived between the mid-16th century and the mid-19th century. © 2010 American Association for the Advancement of Science.
By Judy Stone In one sense, it is refreshing to see men being the target of pharma, after all these years of women being the focus of relentless—and misleading—advertising. On the other, we’re seeing the start of yet another pharma campaign to dupe the public by the unnecessary medicalization of symptoms to create new drug markets. I used to be a fairly enthusiastic pharma fan, but over recent years have become increasingly disillusioned. The hype over testosterone is the latest example of why. With so many pressing problems in the world, I wish pharma would focus their attention on doing something more useful with their energies. I thought it started with drugs for “hot flashes,” but Karen Roush set me straight about hormone therapy, reporting that “It all started with men in ancient civilizations eating the penis and testicles of animals as a cure for impotence.” (And to think that Maryn McKenna just warned us of the dangers of kissing cats! This early hormone therapy sounds a bit dicier.) In the 1940s, estrogen was able to be extracted from horse urine in large quantities, enabling a supply for treating women “suffering from estrogen deficiency.” Dr. Robert Wilson, a prominent New York gynecologist, founded a private trust in 1963 to promote estrogen use. Pharmaceutical companies provided $1.3 million to this “trust;” they, of course, stood to profit handsomely from their investment in Wilson’s endeavor. Wilson is described as being “evangelical” in his crusade to save women from the “decay” of menopause. He was quite successful, with his 1966 book, Feminine Forever, selling 100,000 copies in the first seven months alone. His theme, “A Plea for the Maintenance of Adequate Estrogen from Puberty to Grave,” expounded in a mainstream medical journal, was adopted both by the medical profession and by the popular press. © 2012 Scientific American
By GRETCHEN REYNOLDS It’s widely accepted among scientists that regular exercise transforms the brain, improving the ability to remember and think. And a growing and very appealing body of science has established that exercise spurs the creation of new brain cells, a process known as neurogenesis. But just how jogging or other workouts affect the structure of the brain has remained enigmatic, with many steps in the process unexplained. A new study published last month in Proceedings of the National Academy of Sciences may fill in one piece of the puzzle, by showing that male sex hormones surge in the brain after exercise and could be helping to remodel the mind. The research was conducted on young, healthy and exclusively male rats – but scientists believe it applies to female rats, too, as well as other mammals, including humans. The decision to use only males was carefully considered. “We’ve known for a while that estrogen,” the female sex hormone, “is produced in the brain” not just of female animals but also, to some degree, in males, says Bruce S. McEwen, the director of the Laboratory of Neuroendocrinology at Rockefeller University in New York and an author of the study, which also involved scientists from the University of Tsukuba in Japan and other institutions. Estrogen has been well studied and has many effects, he said, including, scientists suspect, new brain cell growth. But far less has been known about the role of male sex hormones in mammalian brains, particularly after exercise. While both sexes produce male sex hormones, males produce far more of it – mostly in the gonads but, the researchers suspected, also in the brain. Copyright 2012 The New York Times Company
By Matthew Perrone, Associated Press "Do you have a decrease in libido?" "Have you noticed a recent deterioration in your ability to play sports?" "It could be Low-T." Welcome to the latest big marketing push by the nation's drug companies. In this case, it's a web page for Abbott Laboratories' Androgel, a billion-dollar selling testosterone gel used by millions of American men struggling with the symptoms of growing older that are associated with low testosterone, such as poor sex drive, weight gain and fatigue. Androgel is one of a growing number of prescription gels, patches and injections aimed at boosting the male hormone that begins to decline after about age 40. Drugmakers and some doctors claim testosterone therapy can reverse some of the signs of aging — even though the safety and effectiveness of such treatments is unclear. "The problem is that we don't have any evidence that prescribing testosterone to older men with relatively low testosterone levels does any good," says Dr. Sergei Romashkan, who oversees clinical trials for the National Institute on Aging, a part of the National Institutes of Health conglomerate of research centers. Low testosterone is the latest example of a once-natural part of getting old that has become a target for medical treatment. Bladder problems, brittle bones and hot flashes have followed a similar path: from inconvenient facts of life, to ailments that can be treated with drugs. The rise of such therapies is being fueled by both demographics and industry marketing. © 2012 NBCNews.com
By Scicurious We’ve all heard of the legendary monogamous prairie vole, haven’t we? Our adorable rodent friend forms the kind of attachments that make us humans feel slightly ashamed of our more promiscuous habits. And of course, if we know about prairie voles, we know about oxytocin (and I’ve got a whole series on it over at the ‘Science! 101′ page of my other site). Prairie voles are monogamous primarily due to the actions of oxytocin in the female, and vasopressin in the male. Without these two hormones, the prairie voles will love ‘em and leave ‘em just like their close cousins, the meadow vole. But is that all there really is to pair bonding? Just one hormone, a desire to stay with your furry mate forever…and that’s it? No, it’s more complicated than that. There are two real aspects to a pair bond. The first is the prosocial bit, the animal preferring to associate with one particular other animal. In voles, this requires the hormones oxytocin and vasopressin, and the neurotransmitter dopamine. But there’s another aspect to pair bonding: maintenance. And that requires more than fuzzy feelings, it also requires rejection of other potential mates, and guarding your mate against all comers. This aggressive behavior also involves dopamine, but in this case, a different population of receptors. © 2012 Scientific American
By Daisy Yuhas How do I love thee? When neuroscientist Young and journalist Alexander started counting, they found many molecular ways. In The Chemistry between Us, the writers highlight the complex chemical processes that create love in the brain and bolster the argument that love is an addiction. Young has devoted his career to studying the behaviors and neural circuitry of love in the prairie vole, a rodent whose monogamous tendencies resemble our own. Once a prairie vole has found “the one,” the pair will most likely remain companions for life. Young's research has implicated a range of chemical activities—mainly during sex—that build this lifelong bond. In particular, he uncovered how two hormones in the brain, vasopressin in male voles and oxytocin in female voles, regulate social behavior and memory—promoting the recognition of a loved one and the urge to cuddle or defend. In addition, the circulation of dopamine and opioids allows the vole to associate his or her partner with pleasure, thus strengthening their bond. Many of these molecules are identical to those activated in human bonding. That loving feeling comes at a price. A hormone called corticotropin-releasing factor, or CRF, builds up in the brains of paramours and parents alike. The CRF system activates a stress response, and this system elicits the painful sensations you feel when your baby cries or your boyfriend dumps you. The system may seem like a nasty trick, but it has its uses. Even when passion fades or a diaper needs changing, the sharp pangs of the CRF system keep families and loved ones together. The CRF system also contributes to the agony an addict feels after the elation wears off. Thus, the authors argue, the highs of intimacy and withdrawals of separation parallel the highs and lows that drug addicts experience. © 2012 Scientific American
by Sara Reardon Freedom of information requests have revealed that pregnant women may not have been given all the facts before taking an experimental treatment to prevent female fetuses from being masculinised as a result of a rare genetic disorder. Research has provided some evidence that dexamethasone, a drug normally prescribed to relieve inflammation, can prevent girls with a rare hormonal disease from developing male genitalia and same-sex attraction if they are treated as fetuses. But as yet, no clinical studies show that this treatment is safe, says Alice Dreger of Northwestern University in Evanston, Illinois. She claims that researchers have misled an unknown number of pregnant women into taking the experimental treatment without properly informing them of its risks. Since the 1980s, Maria New of Mount Sinai School of Medicine in New York has studied and popularised the idea of prescribing dexamethasone "off-label" to women at risk of having foetuses with congenital adrenal hyperplasia (CAH). The treatment is now taught as standard practice in medical schools. But because the drug must be given very early in pregnancy before the fetus' gender or CAH status is known, many fetuses are treated unnecessarily. A child with two carrier parents has a one-in-four chance of having the disease, and the treatment only works for girls. There is little research available on the effects of dexamethasone, which mimics a steroid hormone. And because dexamethasone doesn't cure CAH but only prevents masculinisation of girls, it can be difficult to distinguish possible effects of the drug from other treatments the children receive after birth. © Copyright Reed Business Information Ltd.
By Susan Milius OTTAWA — Some of the animal kingdom’s showiest extremes, from deer antlers to the outsized horn of the male rhinoceros beetle, may be natural insulin meters. As an animal grows, the nubbins of tissue that will form its big weapons or displays may be more sensitive to insulin than other developing body parts, Douglas Emlen of the University Montana said July 10 at the Evolution Ottawa scientific congress. The proposal “potentially narrows the range of explanations for the evolution of ornaments and weapons,” said Bob Montgomerie of Queen’s University in Kingston, Ontario, who studies courtship-related features in birds. Insulin orchestrates growth in tune with how much food a young animal gets, Emlen explained. A well-fed youngster flush with insulin will grow the most spectacular horns or other paraphernalia, while underfed rivals remain stunted. If the growing antlers or other extreme structures are supersensitive to insulin, they will supersize out of proportion to less sensitive tissue. That’s the case for the horns of the rhinoceros beetle, Trypoxylus dichotomus. Males of the species grow horns about two-thirds as long as the rest of their bodies. They use these fearsome weapons to knock rivals away from sap-oozing wounds on trees where females go to feed. The horns are eight times more responsive to insulin or insulin-like growth factors than some other body parts, Emlen said. That sensitivity fits with reports from other researchers that insulin or related signals affect development of antlers in red deer and the outsized male claws in a type of shrimp and one kind of crab. For those animals though, researchers haven’t yet explored how the weaponry tissues’ sensitivity compares with that of other body parts. © Society for Science & the Public 2000 - 2012
By Helen Shen, Globe Correspondent The International Olympic Committee has issued new rules for the 2012 London Games that would require checking testosterone levels in athletes whose eligibility as females is called into question. Several elite female athletes have previously been accused of secretly being males, including South African runner Caster Semenya , who was investigated and later cleared after her 2009 world championship victory in the 800-meter event drew accusations from competitors. The IOC says its intent is to identify athletes who would be ineligible “by reason of hormonal characteristics” -- not to determine gender, but the policy has drawn criticism. Stanford University bioethicist Katrina Karkazis said the inclusion of a gynecologist and geneticist on the IOC examining panel contradicts this message. “It’s way more than a blood test or a series of blood tests. There will be genital exams, there will be genetic testing,” she said. Athletes will be disqualified to compete as females if they are found with testosterone levels typical of males, and if they possess cellular receptors that respond to the hormone’s effects, which include boosting muscle mass and strength. “They chose something that really does discriminate between males and females,” said Dr. Joshua Safer, an endocrinologist at Boston Medical Center and expert in transgender care. Testosterone levels vary from one individual to another and, for a given individual, can vary widely by time of day. But the overall ranges of testosterone are about 10 times higher in men than in women, he said. © 2012 NY Times Co.
By Nathan Seppa HOUSTON — Men with low testosterone who are given replacement doses of the hormone shed weight steadily for years, researchers in Germany reported June 23 at a meeting of the Endocrine Society. Study participants, nearly all of whom were overweight or obese at the start of the study, lost 36 pounds on average. “This was an unintended effect,” said study coauthor Farid Saad, a research endocrinologist at Bayer Pharma in Berlin. “The big surprise was that when we analyzed the data [we found] that these men had lost weight continuously...year by year.” The men didn’t diet as part of the study, and any increase in their activity was voluntary, Saad said. He and his colleagues studied 116 men, average age 61, who had low testosterone levels. Each received quarterly injections of the hormone for five years. At the start, 71 percent were obese and another 24 percent were overweight. After five years, 97 percent of the men showed a reduction in waist circumference, on average losing “three to four trouser sizes,” Saad said. Average weight dropped from 236 pounds to about 200. “This definitely offers some insight that we can apply to our clinical practices,” said Vineeth Mohan, a clinical endocrinologist at Cleveland Clinic Florida in Weston. High testosterone levels have been linked to prostate cancer risk (SN: 10/8/05, p. 238), and a small portion of men taking high doses of it experience mania (SN: 2/19/00, p. 119). But in this study, Saad said, men received testosterone in doses just high enough to bring them back to normal levels. Three men in the test group were diagnosed with prostate cancer during the study, a rate lower than the incidence found in routine screening programs for men that age, he said. © Society for Science & the Public 2000 - 2012
by Michael Balter Many studies in humans and animals suggest that chronic stress is bad for one’s health, in part because it suppresses the immune system. But nearly 30 years of data on wild baboons shows that top-ranking males, despite showing signs of increased stress, recover more quickly than low-ranking baboons from wounds and illness. The results may help explain why some people escape from the negative effects of stress while others do not. Most studies in humans have shown a clear correlation between higher socioeconomic status and lower risk of death or illness from stress-related diseases such as heart attacks and diabetes. Some of the most famous of these are the so-called Whitehall studies of the British Civil Service, which showed that death and illness rates decreased in a step-wise fashion the higher an employee was on the service’s 6-grade pay and responsibility scale. These and other studies also have found that being at the bottom of the totem pole leads to greater stress as a result of increased work loads and time pressures, as well as more job insecurity. But studies of animals, especially other primates, have shown that the relationship between stress and status largely depends on the social organization of the species in question. For example, in species such as baboons that have rigid social rankings and hierarchies, with so-called alpha males dominating other males and females over extended periods of time, it can apparently be more stressful at the top. In a study reported last year in Science, a team that included ecologist Jeanne Altmann of Princeton University revealed that baboon alpha males had the highest levels of glucocorticoid hormones, such as cortisol, as well as testosterone in their feces, indicators that they were under greater stress than lower-ranking individuals. © 2010 American Association for the Advancement of Science.
Shannon Pettypiece Testosterone replacement has long been prescribed for men who suffer from abnormally low levels of the male sex hormone, but overuse can lead to infertility and can even speed the growth of prostate cancer. That hasn't stopped Michael Murray, a healthy 43-year-old home stager who works in New York and Chicago, from getting frequent testosterone injections to raise his energy level and give his bodybuilding regime a boost. "Am I making a deal with the devil? A little bit, but I have to think about my quality of life," Murray explains. "It is like I'm in my 20s again." In what may become one of the most sought-after lifestyle drugs since the introduction of Pfizer's Viagra 14 years ago, new testosterone drugs from Eli Lilly, Abbott Laboratories, and other drugmakers are hot. Prescriptions for testosterone replacement therapies have more than doubled since 2006 to 5.6 million last year, according to data compiled by Bloomberg. Sales are expected to triple to $5 billion by 2017, forecasts Global Industry Analysts. As many as 13.8 million men older than 45 in the United States have low levels of testosterone, according to a 2006 study in the International Journal of Clinical Practice. The male sex hormone begins to decline after age 30, and tends to drop about 1 percent each year. Lower-than-normal levels can lead to a loss of libido, a decrease in bone and muscle mass, and depression. © 2012 Hearst Communications Inc.
Older obese men could shift excess weight by taking testosterone supplements, suggest findings announced at the European Congress on Obesity. In a study, hormone-deficient men were given testosterone supplements in a similar way to HRT for older women. Men lost an average of 16kg over five years when testosterone levels were increased back to normal. But experts warn that supplements may not be the answer due to possible risks of prostate cancer and heart disease. Prof Richard Sharpe from the University of Edinburgh Centre for Reproductive Health said: "The notion that this is a quick fix for obese older men is, as always, simplistic. It is far more sensible and safer for men to reduce their food intake, reduce their obesity, which will then elevate their own testosterone." The findings announced at the conference also suggest that raising testosterone levels could reduce waist circumference and blood pressure. Dr Farid Saad, lead author of the study said: "We came across this by accident. These men were being given testosterone for a hormone deficiency - they had a range of problems - erectile dysfunction, fatigue and lack of energy. BBC © 2012
By LISA SANDERS, M.D. On Thursday I challenged Well readers to figure out a medical mystery involving a middle-aged woman who learned she had an unusual disease after visiting an ophthalmologist. The case was surprising because the woman didn’t feel sick, yet the doctor made the diagnosis just by looking at her and asking her a few simple questions that confirmed his diagnostic suspicions. The first reader to figure it out completely was Dr. Eric Gierke, a neurologist at Swedish Medical Center in Seattle. He said he recognized the condition because he had a patient who had acromegaly and only a few very subtle physical changes. In submitting his answer, Dr. Gierke also guessed one of the questions that the diagnosing physician asked the patient — “Has your shoe size changed recently?” — making him the clear winner. A few other readers also guessed both the questions and the diagnosis, but Dr. Gierke was first and the most specific. In all, 16 readers figured out the correct diagnosis. Well done! Acromegaly is a disease caused by a tumor, usually found in the pituitary gland, that secretes an excess of growth hormone, the blood chemical that tells our bodies to grow. Children with acromegaly can grow to extraordinary stature. André the Giant, the French professional wrestler and actor whose height was billed at 7 feet 4 inches, and Richard Kiel, the 7-foot-2 actor who played the villain Jaws in two James Bond movies, both had acromegaly from childhood. Their distinctive faces reveal some of the characteristic acromegalic changes: Their brows are prominent, and they have wide, square chins and large noses. Copyright 2012 The New York Times Company
by Daniel Strain Sharks may be known as terrors of the sea, but in some cases they're more like night lights. That's because many deep-sea sharks, like the smalleye pygmy shark (Squaliolus aliae), can make their own light, glowing from tail to snout as a possible means of camouflage. Now, a new study shows how this predator, the world's smallest shark, powers its luminescence. Smalleye pygmy sharks aren't just petite—they grow no more than 22 centimeters long—they're also hard to find, says study co-author Julien Claes, a shark biologist at the Catholic University of Louvain in Belgium. These fish swim hundreds of meters below the water's surface in the Indian and western Pacific oceans. When scientists do manage to pull one of these animals up, they sometimes catch an odd sight: a blue glow coming mostly from the shark's belly. Claes co-authored a paper in 2009 that showed that a second group of luminescent sharks, called lantern sharks (Etmopterus spinax), trigger their own glow using two hormones common in many animals: melatonin and prolactin. But it wasn't clear if smalleye pygmy sharks and their close relatives relied on the same molecules. So Claes and his colleagues launched a second survey, collecting 27 pygmy sharks off the coast of Taiwan. To determine what controlled their unearthly glow, the researchers took patches of the fish's skin and soaked them in various chemicals known to cue luminescence in other species. They then recorded the resulting glow—often so faint that it was tricky to see at a distance even in a dark room—using a light detector. And sure enough, when Claes tried melatonin, which in people helps to control cycles of sleep and waking, voila! There was light. © 2010 American Association for the Advancement of Science.
By Janelle Weaver A micrograph view of crystallized oxytocin. Image: Alfred Pasieka/Photo Researchers, Inc. When we meet new people, we assess their character by watching their gestures and facial expressions. Now a study in the Proceedings of the National Academy of Sciences USA suggests that those nonverbal cues are communicating the presence of a specific form of a gene that makes us more or less responsive to others’ needs. The gene determines which type of receptor a person has for the hormone oxytocin. Oxytocin has been implicated in a variety of positive traits, such as trust, empathy and generosity. The hormone is detected by our body’s cells via their oxytocin receptors. In a past study, psychologist Sarina Rodrigues Saturn of Oregon State University and her collaborators found that people who have a certain variation of the receptor gene are more empathetic than those with the alternative form of the gene. In the new study, Saturn and her team showed volunteers 20-second silent video clips of individuals who were listening to their romantic partner recount an upsetting experience. The study participants watched for nonverbal behaviors, such as head nods and smiles, and rated every individual on a number of character traits. Those with the form of the oxytocin receptor gene associated with empathy were judged by the volunteers as being more trustworthy, compassionate and kind than those with the alternative form of the gene. “These slight genetic variations do have a big impact on not only how you feel internally but also how people perceive you,” Saturn says, adding that impressions based on nonverbal cues can help individuals quickly choose compatible friends or romantic partners. © 2012 Scientific American,
By Stephani Sutherland If you have ever jumped at a loud noise and felt an adrenaline rush, you have experienced the effects of corticotropin-releasing hormone (CRH). In the body, this hormone triggers the familiar fight-or-flight response—racing heart, shortness of breath, sweaty palms. In the brain, however, it acts as a chemical messenger, playing a role in anxiety and depression. That role, a new study suggests, is more complex than anyone expected. Because animal research from the past decade found that CRH contributes to anxiety and depression, drugs were developed that would block its actions in the brain. Clinical trials of these antianxiety and antidepressant drugs in human patients, however, have been disappointing. The new study, published last September in Science, shows why. Jan M. Deussing, a molecular biologist at the Max Planck Institute of Psychiatry in Munich, and his colleagues genetically altered mice so that some of their brain cells would be unable to detect the presence of CRH because they lacked the proper receptors. When the receptors were missing from neurons that produce the neurotransmitter glutamate, the mice displayed less anxiety, as expected. Yet when the receptors were missing from neurons that produce dopamine, the mice became more anxious. These two different neuron types, when interacting with CRH, “have exactly opposite effects in terms of anxiety-related behavior,” Deussing says. Because the unsuccessful drugs limited the amount of the hormone available to all types of neurons, they ended up blocking its actions at neurons that both produce and prevent anxiety. The finding reaffirms scientists’ growing understanding that mood disorders do not result from a simple chemical imbalance—too much or too little of one neurotransmitter—but rather from subtle changes in many systems in the brain. “The network is much more complex than we thought before,” Deussing says. © 2012 Scientific American