Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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Researchers say they have discovered a gene mutation that slows the metabolism of sugar in the gut, giving people who have the mutation a distinct advantage over those who do not. Those with the mutation have a lower risk of diabetes, obesity, heart failure, and even death. The researchers say their finding could provide the basis for drug therapies that could mimic the workings of this gene mutation, offering a potential benefit for the millions of people who suffer with diabetes, heart disease, and obesity. The study, which is largely supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health, appears in the Journal of the American College of Cardiology (link is external). “We’re excited about this study because it helps clarify the link between what we eat, what we absorb, and our risk for disease. Knowing this opens the door to improved therapies for cardiometabolic disease,” said Scott D. Solomon, M.D., a professor of medicine at Harvard Medical School and a senior physician at Brigham and Women’s Hospital in Boston, who led the research. He explained that the study is the first to fully evaluate the link between mutations in the gene mainly responsible for absorbing glucose in the gut — SGLT-1, or sodium glucose co-transporter-1 — and cardiometabolic disease. People who have the natural gene mutation appear to have an advantage when it comes to diet, Solomon noted. Those who eat a high-carbohydrate diet and have this mutation will absorb less glucose than those without the mutation. A high-carbohydrate diet includes such foods as pasta, breads, cookies, and sugar-sweetened beverages.

Keyword: Obesity; Genes & Behavior
Link ID: 25555 - Posted: 10.10.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist

Keyword: Obesity; Neuroimmunology
Link ID: 25536 - Posted: 10.06.2018

By Gretchen Reynolds Are we born to be physically lazy? A sophisticated if disconcerting new neurological study suggests that we probably are. It finds that even when people know that exercise is desirable and plan to work out, certain electrical signals within their brains may be nudging them toward being sedentary. The study’s authors hope, though, that learning how our minds may undermine our exercise intentions could give us renewed motivation to move. Exercise physiologists, psychologists and practitioners have long been flummoxed by the difference between people’s plans and desires to be physically active and their actual behavior, which usually involves doing the opposite. Few of us exercise regularly, even though we know that it is important for health and well being. Typically, we blame lack of time, facilities or ability. But recently an international group of researchers began to wonder whether part of the cause might lie deeper, in how we think. For an earlier review, these scientists had examined past research about exercise attitudes and behavior and found that much of it showed that people sincerely wished to be active. In computer-based studies, for example, they would direct their attention to images of physical activity and away from images related to sitting and similar languor. But, as the scientists knew, few people followed through on their aims to be active. So maybe, the scientists thought, something was going on inside their skulls that dampened their enthusiasm for exercise. To find out, they recruited 29 healthy young men and women. All of the volunteers told the scientists that they wanted to be physically active, although only a few of them regularly were. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25526 - Posted: 10.04.2018

By Diana Kwon How do we decide what we like to eat? Although tasty foods typically top the list, a number of studies suggest preferences about consumption go beyond palatability. Scientists have found both humans and animals can form choices about what to consume based on the caloric content of food, independent of taste. Research spanning many decades has shown nutrients in the gastrointestinal tract can shape animals’ flavor preferences. One of the earliest findings of this effect dates back to the 1960s, when Garvin Holman of the University of Washington reported hungry rats preferred consuming a liquid paired with food injected into the stomach rather than a solution coupled with a gastric infusion of water. More recently Ivan de Araujo, a neuroscientist at the Icahn School of Medicine at Mount Sinai, and his colleagues have shown calories can trump palatability: Their work has demonstrated mice prefer consuming bitter solutions paired with a sugar infusion injected in the gut rather than a calorie-free sweet solution. Advertisement For years De Araujo and his group have been working to tease apart how the contents of the gut produce pleasure in the brain. In mice they have found sugar in the digestive tract can activate the brain’s reward centers. In animals bred without the ability to taste sweetness, sugary snacks still triggered activity in the ventral striatum, a brain region involved in reward processing. But according to De Araujo, the specific pathway that relayed signals between the gut and the brain remained a mystery. © 2018 Scientific American

Keyword: Obesity; Drug Abuse
Link ID: 25523 - Posted: 10.03.2018

Sukanya Charuchandra More and more children around the world are being born to obese mothers than ever before. In the United States, 23.4 percent of women are obese before they become pregnant—a number that represents a growing phenomenon. From 1994 to 2014, the rate of women who were obese prior to pregnancy in the country shot up 86 percent, according to a nationwide nutrition program registry. The increasingly common condition has been associated with children being born obese as well as showing a greater risk of developing heart disease, diabetes, cognitive and behavioral difficulties, and other neurodevelopmental disorders. Incidentally, a growing numbers of children are being diagnosed with mental disorders, with up to one in five children in the US experiencing conditions that challenge their mental health in any single year. This summer alone, multiple studies have found that different facets of moms’ metabolic health and weight are linked with a greater risk for children being diagnosed with autism, attention deficit hyperactivity disorder (ADHD), and mild neurodevelopmental problems. In June, Thomas Buchanan of the University of Southern Carolina and his colleagues reported how expectant mothers’ diabetes—experienced by one in 16 pregnant women in the US—is tied to a baby’s chances developing autism. The researchers found a clear divide: Mothers with a diabetes diagnosis by their 26th week of pregnancy gave birth to children with a higher likelihood of being on the autism spectrum compared to mothers with no diabetes or who received a diagnosis after their 26th week. “There appeared to be not a technical dose-response relationship, but a relationship in severity, according to the severity and timing of the diabetes: the more severe and earlier, the more the risk of autism,” Buchanan tells The Scientist. © 1986 - 2018 The Scientist

Keyword: Autism; Obesity
Link ID: 25522 - Posted: 10.03.2018

Denis Campbell Health policy editor Eating junk food increases the risk of becoming depressed, a study has found, prompting calls for doctors to routinely give dietary advice to patients as part of their treatment for depression. In contrast, those who follow a traditional Mediterranean diet are much less likely to develop depression because the fish, fruit, nuts and vegetables that diet involves help protect against Britain’s commonest mental health problem, the research suggests. Published in the journal Molecular Psychiatry, the findings have come from an analysis by researchers from Britain, Spain and Australia who examined 41 previous studies on the links between diet and depression. “A pro-inflammatory diet can induce systemic inflammation, and this can directly increase the risk for depression,” said Dr Camille Lassale, the study’s lead author. Bad diet heightens the risk of depression to a significant extent, she added. The analysis found that foods containing a lot of fat or sugar, or was processed, lead to inflammation of not just the gut but the whole body, known as “systemic inflammation”. In that respect the impact of poor diet is like that of smoking, pollution, obesity and lack of exercise. © 2018 Guardian News and Media Limited

Keyword: Depression; Obesity
Link ID: 25494 - Posted: 09.26.2018

Sukanya Charuchandra Previous research has shown that the gut-brain connection, which refers to signaling between the digestive and the central nervous systems, is based on the transport of hormones, but a study published today (September 21) in Science suggests there may be a more direct link—the vagus nerve. This research presents “a new set of pathways that use gut cells to rapidly communicate with . . . the brain stem,” Daniel Drucker, who studies gut disorders at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada, and was not involved with the project, tells Science. Building on an earlier study in which the team found that gut cells had synapses, the researchers injected a rabies virus, expressing green fluorescence, into the stomachs of mice and watched it travel speedily from the intestines to the rodents’ brainstems. When they grew sensory gut cells together with neurons from the vagus nerve, the neurons moved across the dish to form synapses with the gut cells and began electrically coupling with them. Adding sugar to the dish sped up the rate of signaling between the gut and brain cells, a finding that suggests glutamate, a neurotransmitter involved in sensing taste, may be key to the process. Blocking glutamate secretion in gut cells brought these signals to a grinding halt. © 1986 - 2018 The Scientist.

Keyword: Obesity
Link ID: 25487 - Posted: 09.25.2018

By Emily Underwood The human gut is lined with more than 100 million nerve cells—it’s practically a brain unto itself. And indeed, the gut actually talks to the brain, releasing hormones into the bloodstream that, over the course of about 10 minutes, tell us how hungry it is, or that we shouldn’t have eaten an entire pizza. But a new study reveals the gut has a much more direct connection to the brain through a neural circuit that allows it to transmit signals in mere seconds. The findings could lead to new treatments for obesity, eating disorders, and even depression and autism—all of which have been linked to a malfunctioning gut. The study reveals “a new set of pathways that use gut cells to rapidly communicate with … the brain stem,” says Daniel Drucker, a clinician-scientist who studies gut disorders at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada, who was not involved with the work. Although many questions remain before the clinical implications become clear, he says, “This is a cool new piece of the puzzle.” In 2010, neuroscientist Diego Bohórquez of Duke University in Durham, North Carolina, made a startling discovery while looking through his electron microscope. Enteroendocrine cells, which stud the lining of the gut and produce hormones that spur digestion and suppress hunger, had footlike protrusions that resemble the synapses neurons use to communicate with each other. Bohórquez knew the enteroendocrine cells could send hormonal messages to the central nervous system, but he also wondered whether they could “talk” to the brain using electrical signals, the way that neurons do. If so, they would have to send the signals through the vagus nerve, which travels from the gut to the brain stem. © 2018 American Association for the Advancement of Science

Keyword: Obesity; Brain imaging
Link ID: 25476 - Posted: 09.21.2018

Diana Kwon Obesity is on the rise across the globe. The worldwide prevalence of the condition has nearly tripled over the last four decades, and approximately 13 percent of adults were obese in 2016. This staggering rise poses a public health concern: not only is obesity tied to bodily ailments such as cardiovascular disease and diabetes, epidemiological investigations have revealed that it is also linked to cognitive decline—and higher chances of developing dementia and other brain-related disorders later in life. Researchers have recently started to shed light on how weight gain affects the brain, and over the last few years, microglia, the brain’s resident immune cells, have emerged as the key culprit. Several rodent studies paint a picture of activated microglia gobbling up dendritic spines that form synapses in obese animals’ brains as the cause of cognitive decline. A study published today (September 10) in the Journal of Neuroscience provides strong new support for this theory. While prior studies have drawn robust associations between microglia and obesity-related cognitive decline, Elise Cope, a postdoc at Princeton University, says none had yet addressed whether those cells were actually causing the behavioral changes. “The novelty of our study was where we decided to see if blocking microglia using three different methods could actually prevent the dendritic spine loss and improve cognitive function,” Cope says. © 1986 - 2018 The Scientist.

Keyword: Obesity; Glia
Link ID: 25443 - Posted: 09.13.2018

Diana Kwon In the early 2000s, Stefano Schiaffino, a muscle physiologist at the University of Padova in Italy, was faced with puzzling results: two seemingly identical experiments involving hind leg muscles in rats had yielded different findings. Schiaffino and his team were investigating nuclear factor of activated T cells (NFAT), a transcription factor that responds to the level of muscle activity. Despite using similar procedures, the researchers found that in the tissues from one set of animals, NFAT had moved from the cytoplasm into the nucleus in a large proportion of cells, while in tissues from another experiment, this change had not occurred. The explanation for this difference turned out to be simple: timing. The researcher responsible for one trial had sacrificed the nocturnal animals in the evening, while another had conducted the same procedure for the second trial in the morning. This meant that the first group of animals was more active at the time of measurement than the second. When the scientists repeated the second experiment late in the day, when the animals were more likely to be awake, they observed high levels of NFAT in the nuclei of the muscle cells, essentially replicating the first experiment. “At that time, I’d been working for many years on muscle, but had never thought about the circadian rhythms,” recalls Schiaffino, whose research now focuses on this aspect of muscle biology. © 1986 - 2018 The Scientist

Keyword: Biological Rhythms; Obesity
Link ID: 25432 - Posted: 09.11.2018

Laura Sanders Obesity can affect brainpower, and a study in mice may help explain how. In the brains of obese mice, rogue immune cells chomp nerve cell connections that are important for learning and memory, scientists report September 10 in the Journal of Neuroscience. Drugs that stop this synapse destruction may ultimately prove useful for protecting the brain against the immune cell assault. Like people, mice that eat lots of fat quickly pack on pounds. After 12 weeks of a high-fat diet, mice weighed almost 40 percent more than mice fed standard chow. These obese mice showed signs of diminished brainpower, neuroscientist Elizabeth Gould of Princeton University and colleagues found. Obese mice were worse at escaping mazes and remembering an object’s location than mice of a normal weight. On nerve cells, microscopic knobs called dendritic spines receive signals. Compared with normal-sized mice, obese mice had fewer dendritic spines in several parts of the mice’s hippocampi, brain structures important for learning and memory. The dendritic spine destruction comes from immune cells called microglia, the results suggest. In obese mice, higher numbers of active microglia lurked among these sparser nerve cell connections compared with mice of normal weights. When the researchers interfered with microglia in obese mice, dendritic spines were protected and the mice’s performance on thinking tests improved. |© Society for Science & the Public 2000 - 2018.

Keyword: Obesity; Learning & Memory
Link ID: 25431 - Posted: 09.11.2018

Increasing time between meals made male mice healthier overall and live longer compared to mice who ate more frequently, according to a new study published in the Sept. 6, 2018 issue of Cell Metabolism. Scientists from the National Institute on Aging (NIA) at the National Institutes of Health, the University of Wisconsin-Madison, and the Pennington Biomedical Research Center, Baton Rouge, Louisiana, reported that health and longevity improved with increased fasting time, regardless of what the mice ate or how many calories they consumed. “This study showed that mice who ate one meal per day, and thus had the longest fasting period, seemed to have a longer lifespan and better outcomes for common age-related liver disease and metabolic disorders,” said NIA Director Richard J. Hodes, M.D. “These intriguing results in an animal model show that the interplay of total caloric intake and the length of feeding and fasting periods deserves a closer look.” The scientists randomly divided 292 male mice into two diet groups. One group received a naturally sourced diet that was lower in purified sugars and fat, and higher in protein and fiber than the other diet. The mice in each diet group were then divided into three sub-groups based on how often they had access to food. The first group of mice had access to food around the clock. A second group of mice was fed 30 percent less calories per day than the first group. The third group was meal fed, getting a single meal that added up to the exact number of calories as the round-the-clock group. Both the meal-fed and calorie-restricted mice learned to eat quickly when food was available, resulting in longer daily fasting periods for both groups.

Keyword: Obesity
Link ID: 25421 - Posted: 09.07.2018

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25408 - Posted: 09.01.2018

A weight-loss pill has been hailed as a potential “holy grail” in the fight against obesity after a major study showed it did not increase the risk of serious heart problems. Researchers say lorcaserin is the first weight-loss drug to be deemed safe for heart health with long-term use. Taken twice a day, the drug is an appetite suppressant which works by stimulating brain chemicals to induce a feeling of fullness. A US study saw 12,000 people who were either obese or overweight given the pills or a placebo – with those who took the drug shedding an average of 4kg (9lbs) in 40 months. Further analysis showed no big differences in tests for heart valve damage. Tam Fry, of Britain’s National Obesity Forum, said the drug is potentially the “holy grail” of weight-loss medicine. “I think it is the thing everybody has been looking for,” he said. “I think there will be several holy grails, but this is a holy grail and one which has been certainly at the back of the mind of a lot of specialists for a long time. “But all of the other things apply – lifestyle change has got to be root and branch part of this.” Prof Jason Halford, an obesity expert at the University of Liverpool, told the Daily Telegraph newspaper that the drug’s availability in the UK would depend on whether it is approved by National Health Service regulators. “We don’t have any appetite suppressants available on the NHS. We have a massive great gap between lifestyle modification and surgery,” he said. © 2018 Guardian News and Media Limited

Keyword: Obesity
Link ID: 25382 - Posted: 08.27.2018

By Bret Stetka Obesity rates in the U.S. and abroad have soared: The world now has more overweight people than those who weigh too little. One reason relates to the way the body reacts to its own fat stores by setting in motion a set of molecular events that impede the metabolic process that normally puts a damper on hunger. A new study published August 22 in Science Translational Medicine provides details of how this process occurs, giving new insight into why obese individuals have trouble shedding pounds. It also suggests a possible treatment approach that targets obesity in the brain, not in the belly. Scientists have long known that a hormone called leptin is instrumental in regulating the human diet. Produced by fat cells, the molecule communicates with a brain region called the hypothalamus, which reins in hunger cravings when our energy stores are full. Yet as we gain weight our bodies become less sensitive to leptin, and it becomes harder and harder to slim down. In other words, weight gain begets more weight gain. In an experiment using mice that became obese on a high-fat diet, an international team found obesity increases the activity of an enzyme called matrix metalloproteinase-2, or MMP-2. By using a technique called western blot analysis—separating and identifying all the proteins in a tissue sample—the authors found MMP-2 cleaves off a portion of the leptin receptor in the hypothalamus, impairing the hormone’s signaling and its ability to suppress appetite. © 2018 Scientific American

Keyword: Obesity
Link ID: 25373 - Posted: 08.24.2018

Hannah Devlin Science correspondent Lack of sleep has long been linked to obesity, but a new study suggests late night snacking may not be the primary culprit. The latest findings provide the most compelling evidence to date that disrupted sleep alters the metabolism and boosts the body’s ability to store fat. The findings add to mounting scientific evidence on how disrupted sleep influences the usual rhythms of the body clock, raising the risk of a wide range of health problems from heart disease to diabetes. Jonathan Cedernaes, a circadian researcher at Uppsala University in Sweden and the paper’s first author, said the findings pointed to “the irreplaceable function that sleep has”. “Sleep is not just to conserve energy, it has so many functions,” he said. Time and again research has linked shift work and lack of sleep to the risk of obesity and diabetes, but the reasons behind this association are complex and have been difficult to elucidate. Insufficient sleep appears to disrupt hormones that control appetite and feelings of fullness. Those who sleep less have more time to eat, may be too tired to exercise and have less self-control when it comes to resisting the temptation of unhealthy snacks. A previous study by Cedernaes and colleagues showed that even a short period of sleep deprivation led people to eat more and opt for higher calorie food. To complicate matters further, obesity increases the risk of sleep apnoea, a breathing problem that itself disturbs sleep quality. © 2018 Guardian News and Media Limited

Keyword: Sleep; Obesity
Link ID: 25365 - Posted: 08.23.2018

By Alex Therrien Health reporter, BBC News A low-carb diet could shorten life expectancy by up to four years, a study suggests. Low-carb diets, such as Atkins, have become increasingly popular for weight loss and have shown promise for lowering the risk of some illnesses. But a US study over 25 years indicates that moderate carb consumption - or switching meat for plant-based protein and fats - is healthier. The study relied on people remembering the amount of carbohydrates they ate. 'Gaining widespread popularity' In the study, published in The Lancet Public Health, 15,400 people from the US filled out questionnaires on the food and drink they consumed, along with portion sizes. From this, scientists estimated the proportion of calories they got from carbohydrates, fats, and protein. After following the group for an average of 25 years, researchers found that those who got 50-55% of their energy from carbohydrates (the moderate carb group and in line with UK dietary guidelines) had a slightly lower risk of death compared with the low and high-carb groups. Carbohydrates include vegetables, fruit and sugar but the main source of them is starchy foods, such as potatoes, bread, rice, pasta and cereals. The NHS Eatwell Guide provides details on how to achieve this kind of healthy, balanced diet and reduce the risk of serious illnesses in the long term. Researchers estimated that, from the age of 50, people in the moderate carb group were on average expected to live for another 33 years. © 2018 BBC

Keyword: Obesity
Link ID: 25342 - Posted: 08.17.2018

By Nicholas Bakalar When it comes to losing weight, more can be better. A lot better, according to a new study. Researchers studied 7,670 overweight or obese people who wanted to lose weight. Using data on current weight, weight a year ago and maximum lifetime weight, they tested the association of long-term weight loss with lowering the risk for metabolic syndrome — a constellation of unhealthy conditions that includes high blood pressure, insulin resistance, excess fat around the waist, high triglycerides and low HDL, or “good,” cholesterol. Compared to people who maintained less than a 5 percent weight loss for one year, those who lost 5 to 10 percent lowered their risk for metabolic syndrome by 22 percent. A 15 to 19 percent loss was associated with a 37 percent lower risk, and those who maintained a loss of 20 percent or more had a 53 percent lower risk. The study is in the Mayo Clinic Proceedings. Only 5.5 percent of the participants succeeded in holding a 20 percent or greater weight loss for one year. “Any weight loss is beneficial,” said the lead author, Gregory Knell of the University of Texas School of Public Health in Houston. “You don’t have to reach 20 percent to have a benefit. But if you are able to lose more weight, you get some really significant numbers related to metabolic health.” © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25335 - Posted: 08.16.2018

By Gretchen Reynolds Don’t skip drinking during exercise in hot weather, a new study reminds us. This advice might seem obvious. But apparently some athletes, especially in team sports, have begun to eschew fluids during hot weather workouts, in hopes that the privation might somehow make them stronger. But the new study finds that it is likely only to make them more physically stressed. And very, very thirsty. Working out in the heat is inherently difficult, as any of us who exercise outside in summer knows. When ambient temperatures are high, we generate internal heat more quickly than if the weather is cool. To remove this heat and maintain a safe body temperature, our hearts pump warm blood toward the skin’s surface, where heat can dissipate, and we sweat copiously, providing evaporative heat loss. These reactions become more pronounced and effective with practice, a process known as heat acclimation (also referred to as acclimatization). During heat acclimation, which can require several weeks of sultry exercise, we begin to sweat earlier and in greater volume. This and other changes help our hearts to labor less, so that, in general, the effort of being physically active in high temperatures starts to feel less wearing. A run on a sizzling summer day in August should feel easier than a similar run on an equally hot evening in June, if we have been running outside in the meantime, because our bodies will have acclimated to the heat. But athletes being athletes, some of them and their coaches began to wonder in recent years whether, if heat acclimation taxes the body and makes it stronger, would exacerbating the physical difficulties of acclimation lead to greater adaptations, in approved Machiavellian style? © 2018 The New York Times Company

Keyword: Miscellaneous
Link ID: 25313 - Posted: 08.10.2018

Lee Daniel Kravetz In 1972, a woman checked into London’s Royal Free Hospital to be treated for anorexia. “I found her symptoms to be unique,” Gerald Russell, the British psychologist who treated her, tells me. “They didn’t match the diagnostic criteria for anorexia at all.” Unlike his emaciated patients with sallow skin and big eyes, Russell’s new patient was of average weight. Her face was full. Her cheeks were pink as the skin of an onion. She was the first of roughly thirty instances of this unusual condition that crossed the threshold of his clinic over the next seven years, each person presenting with perplexing purging behaviors secondary to binge eating. Russell wasn’t dealing with anorexia nervosa, he realized, but something as yet undefined by psychology or medicine. In fact, he had stumbled upon a condition that science had yet to see in large numbers or identify at any time in the long history of eating disorders. Psychological Medicine published Russell’s ensuing paper on these unusual cases; in it, he described the key features of this novel mental illness he was now referring to as bulimia nervosa. Many in the scientific community objected to Russell’s conclusions, pointing to the limited and problematic sample size he’d used. At the time, however, there were simply too few cases for Russell to draw from. The pool in the 1970s was just too small. As bulimia gained further diagnostic legitimacy in 1980 with its inclusion in the third edition of the Diagnostic and Statistical Manual of Mental Disorders, Russell ruefully tracked its unexpectedly swift spread across Europe and North America, where it infiltrated college campuses, affecting 15 percent of female students in sororities, all-women dormitories, and female collegiate sports teams. The disease moved through the halls of American high schools, where binging, fasting, diet pill use, and other eating disorder symptoms easily clustered. He chased its dispersion across Egypt, where the number of new cases grew to 400,000. In Canada, it swelled to 600,000. In Russia, 800,000. In India, 6 million. In China, 7 million. In the UK, one out of every one hundred women was now developing the disorder. © 2018, New York Media LLC.

Keyword: Anorexia & Bulimia
Link ID: 25271 - Posted: 07.30.2018