Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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by Bethany Brookshire For some of us, a weekly case of the Mondays isn’t just because of traffic, work pileups or our soulless office space. It’s because we had to get up early, and sleeping in on the weekend was so incredibly glorious. Besides, because we slept in on Sunday, we didn’t get to the gym until the afternoon, we cooked a late dinner for a friend and then we couldn’t fall asleep at all and so stayed up playing around on the Internet. OK, maybe that’s just me. But you get the general idea. Our obligations — work, family and friends — often don’t line up with when our bodies want to sleep. Scientists call this phenomenon social jetlag. And it may make for more than just miserable Mondays. Social jetlag may also be associated with wider waistlines. As we learn more about how our body clocks work, it might help to think about how our own schedules can shift. Some of us love late nights and can’t help glaring at those who hop out of bed for a 5 a.m. workout (again, maybe that’s just me). But in fact our chronotypes aren’t a result of willpower. Instead they fall in a natural curve. About two-thirds of people are neutral, but a few fall at each end of the spectrum, rising extra early, or staying up until the wee hours. But even those in the middle are still getting up a little bit too early and staying up a little bit too late. We try to make up for it on days off, sleeping in or falling asleep early for a few extra hours of rest. But the result of that shift in sleep schedule? Jetlag. “It’s the equivalent of taking a flight one direction every Friday and going back every Sunday,” says Michael Parsons, a behavioral geneticist at the Medical Research Council Harwell in England. © Society for Science & the Public 2000 - 2015
Allison Aubrey Bite into that bread before your main meal, and you'll spike your blood sugar and amp up your appetite. Waiting until the end of your dinner to nosh on bread can blunt those effects. Bite into that bread before your main meal, and you'll spike your blood sugar and amp up your appetite. Waiting until the end of your dinner to nosh on bread can blunt those effects. iStockphoto Ah, the bread basket. You sit down for a nice meal out, and there it appears: piping hot, giving off a waft of yeasty divinity. There's a reason this age-old tradition prevails. Even in the era of paleo and gluten-free, there are still hordes of us who will gladly nosh on crusty, chewy, soul-warming bread. But the downside may be more than just some extra calories. Turns out, eating all those carbs before a meal can amp up our appetites and spike our blood sugar. "The worst situation is having refined carbohydrates on an empty stomach, because there's nothing to slow down the digestion of that carbohydrate into sugar," explains David Ludwig, director of the Optimal Weight for Life Clinic at Boston Children's Hospital. © 2015 NPR
Link ID: 21108 - Posted: 06.30.2015
By PETER ANDREY SMITH Eighteen vials were rocking back and forth on a squeaky mechanical device the shape of a butcher scale, and Mark Lyte was beside himself with excitement. ‘‘We actually got some fresh yesterday — freshly frozen,’’ Lyte said to a lab technician. Each vial contained a tiny nugget of monkey feces that were collected at the Harlow primate lab near Madison, Wis., the day before and shipped to Lyte’s lab on the Texas Tech University Health Sciences Center campus in Abilene, Tex. Lyte’s interest was not in the feces per se but in the hidden form of life they harbor. The digestive tube of a monkey, like that of all vertebrates, contains vast quantities of what biologists call gut microbiota. The genetic material of these trillions of microbes, as well as others living elsewhere in and on the body, is collectively known as the microbiome. Taken together, these bacteria can weigh as much as six pounds, and they make up a sort of organ whose functions have only begun to reveal themselves to science. Lyte has spent his career trying to prove that gut microbes communicate with the nervous system using some of the same neurochemicals that relay messages in the brain. Inside a closet-size room at his lab that afternoon, Lyte hunched over to inspect the vials, whose samples had been spun down in a centrifuge to a radiant, golden broth. Lyte, 60, spoke fast and emphatically. ‘‘You wouldn’t believe what we’re extracting out of poop,’’ he told me. ‘‘We found that the guys here in the gut make neurochemicals. We didn’t know that. Now, if they make this stuff here, does it have an influence there? Guess what? We make the same stuff. Maybe all this communication has an influence on our behavior.’’ Since 2007, when scientists announced plans for a Human Microbiome Project to catalog the micro-organisms living in our body, the profound appreciation for the influence of such organisms has grown rapidly with each passing year. Bacteria in the gut produce vitamins and break down our food; their presence or absence has been linked to obesity, inflammatory bowel disease and the toxic side effects of prescription drugs. Biologists now believe that much of what makes us human depends on microbial activity. © 2015 The New York Times Company
By Mitch Leslie After years of fasting, the Buddha’s “legs were like bamboo sticks, his backbone was like a rope, his chest was like an incomplete roof of a house, his eyes sank right inside, like stones in a deep well,” according to one account. The Buddha didn’t get what he wanted from this extreme fasting—enlightenment—but a new study suggests that a diet that replicates some effects of milder deprivation may not only lower your weight but also confer other benefits. Researchers report that following the diet for just 5 days a month improves several measures of health, including reducing the risk of developing cardiovascular disease. Eating shortens life, and not just because overindulgence can lead to diseases such as diabetes. A diet that cuts food intake by up to 40%, known as calorie restriction, increases longevity in a variety of organisms and forestalls cancer, heart disease, and other late-life illnesses. Although some short-term studies suggest that calorie restriction provides metabolic benefits to people, nobody has confirmed that it also increases human life span. The closest researchers have come are two large, long-term studies of monkeys, and they conflict about whether meager rations increase longevity. Even if calorie restriction could add years to our lives, almost no one can muster the willpower to eat so little day after day, year after year. An alternative that might be more, er, palatable is fasting, the temporary abstinence from food. Gerontological researcher Valter Longo of the University of Southern California in Los Angeles and colleagues have shown that fasting eases side effects of chemotherapy such as fatigue and weakness, and animal studies suggest that it produces health advantages similar to calorie restriction. © 2015 American Association for the Advancement of Science.
Link ID: 21077 - Posted: 06.20.2015
Aaron E. Carroll One of my family’s favorite shows is “The Biggest Loser.” Although some viewers don’t appreciate how it pushes people so hard to lose weight, the show probably inspires some overweight people to regain control of their lives. But one of the most frustrating parts of the show, at least for me, is its overwhelming emphasis on exercise. Because when it comes to reaching a healthy weight, what you don’t eat is much, much more important. Think about it this way: If an overweight man is consuming 1,000 more calories than he is burning and wants to be in energy balance, he can do it by exercising. But exercise consumes far fewer calories than many people think. Thirty minutes of jogging or swimming laps might burn off 350 calories. Many people, fat or fit, can’t keep up a strenuous 30-minute exercise regimen, day in and day out. They might exercise a few times a week, if that. Or they could achieve the same calorie reduction by eliminating two 16-ounce sodas each day. Proclamations that people need to be more active are ubiquitous in the media. The importance of exercise for proper weight management is reinforced when people bemoan the loss of gym class in schools as a cause of the obesity epidemic. Michelle Obama’s Let’s Move program places the focus on exercise as a critical component in combating excess weight and obesity. Exercise has many benefits, but there are problems with relying on it to control weight. First, it’s just not true that Americans, in general, aren’t listening to calls for more activity. From 2001 to 2009, the percentage of people who were sufficiently physically active increased. But so did the percentage of Americans who were obese. The former did not prevent the latter. © 2015 The New York Times Company
Link ID: 21054 - Posted: 06.15.2015
By Gretchen Reynolds Treadmill desks are popular, even aspirational, in many offices today since they can help those of us who are deskbound move more, burn extra calories and generally improve our health. But an interesting new study raises some practical concerns about the effects of walking at your workspace and suggests that there may be unacknowledged downsides to using treadmill desks if you need to type or think at the office. The drumbeat of scientific evidence about the health benefits of sitting less and moving more during the day continues to intensify. One study presented last month at the 2015 annual meeting of the American College of Sports Medicine in San Diego found that previously sedentary office workers who walked slowly at a treadmill desk for two hours each workday for two months significantly improved their blood pressure and slept better at night. But as attractive as the desks are for health reasons, they must be integrated into a work setting so it seems sensible that they should be tested for their effects on productivity. But surprisingly little research had examined whether treadmill desks affect someone’s ability to get work done. So for the new study, which was published in April in PLOS One, researchers at Brigham Young University in Provo, Utah, recruited 75 healthy young men and women and randomly assigned them to workspaces outfitted with a computer and either a chair or a treadmill desk. The treadmill desk was set to move at a speed of 1.5 miles per hour with zero incline. None of the participants had used a treadmill desk before, so they received a few minutes of instruction and practice. Those assigned a chair were assumed to be familiar with its use. © 2015 The New York Times Company
By SABRINA TAVERNISE WASHINGTON — The global diabetes rate has risen by nearly half over the past two decades, according to a new study, as obesity and the health problems it spawns have taken hold across the developing world. The prevalence of diabetes has been rising in rich countries for several decades, largely driven by increases in the rate of obesity. More recently, poorer countries have begun to follow the trend, with major increases in countries like China, Mexico and India. The study, published Monday in the British medical journal The Lancet, reported a 45 percent rise in the prevalence of diabetes worldwide from 1990 to 2013. Nearly all the rise was in Type 2, which is usually related to obesity and is the most common form of the disease. A major shift is underway in the developing world, in which deaths from communicable diseases like malaria and tuberculosis have declined sharply, and chronic diseases like cancer and diabetes are on the rise. The pattern is linked to economic improvement and more people living longer, but it has left governments in developing countries scrambling to deal with new and often more expensive ways to treat illnesses. The study, led by the Institute for Health Metrics and Evaluation, a research group, was funded by the Bill and Melinda Gates Foundation. It is the largest analysis of global disability data to date, drawing on more than 35,000 data sources in 188 countries. © 2015 The New York Times Company
Link ID: 21026 - Posted: 06.08.2015
By Sarah C. P. Williams Bonobos, endangered great apes considered—along with chimpanzees—the closest living relative to humans, spend most of each day climbing through trees, collecting fruit and leaves. Compare that with the lives of early humans who traversed hot, barren landscapes and it begins to make sense why we’re the fattier, less muscular primate. Over the past 3 decades, two researchers analyzed the hard-to-come-by bodies of 13 bonobos that had died in captivity and compared them with already collected data on 49 human bodies donated by means of autopsy to help understand how evolution drove this change. Although some captive bonobos have become obese, the researchers found that, on average, the apes’ body mass—which is thought to resemble that of the closest common ancestor we share with them—is composed of 10% to 13% skin, whereas humans have only 6% skin. This thinner skin, the team hypothesizes, probably arose around the same time that Homo sapiens gained the ability to sweat, allowing more time spent in hot, open areas. The scientists also found that we pack on more fat than our ape relatives: Female and male humans average 36% and 20% body fat, whereas female and male bonobos average 4% and close to 0% body fat, respectively. Increased fat, the researchers hypothesize, allowed our species to survive—and reproduce—during times of low food availability. As for muscle, the team reports online today in the Proceedings of the National Academy of Sciences, bonobos come out on top, especially when it comes to upper body muscles needed for tree climbing and swinging, which became unnecessary when humans went strictly bipedal. The new findings, the researchers say, help illustrate the forces of natural selection that may have affected H. sapiens’s soft tissues even before our brains started expanding in size and tool use shaped the species. © 2015 American Association for the Advancement of Science.
By Roberto A. Ferdman In 2007, the Food and Drug administration approved the first ever over-the-counter diet drug. Alli, as the pill was (and still is) called, could be taken by anyone, without a prescription. And it worked, so long as those who took it also maintained a healthy lifestyle. That last bit—persuading people who take diet drugs to also eat well and exercise—is the oft overlooked key with weight-loss remedies. And GlaxoSmithKline, which manufactures the drug, knew it. Marketing around the pill made it clear that Alli was not some miracle drug. But getting people to treat diet drugs for what they are—helpers, not fix alls—is actually a lot harder than it sounds. Some diet drugs have been shown to work. But a growing pool of research suggests people are prone to use them improperly. "There's a funny, kind of counterintuitive thing that happens when many people take weight-loss drugs: they gain weight," said Amit Battacharjee, an assistant professor at The Tuck School of Business, whose research focuses on consumer beliefs and well-being. "But it isn't necessarily because the drugs themselves don't work." Battacharjee has a new study titled 'The Perils of Marketing Weight-Management Remedies,' which looks closely at how the way in which weight-loss drugs are pitched to people can significantly affect the way in which people understand them.
Link ID: 20996 - Posted: 05.30.2015
John Bohannon “Slim by Chocolate!” the headlines blared. A team of German researchers had found that people on a low-carb diet lost weight 10 percent faster if they ate a chocolate bar every day. It made the front page of Bild, Europe’s largest daily newspaper, just beneath their update about the Germanwings crash. From there, it ricocheted around the internet and beyond, making news in more than 20 countries and half a dozen languages. It was discussed on television news shows. It appeared in glossy print, most recently in the June issue of Shape magazine (“Why You Must Eat Chocolate Daily”, page 128). Not only does chocolate accelerate weight loss, the study found, but it leads to healthier cholesterol levels and overall increased well-being. The Bild story quotes the study’s lead author, Johannes Bohannon, Ph.D., research director of the Institute of Diet and Health: “The best part is you can buy chocolate everywhere.” I am Johannes Bohannon, Ph.D. Well, actually my name is John, and I’m a journalist. I do have a Ph.D., but it’s in the molecular biology of bacteria, not humans. The Institute of Diet and Health? That’s nothing more than a website. Other than those fibs, the study was 100 percent authentic. My colleagues and I recruited actual human subjects in Germany. We ran an actual clinical trial, with subjects randomly assigned to different diet regimes. And the statistically significant benefits of chocolate that we reported are based on the actual data. It was, in fact, a fairly typical study for the field of diet research. Which is to say: It was terrible science. The results are meaningless, and the health claims that the media blasted out to millions of people around the world are utterly unfounded.
Link ID: 20995 - Posted: 05.28.2015
By ANDREW POLLACK A study of an obesity drug has ended after the manufacturer released early and ultimately misleading data, researchers said on Tuesday. The company, Orexigen Therapeutics, disclosed in March that early results from a clinical trial of its drug Contrave had shown a 41 percent reduction in the risk of heart attacks, strokes and death from cardiovascular causes. Orexigen’s stock shot up, and the information no doubt helped lift sales of Contrave. But the academic researchers who oversaw the study said on Tuesday that Orexigen had violated an agreement that the early results were not going to be shared widely, even within the company. Moreover, as participants in the trial were followed for a longer period of time, the benefit of the drug in reducing cardiovascular risks vanished. The researchers, in a news release issued by the Cleveland Clinic, said they took the unusual step of terminating the study and releasing the more updated results. “We felt it was unacceptable to allow misleading interim data to be in the public domain and be acted upon by patients and providers,” Dr. Steven Nissen, chairman of cardiovascular medicine at the Cleveland Clinic and head of the trial’s steering committee, said in an interview. He said Orexigen had “acted improperly and unethically in violating the data access agreement” and the premature release of data had made it difficult to continue the study. It’s unlikley that patients would want to stay in the trial and risk getting a placebo if they thought the drug, which is already available on the market, could reduce their risk of heart attacks. © 2015 The New York Times Company
Link ID: 20921 - Posted: 05.13.2015
By David Shultz We no longer live in a world governed by the sun. Artificial light lets millions of people stay up late, or work in the predawn hours. But the price many of us pay for this extra illumination is a disrupted internal clock—and, growing evidence suggests, obesity. Now, a study of mice suggests that excessive light exposure causes the rodents to burn less fat, a finding that if confirmed could lead to new paths to weight loss in humans. Many mammals have two types of tissues that store fat: brown fat and white fat. Both store energy, but white fat releases its energy stores to power other cells, while brown fat produces heat from metabolizing its contents. For years, scientists have been trying to coax brown fat into action as a way to stimulate weight loss. They’ve identified a protein called β3 adrenergic receptor that, when activated, encourages brown fat cells to burn off more fat and produce more heat. To test the relationship between light exposure and brown fat activity, researchers exposed groups of mice to artificial light for 12, 16, or 24 hours per day and monitored their levels of β3 adrenergic receptor activity. The team also monitored the rate at which energy molecules such as glucose and fatty acids were absorbed from the bloodstream by brown fat tissue to test whether the tissue was using less energy to begin with. Both metrics showed the same trend: Brown fat in mice exposed to prolonged periods of light, 16 or 24 hours compared with a normal 12, absorbed less nutrients from the blood and burned less fat as a result of reduced β3 adrenergic receptor activity. In essence, their furnaces were using less fuel and burning less intensely. To compound the problem, the fatty molecules left in the blood stream were absorbed elsewhere—often in white adipose tissue that makes up the classical body fat that causes obesity, says team leader Patrick Rensen, a biochemist at Leiden University Medical Center in the Netherlands. © 2015 American Association for the Advancement of Science.
By Nicholas Bakalar The type of sugar you eat may affect your cravings for high-calorie foods, researchers report. An experiment with 24 healthy volunteers found that compared with consuming glucose, consuming fructose — the sugar found in fruits, honey and corn syrup — resulted in more activity in the brain’s reward regions, increased responses to images of food and a tendency to choose eating a high-calorie food over a future monetary reward. The volunteers drank a 10-ounce glass of cherry-flavored liquid that contained two and a half ounces of fructose or glucose. (Table sugar, or sucrose, extracted from sugar cane or sugar beets, is a compound of glucose and fructose.) Researchers also took blood samples to measure levels of glucose, fructose and insulin, and of leptin and ghrelin, enzymes involved in controlling hunger and feelings of fullness. Before having their drinks, the participants rated their desire to eat on a one-to-10 scale from “not at all” to “very much.” Then they drank the liquids and had functional magnetic resonance imaging brain scans while looking at images of food and of neutral objects like buildings or baskets. As they did so, they rated their hunger using the scale. The volunteers were then presented with images of high-calorie foods and asked whether they would like to have the food now, or a monetary award a month later instead. The study, published in the journal PNAS, found that compared with glucose, consuming fructose produced greater responses to food cues in the orbital frontal cortex of the brain, a region that plays an important role in reward processing. The fructose drink also produced greater activity in the visual cortex when volunteers looked at images of food, a finding that suggests increased craving compared with glucose. © 2015 The New York Times Company
Link ID: 20883 - Posted: 05.05.2015
By Nicholas Bakalar Many people consume sweets in response to stress. Now researchers may have discovered why. Sugar reduces levels of cortisol, the stress hormone. Scientists recruited 19 female volunteers. For 12 days, eight of them consumed beverages sweetened with aspartame, an artificial sweetener. The rest drank an identical beverage containing 25 percent sucrose, or table sugar. Before and after the experiment, researchers measured the volunteers’ saliva cortisol levels and performed functional M.R.I. scans while they took arithmetic tests designed to be just beyond their abilities — a procedure known to increase cortisol levels. The study, in the Journal of Clinical Endocrinology and Metabolism, found no differences in the tests between the two groups before the 12-day diet. But in tests afterward, cortisol levels were lower in the sugar consumers and higher in the aspartame group. The post-diet M.R.I. showed increased activity in the areas of the brain controlling fear and stress in the sugar group. The aspartame group showed decreased activity in those areas. The senior author, Kevin D. Laugero, a nutritionist with the federal Department of Agriculture, said no one should conclude that sugar should be used as a stress reducer. But, he said, “the finding is intriguing because it suggests that there is a metabolic pathway sensitive to sugar outside the brain that may expose new targets for treating neurobehavioral and stress-related conditions.” © 2015 The New York Times Company
Physical activity has little role in tackling obesity - and instead public health messages should squarely focus on unhealthy eating, doctors say. In an editorial in the British Journal of Sports Medicine, three international experts said it was time to "bust the myth" about exercise. They said while activity was a key part of staving off diseases such as diabetes, heart disease and dementia, its impact on obesity was minimal. Instead excess sugar and carbohydrates were key. The experts, including London cardiologist Dr Aseem Malhotra, blamed the food industry for encouraging the belief that exercise could counteract the impact of unhealthy eating. They even likened their tactics as "chillingly similar" to those of Big Tobacco on smoking and said celebratory endorsements of sugary drinks and the association of junk food and sport must end. They said there was evidence that up to 40% of those within a normal weight range will still harbour harmful metabolic abnormalities typically associated with obesity. But despite this public health messaging had "unhelpfully" focused on maintaining a healthy weight through calorie counting when it was the source of calories that mattered most - research has shown that diabetes increases 11-fold for every 150 additional sugar calories consumed compared to fat calories. And they pointed to evidence from the Lancet global burden of disease programme which shows that unhealthy eating was linked to more ill health than physical activity, alcohol and smoking combined. © 2015 BBC
Link ID: 20840 - Posted: 04.23.2015
|By Cari Nierenberg and LiveScience Women who develop gestational diabetes early in their pregnancy have a higher chance of having a child with autism than women who don't develop the condition, a new study suggests. Researchers found that mothers-to-be who developed gestational diabetes — high blood sugar during pregnancy in women who have never had diabetes — by their 26th week of pregnancy were 63 percent more likely to have a child diagnosed with an autism spectrum disorder (ASD) compared with women who did not have gestational diabetes at any point during their pregnancy (and who also did not have type 2 diabetes prior to pregnancy). The finding does not mean that autism is common among children born to women who had gestational diabetes. "Autism is still rare," said study co-author Anny Xiang, a research scientist at Kaiser Permanente Southern California in Pasadena. The findings show that, although the risk of having a child with autism is still low among women who have gestational diabetes early in pregnancy (before 26 weeks), the study did find a relationship between these women and an increased risk that the child would have autism, Xiang said. The study, published today (April 14) in the Journal of the American Medical Association, looked at more than 320,000 children born in Southern California between 1995 and 2009. About 8 percent of the kids were born to mothers who had pregnancy-related diabetes, and 2 percent had mothers with type 2 diabetes. © 2015 Scientific American
By James Gallagher Health editor, BBC News website Those who were overweight had an 18% reduction in dementia, researchers found Being overweight cuts the risk of dementia, according to the largest and most precise investigation into the relationship. The researchers admit they were surprised by the findings, which run contrary to current health advice. The analysis of nearly two million British people, in the Lancet Diabetes & Endocrinology, showed underweight people had the highest risk. Dementia charities still advised not smoking, exercise and a balanced diet. Dementia is one of the most pressing modern health issues. The number of patients globally is expected to treble to 135 million by 2050. There is no cure or treatment, and the mainstay of advice has been to reduce risk by maintaining a healthy lifestyle. Yet it might be misguided. The team at Oxon Epidemiology and the London School of Hygiene and Tropical Medicine analysed medical records from 1,958,191 people aged 55, on average, for up to two decades. Their most conservative analysis showed underweight people had a 39% greater risk of dementia compared with being a healthy weight. But those who were overweight had an 18% reduction in dementia - and the figure was 24% for the obese. "Yes, it is a surprise," said lead researcher Dr Nawab Qizilbash. He told the BBC News website: "The controversial side is the observation that overweight and obese people have a lower risk of dementia than people with a normal, healthy body mass index. "That's contrary to most if not all studies that have been done, but if you collect them all together our study overwhelms them in terms of size and precision." Loss of tissue in a demented brain compared with a healthy one © 2015 BBC
By Rachel Feltman If you give a mouse an eating disorder, you might just figure out how to treat the disease in humans. In a new study published Thursday in Cell Press, researchers created mice who lacked a gene associated with disordered eating in humans. Without it, the mice showed behaviors not unlike those seen in humans with eating disorders: They tended to be obsessive compulsive and have trouble socializing, and they were less interested in eating high-fat food than the control mice. The findings could lead to novel drug treatments for some of the 24 million Americans estimated to suffer from eating disorders. In a 2013 study, the same researchers went looking for genes that might contribute to the risk of an eating disorder. Anorexia nervosa and bulimia nervosa aren't straightforwardly inherited -- there's definitely more to an eating disorder than your genes -- but it does seem like some families might have higher risks than others. Sure enough, the study of two large families, each with several members who had eating disorders, yielded mutations in two interacting genes. In one family, the estrogen-related receptor α (ESRRA) gene was mutated. The other family had a mutation on another gene that seemed to affect how well ESRRA could do its job. So in the latest study, they created mice that didn't have ESRRA in the parts of the brain associated with eating disorders. "You can't go testing this kind of gene expression in a human," lead author and University of Iowa neuorscientist Michael Lutter said. "But in mice, you can manipulate the expression of the gene and then look at how it changes their behavior."
by Alison George Misguided notions about our sexual appetites are missing the bigger picture and making people unhappy, says Emily Nagoski Why is there no such thing as a sex drive? A drive is a motivational system to deal with life-or-death issues, like hunger or being too cold. You're not going to die if you don't have sex. But biologists might say that if you don't reproduce, that is a form of death Yes. That's the argument that was used when desire was being added to the way sexual dysfunctions were diagnosed in the 1970s, to justify the framing of sexual desire as a drive. But when it comes to sex, there just isn't any physical evidence of a drive mechanism. So what's going on? If sex is a drive then desire should be spontaneous, like a hunger. When you see a sexy person or have a stray sexy thought, it activates an internal craving or urge for sex. That's called "spontaneous desire". It feels like it comes out of the blue. But there is another way of experiencing desire which is also healthy and normal, called "responsive desire", where your interest only emerges in response to arousal. So, your partner comes over and starts kissing your neck and you're like, "oh, right, sex, that's a good idea". Do you think an absence of spontaneous desire is normal? Yes. If our metaphor for desire is hunger, if you are never hungry for food there will be dire consequences and that's clearly a disorder, right? That's a medical problem that needs to be fixed. But not experiencing spontaneous hunger for sex doesn't have dire consequences; it is not a medical disorder. I think the reason we expect everyone to have spontaneous desire is because that's how most men experience it. © Copyright Reed Business Information Ltd
Keyword: Sexual Behavior
Link ID: 20759 - Posted: 04.06.2015
By Harriet Brown If you’re one of the 45 million Americans who plan to go on a diet this year, I’ve got one word of advice for you: Don’t. You’ll likely lose weight in the short term, but your chance of keeping if off for five years or more is about the same as your chance of surviving metastatic lung cancer: 5 percent. And when you do gain back the weight, everyone will blame you. Including you. This isn’t breaking news; doctors know the holy trinity of obesity treatments—diet, exercise, and medication—don’t work. They know yo-yo dieting is linked to heart disease, insulin resistance, higher blood pressure, inflammation, and, ironically, long-term weight gain. Still, they push the same ineffective treatments, insisting they’ll make you not just thinner but healthier. In reality, 97 percent of dieters regain everything they lost and then some within three years. Obesity research fails to reflect this truth because it rarely follows people for more than 18 months. This makes most weight-loss studies disingenuous at best and downright deceptive at worst. One of the principles driving the $61 billion weight-loss industries is the notion that fat is inherently unhealthy and that it’s better, health-wise, to be thin, no matter what you have to do to get there. But a growing body of research is beginning to question this paradigm. Does obesity cause ill health, result from it, both, or neither? Does weight loss lead to a longer, healthier life for most people? Studies from the Centers for Disease Control and Prevention repeatedly find the lowest mortality rates among people whose body mass index puts them in the “overweight” and “mildly obese” categories.
Link ID: 20718 - Posted: 03.25.2015