Chapter 9. Homeostasis: Active Regulation of the Internal Environment
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Ian Sample Science editor Selling high calorie foods in plain packaging could help in the battle against obesity according to a leading researcher who has won a share of the most lucrative prize in neuroscience for his work on the brain’s reward system. The colourful wrapping and attractive advertising of calorie-rich foods encourage people to buy items that put them at risk of overeating and becoming obese in the future, said Wolfram Schultz, a professor of neuroscience at the University of Cambridge. “We should not advertise, propagate or encourage the unnecessary ingestion of calories,” Schultz said at a press conference held on Monday to announce the winners of the 2017 Brain Prize. “There should be some way of regulating the desire to get more calories. We don’t need these calories.” “Colourful wrapping of high energy foods of course makes you buy more of that stuff and once you have it in your fridge, it’s in front of you every time you open the fridge and ultimately you’re going to eat it and eat too much,” he added. Schultz shares the €1m prize from the Lundbeck Foundation in Denmark with professors Peter Dayan, director of the Gatsby Computational Neuroscience Unit at UCL, and Ray Dolan, director of the Max Planck UCL Centre for Computational Psychiatry and Ageing. Together, the scientists unravelled how the brain uses rewards to learn and shape behaviour.
Aaron E. Carroll While we have long known about the existence of microbes — the tiny bacteria, fungi and archaea that live all around, on and in us — our full relationship has become one of the hottest topics for research only in recent years. Scientists believe that every person contains as many independent microbial cells as human cells. This collection of life, known as the microbiome, provides useful functions for us. Indeed, some of the things we think our bodies do are actually the abilities and enzymes of life-forms living within us. They can help with digestion, vitamin synthesis and even immunological responses. But, as with many new breakthroughs and advances, the hype of the microbiome often outweighs the reality. This seems especially likely in the field of nutrition. Doing research on the microbiome is not easy, and there are many opportunities to foul things up. To accomplish human studies, large samples of people and microbiomes are needed to account for potential confounding variables. Specimens have to be collected and stored carefully because contamination has been a big problem. DNA has to be extracted, amplified and sequenced. Finally, powerful bioinformatics tools are necessary to assemble and analyze the huge amount of data contained in a sequence of nucleotides — all of which has resulted in a wide range of new “omics,” including genomics, proteomics, transcriptomics and metabolomics. Of course, if we think that microbes play a large role in health, we have to rethink the role that antimicrobials play in our lives. In this thinking, antibiotics and antifungals could be life-changing or life-threatening. But that’s not the case. There are many reasons to avoid unnecessary use of these medications, but the microbiome appears able to withstand most treatment. © 2017 The New York Times Company
Link ID: 23318 - Posted: 03.06.2017
By NICHOLAS BAKALAR There is some evidence that stress prompts people to turn to sweet, high-calorie “comfort foods.” Now scientists have confirmed a link between long-term stress and obesity. The study, published in Obesity, tested 2,527 men and women over 50 years old, quantifying stress by measuring levels of cortisol, the stress hormone, in 2-centimeter hair clippings, or about two months’ growth. After controlling for age, sex, ethnicity, smoking, diabetes and other factors that might be linked to obesity, they found that the higher the level of cortisol, the greater the body weight, B.M.I. and waist circumference. Higher cortisol levels were also associated with persistence of obesity over time. Other studies have relied on measures of cortisol in blood, urine or saliva, which can vary by time of day and be affected by temporary stressors and other factors. But this study was able to measure general stress levels over two months to get a picture of the long-term effect. The researchers acknowledge that they were unable to determine whether chronically high cortisol levels are a cause or a consequence of obesity (feeling “fat,” for example, could raise your stress levels). The lead author, Sarah E. Jackson, an epidemiologist at University College London, said that while it may not be possible to eliminate stress, “you may be able to find ways to control it. Even just being aware that stress might make you eat more may help.” © 2017 The New York Times Company
By Emma Hiolski There’s more to those love handles than meets the eye. Fat tissue can communicate with other organs from afar, sending out tiny molecules that control gene activity in other parts of the body, according to a new study. This novel route of cell-to-cell communication could indicate fat plays a much bigger role in regulating metabolism than previously thought. It could also mean new treatment options for diseases such as obesity and diabetes. “I found this very interesting and, frankly, very exciting,” says Robert Freishtat of Children’s National Health System in Washington, D.C., a pediatrician and researcher who has worked with metabolic conditions like obesity and diabetes. Scientists have long known that fat is associated with all sorts of disease processes, he says, but they don’t fully understand how the much-reviled tissue affects distant organs and their functions. Scientists have identified hormones made by fat that signal the brain to regulate eating, but this new study—in which Freishtat was not involved—takes a fresh look at another possible messenger: small snippets of genetic material called microRNAs, or miRNAs. MiRNAs, tiny pieces of RNA made inside cells, help control the expression of genes and, consequently, protein production throughout the body. But some tumble freely through the bloodstream, bundled into tiny packets called exomes. There, high levels of some miRNAs have been associated with obesity, diabetes, cancer, and cardiovascular disease. © 2017 American Association for the Advancement of Science.
Link ID: 23247 - Posted: 02.17.2017
By Alice Callahan Once fat cells are formed, can you ever get rid of them? The number of fat cells in a person’s body seems to be able to change in only one direction: up. Fat cell number increases through childhood and adolescence and generally stabilizes in adulthood. But this doesn’t mean that fat cells, or adipocytes, are stagnant. The size of individual fat cells is remarkably variable, expanding and contracting with weight gain or weight loss. And as with most cell types in the body, adipocytes die eventually. “Usually when old ones die, they are replaced by new fat cells,” said Dr. Michael Jensen, an endocrinologist and obesity researcher at the Mayo Clinic. Cell death and production appear to be tightly coupled, so although about 10 percent of adipocytes die each year, they’re replaced at the same rate. Even among bariatric surgery patients, who can lose massive amounts of weight, the number of fat cells tends to remain the same, although the cells shrink in size, studies show. Liposuction reduces the number of fat cells in a person’s body, but studies show the weight lost is typically regained within a year. It isn’t known whether this regain occurs through the production of new fat cells or expansion of existing ones. People who are obese tend to have more fat cells than those who are not, and several studies have found an increase in fat cell number with weight regain following weight loss. The fact that fat cell number can be increased but not decreased most likely contributes to the body’s drive to regain weight after weight loss, said Dr. Kirsty L. Spalding, a cell biologist at the Karolinska Institute in Sweden and the lead author of a 2008 study showing that fat cells die and are replaced. Beyond their role in storing fat, adipocytes secrete proteins and hormones that affect energy metabolism. © 2017 The New York Times Company
Link ID: 23246 - Posted: 02.17.2017
By Mitch Leslie Fasting is all the rage. Self-help books promise it will incinerate excess fat, spruce up your DNA, and prolong your life. A new scientific study has backed up some health claims about eating less. The clinical trial reveals that cutting back on food for just 5 days a month could help prevent or treat age-related illnesses like diabetes and cardiovascular disease. “It’s not trivial to do this kind of study,” says circadian biologist Satchidananda Panda of the Salk Institute for Biological Studies in San Diego, California, who wasn’t connected to the research. “What they have done is commendable.” Previous studies in rodents and humans have suggested that periodic fasting can reduce body fat, cut insulin levels, and provide other benefits. But there are many ways to fast. One of the best known programs, the 5:2 diet, allows you to eat normally for 5 days a week. On each of the other 2 days, you restrict yourself to 500 to 600 calories, about one-fourth of what the average American consumes. An alternative is the so-called fasting-mimicking diet, devised by biochemist Valter Longo of the University of Southern California in Los Angeles and colleagues. For most of the month, participants eat as much of whatever they want. Then for five consecutive days they stick to a menu that includes chips, energy bars, and soups, consuming about 700 to 1100 calories a day. © 2017 American Association for the Advancement of Science
Link ID: 23236 - Posted: 02.16.2017
Laura Beil People who undergo gastric bypass surgery are more likely to experience a remission of their diabetes than patients who receive a gastric sleeve or intensive management of diet and exercise, according to a new study. Bypass surgery had already shown better results for diabetes than other weight-loss methods in the short term, but the new research followed patients for five years. “We knew that surgery had a powerful effect on diabetes,” says Philip Schauer of the Bariatric & Metabolic Institute at the Cleveland Clinic. “What this study says is that the effect of surgery is durable.” The results were published online February 15 in the New England Journal of Medicine. The study followed 134 people with type 2 diabetes for five years in a head-to-head comparison of weight-loss methods. At the end of that time, two of 38 patients who only followed intensive diet and exercise plans were no longer in need of insulin to manage blood sugar levels. For comparison, 11 of 47 patients who had a gastric sleeve, which reduces the size of the stomach, and 14 of 49 who underwent gastric bypass, a procedure that both makes the stomach smaller and shortens digestion time, did not need the insulin anymore. In general, patients who had been diabetic for fewer than eight years were more likely to be cured, Schauer says. Even those surgical patients who still needed to take insulin had greater weight loss and lower median glucose levels than others in the study. This study was also one of the few to show that bariatric surgery could help those with only mild obesity, defined as a body mass index between 27 and 34. How bariatric surgery might improve diabetes is still unknown, but scientists have pointed to effects on the body’s metabolism (SN: 8/24/13, p. 14) and gut microbes (SN: 9/5/15, p. 16). |© Society for Science & the Public 2000 - 2016.
Link ID: 23235 - Posted: 02.16.2017
By Andy Coghlan It’s as if a switch has been flicked. Evidence is mounting that chronic fatigue syndrome (CFS) is caused by the body swapping to less efficient ways of generating energy. Also known as ME or myalgic encephalomyelitis, CFS affects some 250,000 people in the UK. The main symptom is persistent physical and mental exhaustion that doesn’t improve with sleep or rest. It often begins after a mild infection, but its causes are unknown. Some have argued that CFS is a psychological condition, and that it is best treated through strategies like cognitive behavioural therapy. But several lines of investigation are now suggesting that the profound and painful lack of energy seen in the condition could in many cases be due to people losing their ability to burn carbohydrate sugars in the normal way to generate cellular energy. Instead, the cells of people with CFS stop making as much energy from sugar as usual, and start relying more on lower-yielding fuels, such as amino acids and fats. This kind of metabolic switch produces lactate, which can cause pain when it accumulates in muscles. Together, this would explain both the shortness of energy, and why even mild exercise can be exhausting and painful. © Copyright Reed Business Information Ltd.
Link ID: 23226 - Posted: 02.14.2017
Moises Velasquez-Manoff This Valentine’s Day, as you bask in the beauty of your beloved, don’t just thank his or her genes and your good fortune; thank microbes. Research on the microbes that inhabit our bodies has progressed rapidly in recent years. Scientists think that these communities, most of which live in the gut, shape our health in myriad ways, affecting our vulnerability to allergic diseases like hay fever, how much weight we put on, our susceptibility to infection and maybe even our moods. They can also, it seems, make us sexy. Susan Erdman, a microbiologist at M.I.T., calls it the “glow of health.” The microbes you harbor, she argues, can make your skin smooth and your hair shiny; they may even put a spring in your step. She stumbled on the possibility some years ago when, after feeding mice a probiotic microbe originally isolated from human breast milk, a technician in her lab noticed that the animals grew unusually lustrous fur. Further observation of males revealed thick skin bristling with active follicles, elevated testosterone levels and oversize testicles, which the animals liked showing off. Microbes had transformed these animals into rodent heartthrobs. When given to females, the probiotic also prompted deeper changes. Levels of a protein called interleukin 10, which helps to prevent inflammatory disease and ensure successful pregnancy, went up, as did an important hormone called oxytocin. Oxytocin, often called the love hormone, helps mammals bond with one another. Our bodies may release it when we kiss (and mean it), when women breast-feed, even when people hang out with good friends. And the elevated oxytocin Dr. Erdman saw had important effects during motherhood. Some of the mice in her studies were eating a high-fat, high-sugar diet — junk-foody fare that’s known to shift the microbiome into an unhealthy state. Not surprisingly perhaps, mothers that didn’t imbibe the probiotics were less caring and tended to neglect their pups. But mothers that had high oxytocin thanks to the probiotic were nurturing and reared their pups more successfully. © 2017 The New York Times Company
By JANE E. BRODY “Bariatric surgery is probably the most effective intervention we have in health care,” says Laurie K. Twells, a clinical epidemiologist at Memorial University of Newfoundland. She bases this bold claim on her experience with seriously obese patients and a detailed analysis of the best studies yet done showing weight-loss surgery’s ability to reverse the often devastating effects of being extremely overweight on health and quality of life. “I haven’t come across a patient yet who wouldn’t recommend it,” Dr. Twells said in an interview. “Most say they wish they’d done it 10 years sooner.” She explained that the overwhelming majority of patients who undergo bariatric surgery have spent many years trying — and failing — to lose weight and keep it off. And the reason is not a lack of willpower. “These patients have lost hundreds of pounds over and over again,” Dr. Twells said. “The weight that it takes them one year to lose is typically back in two months,” often because a body with longstanding obesity defends itself against weight loss by drastically reducing its metabolic rate, an effect not seen after bariatric surgery, which permanently changes the contours of the digestive tract. In reviewing studies that followed patients for five to 25 years after weight-loss surgery, Dr. Twells and colleagues found major long-lasting benefits to the patients’ health and quality of life. Matched with comparable patients who did not have surgery, those who did fared much better physically, emotionally and socially. They rated themselves as healthier and were less likely to report problems with mobility, pain, daily activities, social interactions and feelings of depression and anxiety, among other factors that can compromise well-being. © 2017 The New York Times Company
Link ID: 23219 - Posted: 02.13.2017
By Tamar Haspel In his new book “The Case Against Sugar,” journalist Gary Taubes makes, as you might easily guess, a spirited case against sugar. His argument is based on the straightforward idea that sugar contributes to obesity and disease well beyond its calorie content, because it affects human metabolism in a way that encourages fat storage. In his new book, the science journalist Gary Taubes takes a hard-nosed look at sugar — and further advances the idea that not all calories are created equal. But there are competing theories of obesity. Who’s right? The debate is often framed as being over the nature of calories themselves, with scientists holding that calories are units of energy — each one no different than the other. Sugar is a carbohydrate, and the body converts carbs to glucose which is then absorbed into the bloodstream. This, in turn, triggers the pancreas to release insulin, the hormone that enables the body to use energy or store it as fat. If a person doesn’t eat many carbohydrates, the pancreas doesn’t release as much insulin, and less fat is stored, forcing the body’s metabolism to increase and burn off that energy. In practical terms, the theory goes, such a person will have an easier time losing weight — or avoiding gaining it. This hypothesis is called, appropriately, the carbohydrate/insulin, or C/I, model, and it is the basis for any number of popular low-carb diets, including Atkins, the Paleo diet, and others. It is also a “minority position” among food scientists, Taubes concedes, and many mainstream nutrition authorities reject it. Copyright 2017 Undark
Link ID: 23208 - Posted: 02.09.2017
By Simon Oxenham Ever felt hungry and angry at the same time? There’s evidence that “hanger” is a real phenomenon, one that can affect your work and relationships. The main reason we become more irritable when hungry is because our blood glucose level drops. This can make it difficult for us to concentrate, and more likely to snap at those around us. Low blood sugar also triggers the release of stress-related hormones like cortisol and adrenaline, as well as a chemical called neuropeptide Y, which has been found to make people behave more aggressively towards those around them. This can all have an alarming effect on how you feel about other people – even those you love. A classic study of married couples asked them to stick pins into “voodoo dolls” that represented their loved ones, to reflect how angry they felt towards them. The volunteers then competed against their spouse in a game, in which the winner could blast loud noise through the loser’s headphones. The researchers tracked the participants’ blood glucose levels throughout. They found that when people had lower sugar levels, the longer the blasts of unpleasant noise they subjected their spouse to, and the more pins they stuck into their dolls. But while being hungry really does change your behaviour, the effects of hanger have sometimes been overstated. One study that attracted attention a few years ago found that judges are less likely to set lenient sentences the closer it gets to lunch. © Copyright Reed Business Information Ltd.
Link ID: 23172 - Posted: 02.01.2017
By Mitch Leslie When we have food poisoning, the last thing we want to do is eat. But in mice, a microbe that causes this ailment actually increases appetite, a new study reveals. Researchers say they might be able to use the same trick to increase eating in cancer patients and old folks, who often lose their desire for food. “I think it’s a fantastic paper,” says immunophysiologist Keith Kelley of the University of Illinois in Urbana, who wasn’t connected to the study. The researchers deserve praise for combining approaches from several disciplines such as microbiology, neurobiology, and immunology to draw a surprising conclusion, he says. “It’s the way disease responses should be investigated.” Some of the symptoms you endure when you are ill, such as lethargy and fever, are actually good for you. Lolling on the couch all day, for instance, saves energy for your immune cells. But the picture is more complex for another of these so-called sickness behaviors—reduced appetite. Animal studies have found that eating less seems to improve the odds of surviving some infections, perhaps because it robs the invading microbes of key nutrients, but in other cases the loss of appetite often proves fatal. © 2017 American Association for the Advancement of Science
Eating disorders, including anorexia and bulimia, affect a small but substantial number of women in their 40s and 50s, UK research suggests. The study, involving more than 5,000 women, found just over 3% reported having an eating disorder. Some said they had experienced it since their teens, others developed it for the first time in their middle age. Julie Spinks, from Beaconsfield, is 48. She was not involved in the study, but can relate first-hand to its findings. She developed anorexia for the first time when she was 44. "It was a complete shock at the time," she recalls. "I knew that I was restricting my food but I didn't ever think I had anorexia. "I'd been really unhappy at work and had very low self-esteem. To begin with I just thought I had lost my appetite. "I felt depressed, like I was not worth feeding or existing. I wanted to disappear and fade away." Julie started to lose weight quite quickly and began to exercise as well. She realised something was very wrong one day after she had been to the gym. Mind struggle "I'd run for about an hour and burnt off about 500 calories. I remember thinking that's about the same as a chocolate bar. That's when I started to link food and exercise." Julie still did not recognise she had anorexia though. "I thought anorexia was something that happened to other people. It didn't occur to me that I might have it." After a breakdown at work she went for a mental health assessment. Her doctors then diagnosed her with anorexia and depression. Julie was given antidepressants and began therapy sessions to help with her eating disorder. © 2017 BBC.
Keyword: Anorexia & Bulimia
Link ID: 23112 - Posted: 01.17.2017
By GARY TAUBES The first time the sugar industry felt compelled to “knock down reports that sugar is fattening,” as this newspaper put it, it was 1956. Papers had run a photograph of President Dwight D. Eisenhower sweetening his coffee with saccharin, with the news that his doctor had advised him to avoid sugar if he wanted to remain thin. The industry responded with a national advertising campaign based on what it believed to be solid science. The ads explained that there was no such thing as a “fattening food”: “All foods supply calories and there is no difference between the calories that come from sugar or steak or grapefruit or ice cream.” More than 60 years later, the sugar industry is still making the same argument, or at least paying researchers to do it for them. The stakes have changed, however, with a near tripling of the prevalence of obesity in the intervening decades and what the Centers for Disease Control and Prevention figures reveal to be an almost unimaginable 655 percent increase in the percentage of Americans with diabetes diagnoses. When it comes to weight gain, the sugar industry and purveyors of sugary beverages still insist, a calorie is a calorie, regardless of its source, so guidelines that single out sugar as a dietary evil are not evidence-based. Surprisingly, the scientific consensus is technically in agreement. It holds that obesity is caused “by a lack of energy balance,” as the National Institutes of Health website explains — in other words, by our taking in more calories than we expend. Hence, the primary, if not the only, way that foods can influence our body weight is through their caloric content. Another way to say this is that what we eat doesn’t matter; it’s only how much — just as the sugar industry would have us believe. A 2014 article in an American Diabetes Association journal phrased the situation this way: “There is no clear or convincing evidence that any dietary or added sugar has a unique or detrimental impact relative to any other source of calories on the development of obesity or diabetes.” © 2017 The New York Times Company
Link ID: 23105 - Posted: 01.14.2017
By Anthony Warner Other things being equal, you’d think the strongest influence on expanding midriffs might be fizzy drinks or fried food. But a study out yesterday reinforces the growing idea that poverty is a bigger factor. It found socio-economic status offered the best explanation for greater weight gain when comparing people in the UK with the same genetic vulnerability to obesity (International Journal of Epidemiology, DOI: 10.1093/ije/dyw337). Mounting evidence of poverty’s role in this health crisis makes even more repulsive the rise in vile and deeply offensive prejudice based solely on a failure to fit with the physical ideals of privileged society. This is no longer just about random acts of unkindness. It is everywhere. These views were aired without challenge at a large food and health conference recently. I heard open expression of the idea that obese people should be banned from working in the public sector or that food prices should be increased to force poorer people to eat less. This is the respectable face of prejudice and it has crept into just about every walk of life, stoked by extreme media commentators. It risks creating bigger divides within already fragmented societies. In countries battling obesity, such vitriol extends to repeated talk of denying access to healthcare. It seems this prejudice is OK if its intention is to help people lose weight and often portrays them as slovenly, lazy, lacking self-control, a drain on our health system and morally weak. © Copyright Reed Business Information Ltd.
Link ID: 23093 - Posted: 01.13.2017
By Catherine Caruso If you give a mouse a beer, he’s going to ask for a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos. But why does binge drinking make us binge eat as well? The reason may lie not in the stomach but in the brain, recent research suggests. A study published today in Nature Communications found alcohol activated brain cells that control hunger, sending drunk mice scampering for snacks even when they were not really hungry. Researchers from The Francis Crick Institute Mill Hill Laboratory in London got mice drunk, then tagged and recorded the electrical activity in brain cells linked to hunger, uncovering a neural mechanism that could explain why the animals ate significantly more after binge-drinking sessions even though their bodies did not need the calories. Although hunger pangs in our stomach usually alert us that it is time to eat, the impulse to consume food originates in our brains, and brain cells located in the hypothalamus called agouti-related protein (AgRP) neurons play a key role in controlling hunger. A previous study showed that when AgRP neurons are activated, mice almost immediately seek out food and start eating, even if their stomachs are full. By contrast, when AgRP neurons are deactivated, hungry mice will not eat. AgRP neurons play a similar role in human hunger: Under natural conditions they are activated when our bodies need calories, signaling to us that we should find food. Something different happens, however, when alcohol is involved. Although alcohol is second only to fat in caloric density, previous studies have shown drinking causes humans to eat more, a paradox that made lead authors Craig Blomeley and Sarah Cains and colleagues wonder whether the brain could be to blame. © 2017 Scientific American,
Brandie Jefferson When I told my coworker that I was participating in a study that involved fasting, she laughed until she nearly cried. My boyfriend, ever supportive, asked hesitantly, "Are you sure you want to try this?" Note the use of "try" instead of "do." When I told my father over the phone, the line went silent for a moment. Then he let out a long, "Welllllll," wished me luck, and chuckled. Turns out, luck might not be enough. I like to eat. Often and a lot. Now, however, my eating habits have become more than a source of amusement for friends and coworkers. Now they are data in a study focusing on people with multiple sclerosis, like me. The pilot study, led by Dr. Ellen Mowry at the Johns Hopkins University in Baltimore, is looking at the impact of intermittent fasting on our microbiomes — the universe of trillions of microbes, mainly bacteria, that live in our guts. Intermittent fasting is pretty much what it sounds like. For six months, participants are allowed to eat during an 8-hour period each day. The remaining 16 hours we are limited to water, tea and coffee. No added sugar, cream, honey or sweetener. Several studies have suggested that the predominant bacteria in the guts of people with MS tend to be different than those in the guts of those without the chronic autoimmune inflammatory disease, according to Samantha Roman, the study's research coordinator. Depending on their makeup, bacteria have the ability to soothe or trigger inflammation, potentially affecting the symptoms of MS and other diseases. Exactly how gut bacteria and inflammation are related, though, is not well understood. © 2017 npr
Keyword: Multiple Sclerosis
Link ID: 23070 - Posted: 01.09.2017
Eating a Mediterranean diet has been linked to less brain shrinkage in older adults. Human brains naturally shrink with age. But a study that followed 401 people in their 70s found that the brains of those who adhered more closely to a Mediterranean-style diet shrank significantly less over a period of three years. A typical Mediterranean diet contains a high amount of vegetables, fruits, olive oil, beans and cereal grains, moderate amounts of fish, dairy products, and wine, and only a small amount of red meat and poultry. “As we age, the brain shrinks and we lose brain cells, which can affect learning and memory,” says Michelle Luciano, at the University of Edinburgh, UK, who led the study. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.” The differences in brain shrinkage were measured using brain scans. Statistical analysis of diet data found that simply eating more fish and less meat were not associated with reduced shrinking. “While the study points to diet having a small effect on changes in brain size, it didn’t look at the effect on risk of dementia,” says David Reynolds, at the charity Alzheimer’s Research UK. “We would need to see follow-up studies in order to investigate any potential protective effects against problems with memory and thinking.” Other studies have found that being overweight seems to accelerate shrinking of the brain’s white matter. © Copyright Reed Business Information Ltd.
By Joshua A. Krisch Experiments in mice find that obesity reinforces a sedentary lifestyle. According to a December 29 study in Cell, obese mice were less active due to changes in their dopamine receptors—specifically, a drop in activity in DR2 receptors in the brain’s striatum, which plays a role in motor control. “There’s a common belief that obese animals don’t move as much because carrying extra body weight is physically disabling,” coauthor Alexxai Kravitz of the National Institute of Diabetes and Digestive and Kidney Diseases said in a press release. “But our findings suggest that assumption doesn't explain the whole story.” Kravitz and colleagues fed mice either a standard diet or a high-fat diet for 18 weeks, and then examined their dopamine signaling pathways. They found that the least active mice had less-active DR2 dopamine receptors in the striatum. Then they genetically engineered mice to have the same DR2 deficiency, and found that even those that remained lean engaged in less physical activity than other mice. Together, the findings suggest that the DR2 deficiency may account for a lack of movement in obese mice. “Other studies have connected dopamine signaling defects to obesity, but most of them have looked at reward processing—how animals feel when they eat different foods,” Kravitz said in the press release. “We looked at something simpler: dopamine is critical for movement, and obesity is associated with a lack of movement. Can problems with dopamine signaling alone explain the inactivity?” © 1986-2017 The Scientist