Posts Tagged ‘metabolism’

by MARY JO DILONARDO

When you want to lose weight, there are two things you do: eat less and exercise more.

Just cutting calories should cause you to drop pounds. But exercise alone is rarely enough for weight loss. Life isn’t fair, after all.

Think of it this way: When going on a 30-minute brisk walk at about 4 miles per hours (that’s a 15-minute mile), a 155-pound person burns about 167 calories, according to Harvard Medical School. Want to celebrate your accomplishment? That exercise is quickly erased by a large scoop of vanilla ice cream or two small chocolate chip cookies.

If more serious exercise is your thing, 30 minutes of vigorous stationary bicycling burns 391 calories. But that gets wiped away with one slice of pepperoni pizza.

It doesn’t seem fair how all that effort can be nullified by a few bites of tasty food.

Is more exercise the answer?

It seems like simple math: If exercising for x minutes burns y calories, then just exercise longer and burn more calories. But research shows it’s not that easy.

Recently, New Scientist explained it with a story called, “Why doing more exercise won’t help you burn more calories.” Science writer Teal Burrell explored the idea of the so-called exercise paradox. People who dramatically increase their workout regimens often find that despite all the sweat and motion, they shed few pounds. Scientists have several theories why that might happen.

They eat more. You went for a grueling hike and are so proud of yourself, so you reward yourself later with a chocolate shake. People tend to overestimate the calories they burn when they exercise. In one study, people worked out on a treadmill and then were told to eat from a buffet the amount of food that equaled the calories they thought they burned. They guessed they had burned about 800 calories and ate about 550, when they had really burned just 200.

They move less. You went on that grueling hike in the morning, so you sprawled on the couch the rest of the day. Another theory is that people make up for their workouts by spending the rest of the time being sedentary. These are called “compensatory behaviors” when the moving and not moving balance each other out. But exercise physiologist Lara Dugas of Loyola University doesn’t buy this idea. “That doesn’t mean you lose that 500-calorie run because you’re sedentary for the rest of the day,” she tells New Scientist. “That doesn’t make sense.”

The body adapts. The theory that seems to make the most sense is that when you exercise more, your body adjusts by spending less energy on internal functions, from the immune system to digestion. Those systems that are working in the background, spending calories, just become more efficient when you exercise more, researchers think.

The role of exercise

Mathematician and obesity researcher Kevin Hall explained to Vox why adding more exercise probably won’t lead to much weight loss. Hall used the National Institutes of Health’s Body Weight Planner to calculate that if a 200-pound man added 60 minutes of medium-intensity running four days per week for a month while keeping his calorie intake the same, he’d lose five pounds. “If this person decided to increase food intake or relax more to recover from the added exercise, then even less weight would be lost,” Hall added.

So if someone is trying to lose a lot of weight, it would take a lot of time and effort to try to lose pounds based on exercise alone.

But of course, that doesn’t mean you should cancel your gym membership and toss your sneakers into the back of your closet. Exercise is still a key part of the one-two punch to weight loss. You just have to combine it with calorie control.

Nutritionists will say that weight loss is about 80% diet and 20% exercise. So yes, watch the brownies and the snacks if you’re trying to lose the love handles, but keep moving. It’s an eat-move combination that does require smart eating and regular movement to be healthy.

https://www.mnn.com/health/fitness-well-being/stories/why-exercise-doesnt-matter-all-much-weight-loss?utm_source=Weekly+Newsletter&utm_campaign=10b270682b-RSS_EMAIL_CAMPAIGN_FRI0802_2019&utm_medium=email&utm_term=0_fcbff2e256-10b270682b-40844241

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By Ben Tinker

There’s no shortage of things people swore to leave behind in 2018: bad jobs, bad relationships, bad habits. But chances are, you’re beginning 2019 with something you didn’t intend: a few extra pounds.

Every January, one of the top New Year’s resolutions is to lose weight. And if you’re looking to be successful, there’s something you should know: Diet is far more important than exercise — by a long shot.

“It couldn’t be more true,” nutritionist and CNN contributor Lisa Drayer said. “Basically, what I always tell people is, what you omit from your diet is so much more important than how much you exercise.”

Think of it like this: All of your “calories in” come from the food you eat and the beverages you drink, but only a portion of your “calories out” are lost through exercise.

According to Alexxai Kravitz, an investigator at the National Institute of Diabetes and Digestive and Kidney Diseases — part of the National Institutes of Health, “it’s generally accepted that there are three main components to energy expenditure”:

(1) Basal metabolic rate, the amount of energy it takes just to keep your body running (blood pumping, lungs breathing, brain functioning)

(2) Breaking down food, scientifically referred to as “diet-induced thermogenesis,” “specific dynamic action” or the “thermic effect of food”

(3) Physical activity

For most people, basal metabolic rate accounts for 60% to 80% of total energy expenditure, Kravitz said. He cited a study that defines this as “the minimal rate of energy expenditure compatible with life.” As you get older, your rate goes down, but increasing your muscle mass makes it go up.

About 10% of your calories are burned digesting the food you eat, which means roughly 10% to 30% are lost through physical activity.

“An important distinction here is that this number includes all physical activity: walking around, typing, fidgeting and formal exercise,” Kravitz said. “So if the total energy expenditure from physical activity is 10% to 30%, exercise is a subset of that number.

“The average person — professional athletes excluded — burns 5% to 15% of their daily calories through exercise,” he said. “It’s not nothing, but it’s not nearly equal to food intake, which accounts for 100% of the energy intake of the body.”

What’s more, as anyone who’s worked out a day in their life can tell you, exercising ramps up appetite — and that can sabotage even the best of intentions.

According to calculations by Harvard Medical School, a 185-pound person burns 200 calories in 30 minutes of walking at 4 miles per hour (a pace of 15 minutes per mile). You could easily undo all that hard work by eating four chocolate chip cookies, 1½ scoops of ice cream or less than two glasses of wine.

Even a vigorous cycling class, which can burn more than 700 calories, can be completely canceled out with just a few mixed drinks or a piece of cake.

“It’s so disproportionate — the amount of time that you would need to [exercise] to burn off those few bites of food,” Drayer said.

The sentiment here is that you’ve “earned” what you eat after working out, when instead — if your goal is to lose weight — you’d be better off not working out and simply eating less.

Of course, not all calories are created equal, but for simplicity’s sake, 3,500 calories equal 1 pound of fat. So to lose 1 pound a week, you should aim to cut 500 calories every day. If you drink soda, cutting that out of your diet is one of the easiest ways to get there.

“The other thing is that exercise can increase your appetite, especially with prolonged endurance exercise or with weight lifting,” Drayer said. “It’s another reason why I tell people who want to lose weight to really just focus on diet first.”

It is cliché — but also true — that slow and steady wins the race when it comes to weight loss. According to the US Centers for Disease Control and Prevention, “evidence shows that people who lose weight gradually (about 1 to 2 pounds per week) are more successful at keeping weight off.”

“All this is not to say that exercise doesn’t have its place,” Drayer said. “It’s certainly important for building strength and muscle mass and flexibility. It can help to manage diseases, including heart disease and diabetes. It can improve your mood. It can help fight depression. But although exercise can help with weight loss, diet is a much more important lifestyle factor.”

As the saying goes: Abs are made in the kitchen, not the gym.

https://www.cnn.com/2019/01/04/health/diet-exercise-weight-loss/index.html


Adipose Connective Tissue Stores Fat in Our Body. Credit: Berkshire Community College Bioscience Image Library

A new technique to study fat stores in the body could aid efforts to find treatments to tackle obesity.

The approach focuses on energy-burning tissues found deep inside the body – called brown fat – that help to keep us warm when temperatures drop.

Experts are aiming to find it this calorie-burning power can be harnessed to stop weight gain, but little is known about how the process works.

Previous studies have mainly relied on a medical imaging technique called PET/CT to watch brown fat in action deep inside the body. But the method is unable to directly measure the chemical factors in the tissue.

Scientists at the University of Edinburgh developed a technique called microdialysis to measure how brown fat generates heat in people.

The approach involves inserting a small tube into an area of brown fat in the body and flushing it with fluid to collect a snapshot of the tissues’ chemical make-up.

The team tested the technique in six healthy volunteers, using PET/CT to guide the tube to the right location.

They discovered that in cold conditions, brown fat uses its own energy stores and other substances to generate heat.

Brown fat was active under warm conditions too, when the body does not need to generate its own heat, an outcome that had not been seen before.

Researchers hope the technique will help them to analyse the specific chemicals involved, so that they can better understand how brown fat works.

Most of the fat in our body is white fat, which is found under the skin and surrounding internal organs. It stores excess energy when we consume more calories than we burn.

Brown fat is mainly found in babies and helps them to stay warm. Levels can decrease with age but adults can still have substantial amounts of it, mainly in the neck and upper back region. People who are lean tend to have more brown fat.

The study, published in Cell Metabolism, was funded by the Medical Research Council and Wellcome.

Lead researcher Dr Roland Stimson, of the British Heart Foundation Centre for Cardiovascular Science at the University of Edinburgh, said: “Understanding how brown fat is activated could reveal potential targets for therapies that boost its energy-burning power, which could help with weight loss.”

This article has been republished from materials provided by the University of Edinburgh. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference: Weir, G., Ramage, L. E., Akyol, M., Rhodes, J. K., Kyle, C. J., Fletcher, A. M., … Stimson, R. H. (2018). Substantial Metabolic Activity of Human Brown Adipose Tissue during Warm Conditions and Cold-Induced Lipolysis of Local Triglycerides. Cell Metabolism, 0(0). https://doi.org/10.1016/j.cmet.2018.04.020

https://www.technologynetworks.com/proteomics/news/how-brown-fat-keeps-us-warm-304351?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=63228690&_hsenc=p2ANqtz-9oqDIw3te1NPoj51s94kxnA1ClK8Oiecfela6I4WiITEbm_-SWdmw6pjMTwm2YP24gqSzRaBvUK1kkb2kZEJKPcL5JtQ&_hsmi=63228690


A fluorescent probe creates a heat map of copper in white fat cells. Higher levels of copper are shown in yellow and red. The left panel shows normal levels of copper from fat cells of control mice, and the right panel shows cells deficient in copper.
Credit: Lakshmi Krishnamoorthy and Joseph Cotruvo Jr./UC Berkeley

A new study is further burnishing copper’s reputation as an essential nutrient for human physiology. A research team led by a scientist at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) and at the University of California, Berkeley, has found that copper plays a key role in metabolizing fat.

Long prized as a malleable, conductive metal used in cookware, electronics, jewelry and plumbing, copper has been gaining increasing attention over the past decade for its role in certain biological functions. It has been known that copper is needed to form red blood cells, absorb iron, develop connective tissue and support the immune system.

The new findings, to appear in the July print issue of Nature Chemical Biology but published online today, establishes for the first time copper’s role in fat metabolism.

The team of researchers was led by Chris Chang, a faculty scientist at Berkeley Lab’s Chemical Sciences Division, a UC Berkeley professor of chemistry and a Howard Hughes Medical Institute investigator. Co-lead authors of the study are Lakshmi Krishnamoorthy and Joseph Cotruvo Jr, both UC Berkeley postdoctoral researchers in chemistry with affiliations at Berkeley Lab.

“We find that copper is essential for breaking down fat cells so that they can be used for energy,” said Chang. “It acts as a regulator. The more copper there is, the more the fat is broken down. We think it would be worthwhile to study whether a deficiency in this nutrient could be linked to obesity and obesity-related diseases.”

Dietary copper

Chang said that copper could potentially play a role in restoring a natural way to burn fat. The nutrient is plentiful in foods such as oysters and other shellfish, leafy greens, mushrooms, seeds, nuts and beans.

According to the Food and Nutrition Board of the Institute of Medicine, an adult’s estimated average dietary requirement for copper is about 700 micrograms per day. The Food and Nutrition Board also found that only 25 percent of the U.S. population gets enough copper daily.

“Copper is not something the body can make, so we need to get it through our diet,” said Chang. “The typical American diet, however, doesn’t include many green leafy vegetables. Asian diets, for example, have more foods rich in copper.”

But Chang cautions against ingesting copper supplements as a result of these study results. Too much copper can lead to imbalances with other essential minerals, including zinc.

Copper as a ‘brake on a brake’

The researchers made the copper-fat link using mice with a genetic mutation that causes the accumulation of copper in the liver. Notably, these mice have larger than average deposits of fat compared with normal mice.

The inherited condition, known as Wilson’s disease, also occurs in humans and is potentially fatal if left untreated.

Analysis of the mice with Wilson’s disease revealed that the abnormal buildup of copper was accompanied by lower than normal lipid levels in the liver compared with control groups of mice. The researchers also found that the white adipose tissue, or white fat, of the mice with Wilson’s disease had lower levels of copper compared with the control mice and correspondingly higher levels of fat deposits.

They then treated the Wilson’s disease mice with isoproterenol, a beta agonist known to induce lipolysis, the breakdown of fat into fatty acids, through the cyclic adenosine monophosphate (cAMP) signaling pathway. They noted that the mice with Wilson’s disease exhibited less fat-breakdown activity compared with control mice.

The results prompted the researchers to conduct cell culture analyses to clarify the mechanism by which copper influences lipolysis. The researchers used inductively coupled plasma mass spectroscopy (ICP-MS) equipment at Berkeley Lab to measure levels of copper in fat tissue.

“It had been noted in cattle that levels of copper in the feed would affect how fatty the meat was,” said Chang. “This effect on fat deposits in animals was in the agricultural literature, but it hadn’t been clear what the biochemical mechanisms were linking copper and fat.”

The new work builds upon prior research from Chang’s lab on the roles of copper and other metals in neuroscience. In support of President Barack Obama’s BRAIN Initiative, Berkeley Lab provided Chang seed funding in 2013 through the Laboratory Directed Research and Development program. Chang’s work continued through the BRAIN Tri-Institutional Partnership, an alliance with Berkeley Lab, UC Berkeley and UC San Francisco.

Of the copper in human bodies, there are particularly high concentrations found in the brain. Recent studies, including those led by Chang, have found that copper helps brain cells communicate with each other by acting as a brake when it is time for neural signals to stop.

While Chang’s initial focus was on the role of copper in neural communications, he branched out to investigations of metals in fat metabolism and other biological pathways. This latest work was primarily funded by the National Institutes of Health.

https://www.sciencedaily.com/releases/2016/06/160606200439.htm

They found that copper binds to phosphodiesterase 3, or PDE3, an enzyme that binds to cAMP, halting cAMP’s ability to facilitate the breakdown of fat.

“When copper binds phosphodiesterase, it’s like a brake on a brake,” said Chang. “That’s why copper has a positive correlation with lipolysis.”

Hints from cows

The connection between copper and fat metabolism is not altogether surprising. The researchers actually found hints of the link in the field of animal husbandry.

While it’s known that the brain is responsible for instructing our fat stores to break down and release energy as we need it, scientists haven’t yet been able to pin down exactly how this process plays out. Leptin, a hormone produced by our fat cells, travels to the brain to regulate appetite, metabolism and energy, but it hasn’t been clear what communication was coming back the other way. New research has now uncovered this missing link for the first time, revealing a set of nerves that connect with fat tissue to stimulate the process in a development that could lead to new types of anti-obesity treatments.

The leptin hormone was identified around 20 years ago as a regulator of the body’s metabolism. Low levels of the hormone serve to boost one’s appetite and slow metabolism, while conversely, high leptin levels dull the appetite and facilitate better fat breakdown. Using a combination of techniques, a research team led by Ana Domingos from Portugal’s Instituto Gulbenkian de Ciência were able to shed light on how leptin behaves when sending signals back to the fat by finding the nerves that meet with white fat tissue to prompt its breakdown.

“We dissected these nerve fibers from mouse fat, and using molecular markers identified these as sympathetic neurons,” explains Domingos. “When we used an ultra sensitive imaging technique, on the intact white fat tissue of a living mouse, we observed that fat cells can be encapsulated by these sympathetic neural terminals.”

But to determine the extent of these neurons’ role in obesity, the team carried out further research on mice. The rodents were genetically engineered so that these neurons could be switched on and off through optogenetics, where brain cells are made to behave differently by exposing them to light. Optogenetics is an emerging technique we have seen explored as a means of treating blindness and altering our pain threshold, among other things.

Domingos’ team found that flicking the switch on the neurons locally triggered the release of a neurotransmitter called norepinephrine, which in turn flooded the fat cells with signals that brought about fat breakdown. The team report that without these sympathetic neurons, leptin was not able to stimulate fat breakdown on its own. Therefore the findings suggest that these sympathetic neurons offer a potential target for obesity treatments other than leptin, which the brains of many obese people have a resistance to.

“This result provides new hopes for treating central leptin resistance, a condition in which the brains of obese people are insensitive to leptin,” says Domingos.

The team’s research was published in the journal Cell.

http://www.gizmag.com/neural-mechanism-fat-breakdown-anti-obesity-therapies/39601/


Dr. Justin Grobe, PhD


Dr. Michael Lutter, MD PhD

In a study that seems to defy conventional dietary wisdom, University of Iowa scientists have found that adding high salt to a high-fat diet actually prevents weight gain in mice.

As exciting as this may sound to fast food lovers, the researchers caution that very high levels of dietary salt are associated with increased risk for cardiovascular disease in humans. Rather than suggest that a high salt diet is suddenly a good thing, the researchers say these findings really point to the profound effect non-caloric dietary nutrients can have on energy balance and weight gain.

“People focus on how much fat or sugar is in the food they eat, but [in our experiments] something that has nothing to do with caloric content – sodium – has an even bigger effect on weight gain,” say Justin Grobe, PhD, assistant professor of pharmacology at the UI Carver College of Medicine and co-senior author of the study, which was published in the journal Scientific Reports on June 11.

The UI team started the study with the hypothesis that fat and salt, both being tasty to humans, would act together to increase food consumption and promote weight gain. They tested the idea by feeding groups of mice different diets: normal chow or high-fat chow with varying levels of salt (0.25 to 4 percent). To their surprise, the mice on the high-fat diet with the lowest salt gained the most weight, about 15 grams over 16 weeks, while animals on the high-fat, highest salt diet had low weight gain that was similar to the chow-fed mice, about 5 grams.

“We found out that our ‘french fry’ hypothesis was perfectly wrong,” says Grobe, who also is a member of the Fraternal Order of Eagles Diabetes Research Center at the UI and a Fellow of the American Heart Association. “The findings also suggest that public health efforts to continue lowering sodium intake may have unexpected and unintended consequences.”

To investigate why the high salt prevented weight gain, the researchers examined four key factors that influence energy balance in animals. On the energy input side, they ruled out changes in feeding behavior – all the mice ate the same amount of calories regardless of the salt content in their diet. On the energy output side, there was no difference in resting metabolism or physical activity between the mice on different diets. In contrast, varying levels of salt had a significant effect on digestive efficiency – the amount of fat from the diet that is absorbed by the body.

“Our study shows that not all calories are created equal,” says Michael Lutter, MD, PhD, co-senior study author and UI assistant professor of psychiatry. “Our findings, in conjunction with other studies, are showing that there is a wide range of dietary efficiency, or absorption of calories, in the populations, and that may contribute to resistance or sensitivity to weight gain.”

“This suppression of weight gain with increased sodium was due entirely to a reduced efficiency of the digestive tract to extract calories from the food that was consumed,” explains Grobe.

It’s possible that this finding explains the well-known digestive ill effects of certain fast foods that are high in both fat and salt, he adds.

Through his research on hypertension, Grobe knew that salt levels affect the activity of an enzyme called renin, which is a component in the renin- angiotensin system, a hormone system commonly targeted clinically to treat various cardiovascular diseases. The new study shows that angiotensin mediates the control of digestive efficiency by dietary sodium.

The clinical usefulness of reducing digestive efficiency for treating obesity has been proven by the drug orlistat, which is sold over-the-counter as Alli. The discovery that modulating the renin-angiotensin system also reduces digestive efficiency may lead to the developments of new anti-obesity treatments.

Lutter, who also is an eating disorders specialist with UI Health Care, notes that another big implication of the findings is that we are just starting to understand complex interactions between nutrients and how they affect calorie absorption, and it is important for scientists investigating the health effects of diet to analyze diets that are more complex than those currently used in animal experiments and more accurately reflect normal eating behavior.

“Most importantly, these findings support continued and nuanced discussions of public policies regarding dietary nutrient recommendations,” Grobe adds.

http://www.eurekalert.org/pub_releases/2015-06/uoih-hsp061115.php

By Elizabeth Norton

A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood.

That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. “Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn’t seem to be there before, if only for a short time during a fever or other stress” says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders.

Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child.

As a specialist in the cell’s life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay “higher up” in the cell’s metabolism.

To test the idea, he and colleagues focused on a process called the cell danger response, by which the cell protects itself from threats like infection, temperature changes, and toxins. As part of this strategy, Naviaux explains, “the cells behave like countries at war. They harden their borders. They don’t trust their neighbors.” If the cells in question are neurons, he says, disrupted communication could result—perhaps underlying the social difficulties; heightened sensitivity to sights, sounds, and sensations; and intolerance for anything new that often afflict patients with autism.

The key player may be ATP, the chief carrier of energy within a cell, which can also relay messages to other nearby cells. When too much ATP is released for too long, it can induce a hair-trigger cell danger response in neighboring neurons. In 2013, Naviaux spelled out his hypothesis that autism involves a prolonged, heightened cell danger response, disrupting pathways within and between neurons and contributing to the symptoms of the disorder.

The same year, he and his colleagues homed in on the drug suramin as a way to call off the response. The medication has been in use since the early 20th century to kill the organisms that cause African sleeping sickness. In 1988, it was found to block the so-called purinergic receptors, which bind to compounds called purines and pyrimidines—including ATP. These receptors are found on every cell in the body; on neurons, they help orchestrate many of the processes impaired in autism—such as brain development, the production of new synapses, inflammation, and motor coordination.

To determine if suramin could protect these receptors from overstimulation by ATP, Naviaux’s team worked with mice that developed an autism-like disorder after their mothers had been exposed to a simulated viral infection (and heightened cell danger responses) during pregnancy. Like children with autism, the mice born after these pregnancies were less social and did not seek novelty; they avoided unfamiliar mice and passed up the chance to explore new runs of a maze. In the 2013 paper, the researchers reported that these traits vanished after weekly injections of suramin begun when the mice were 6 weeks old (equivalent to 15-year-old humans). Many consequences of altered metabolism—including the structure of synapses, body temperature, the production of key receptors, and energy transport within neurons—were either corrected or improved.

In the new study, published online today in Translational Psychiatry, the researchers found equally compelling results after a single injection of suramin given to 6-month-old mice (equivalent to 30-year-old humans) with the same autism-like condition. Once again, previously reclusive animals approached unknown mice and investigated unfamiliar parts of a maze, suggesting that the animals had overcome the aversion to novelty that’s a hallmark of autism in children. After the single injection, the team lowered the levels of suramin by half each week. Within 5 weeks most, but not all, of the benefits of treatment had been lost. The drug also corrected 17 of 18 metabolic pathways that are disrupted in mice with autism-like symptoms.

Naviaux cautions that mice aren’t people, and therapies that are promising in rodents have a track record of not panning out in humans. He also says that prolonged treatment with suramin is not an option for children, because it can have side effects such as anemia with long-term use. He notes that there are 19 different kinds of purinergic receptors; if suramin does prove to be helpful in humans, newer drugs could be developed that would target only one or a few key receptors. The researchers are beginning a small clinical trial in humans of a single dose of suramin that they hope will be completed by the end of the year.

The study is exciting, says Bruce Cohen, a pediatric neurologist at Akron Children’s Hospital in Ohio. “The authors have come up with a novel idea, tested it thoroughly, and got a very positive response after one dose.” He notes, however, that the mice with a few characteristics of autism don’t necessarily reflect the entire condition in humans. “Autism isn’t a disease. It’s a set of behaviors contributing to hundreds of conditions and resulting from multiple genes and environmental effects. Great work starts with a single study like this one, but there’s more work to be done.”

http://news.sciencemag.org/biology/2014/06/century-old-drug-reverses-signs-autism-mice