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Scientific evidence that macaroni and cheese, ice cream, and chocolate do indeed comfort. August 2, 2011

Posted by ADAM PARTNERS in Carbohydrates, COMFORT FOODS, DRUG ADDICTION, FOOD, Obesity, Pharmacology, Uncategorized.
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High resolution fMRI of the Human brain.


In an experiment with healthy volunteers, researchers found fatty acids administered to the stomach blunt the behavioral and nerve cell responses to sad emotion, providing scientific evidence that comfort foods such as macaroni and cheese, ice cream, and chocolate do indeed comfort.

The brief report was published online July 25 in the Journal of Clinical Investigation. “Everyone knows this from personal experience,” lead author Lukas Van Oudenhove, MD, PhD, from the University of Leuven, Belgiumtold Medscape Medical News. “Now we have scientific proof that this widely known phenomenon has a scientific basis.”Dr. Van Oudenhove explained that he has always been interested in gut brain signalling in the context of gastrointestinal pain.

“I have performed studies where we do distention of the stomach and the esophagus and look at the brain mechanisms that are involved in processing these painful and nonpainful sensations. Those studies showed that emotions could modulate or interact with these sensations,” he said.

By chance, his colleagues at the University of Manchester, in the United Kingdom, had been studying signals in the brain induced by fatty acids in the stomach when Dr. Van Oudenhove arrived there to do a fellowship. It was then that the researchers decided to see just how emotions interact with the gut brain signals generated by fatty acids.

To do this, they recruited healthy volunteers to undergo four 40-minute functional magnetic resonance imaging (fMRI) examinations while listening to emotional music and viewing sad, fearful faces to induce sad emotion. At the same time, the participants randomly received either a saline or a fatty-acid intragastric infusion.

The researchers rated the participants’ sensations of hunger, fullness, and mood.

The investigators found that participants receiving the fatty acids reported feeling less sad when they were viewing the sad faces or hearing the sad music. In addition, the fMRI images of the brain showed that fatty-acid infusion lessened the neural responses to sad emotions in regions of the brain, including the medulla/pons, midbrain, hypothalamus, thalamus, striatum, cerebellum, insula, hippocampus, amygdala, and cingulate cortex.

“We already knew that there was some interactions between emotions and food, but mostly we were thinking about that in terms of the sensory aspects of feeding, like smell and taste and sight,” Dr. Van Oudenhove said.

“Here, we showed for the first time that if you bypass all of this and you administer foods in a completely subconscious way, without anyone knowing whether they were getting saline or fatty acids, we still see this effect on emotion. This is where the novelty of this study lies.”

Not Ready for Prime Time

As intriguing as the finding is, there is still a long way to go before it can be applied clinically, Dr. Van Oudenhove said.

“This study needs to be replicated in a larger sample of healthy volunteers to confirm our results and also to tease out the mechanisms of communication between the gut and the brain that are actually involved in the phenomenon that we described. We need to establish exactly how this works,” he said.

If this pans out, the next step would be to see whether these mechanisms are abnormal in people with certain disorders, such as depression, obesity, and eating disorders.

“It’s only after we show that gut brain signalling is abnormal in these conditions that we can start thinking about any therapeutic implications. So I see this more as a preclinical study,” Dr. Van Oudenhove said.

In an accompanying editorial, Giovanni Cizza, MD, PhD, and Kristina I. Rother, MD, from the National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, write that the field of research on the mind-body connection “has suffered from a Cartesian top-down approach, in which the brain or mind is presumed to influence the body.”

This study shows that this mind-body relationship is bi-directional and that the body can be a powerful modulator of emotions, they note, citing as an example the practice by neonatologists of giving sugar to a neonate before they perform an invasive procedure to shorten the time the baby cries in pain.

The study broadens “our understanding of the ties between food and mood and underscore promising targets for obesity treatments,” they write.



Posted by ADAM PARTNERS in Atkins Diet, DIETRY GUIDELINES FOR AMERICANS, Dr Atkins, High Fat Low Carb Diet, Obesity.
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Railroad tank car transporting high fructose c...

Railroad tank car transporting high fructose corn syrup.

Results from a new study show that adults who consumed 25% of their daily calories as fructose or high-fructose corn syrup beverages (a percentage within current government guidelines) for 2 weeks experienced increases in serum levels of cholesterol and triglycerides, to prove Dr Atkins true on his account that sugar consumption was directly linked to high cholesterol.

The authors of the study, recently accepted for publication in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolismand slated to be published in the October 2011 print issue, say the results should spur the government to reevaluate the guidelines.

Senior author Kimber Stanhope, PhD, from the departments of nutrition and molecular biosciences, University of California, Davis, and colleagues say the study was conducted to help sort out a discrepancy in 2 prominent sets of recommendations: The Dietary Guidelines for Americans, jointly published by the US Department of Health and Human Services and the US Department of Agriculture, recommend that people consume a maximum of 25% of their daily calories as added sugars. In contrast, the American Heart Association recommends an upper limit of 5%.

“While there is evidence that people who consume sugar are more likely to have heart disease or diabetes, it is controversial as to whether high sugar diets may actually promote these diseases, and dietary guidelines are conflicting,” remarked Dr. Stanhope in a press release.

To shed light on the effects of the higher government-recommended threshold, the researchers had 48 overweight and normal-weight adults (age, 18-40 years; body mass index, 18-35 kg/m2) consume beverages that contained fructose, high-fructose corn syrup, or glucose at the 25% upper limit for calorie intake for 2 weeks.

During the first 3.5 days of the trial, the participants stayed at an inpatient facility for baseline testing while consuming a balanced diet consisting of 55% complex carbohydrates. The following 12 days were at home on an ad libitum diet with the addition of 3 daily drinks of glucose-, fructose-, or high-fructose corn syrup-sweetened beverages (n = 16/group) that provided 25% of their energy requirements. The last 3.5 days were spent back at the inpatient facility for repeated testing while the participants were consuming energy-balanced diets containing 25% sugar-sweetened beverages and 30% complex carbohydrate.

At the end of the study period, participants who consumed fructose or high-fructose corn syrup in their drinks exhibited elevated blood levels of low-density lipoprotein (LDL) cholesterol, triglycerides, and apolipoprotein B (apo B).

Participants who consumed glucose in their beverages exhibited no such changes. More specifically, the 24-hour triglyceride area under the curve (AUC) increased compared with baseline during consumption of fructose (increase, 4.7 ± 1.2 mmol/L x 24 hours; = .0032) and high-fructose corn syrup (increase, 1.8 ± 1.4 mmol/L x 24 hours; = .035), but not glucose (decrease, 1.9 ± 0.9 mmol/L x 24 hours; = .14). Similarly, fasting LDL and apoB concentrations were increased during consumption of fructose (LDL increase, 0.29 ± 0.082 mmol/L; = .0023; apoB increase, 0.093 ± 0.022 g/L; = .0005) and high-fructose corn syrup (LDL increase, 0.42 ± 0.11 mmol/L; < .0001; apoB, 0.12 ± 0.031 g/L; < .0001), but not glucose (LDL increase, 0.012 ± 0.071 mmol/L, P= .86; apoB increase, 0.0097 ± 0.019 g/L; = .91).

One limitation is the lack of inclusion of sucrose in the study.

“There is growing evidence linking increases of postprandial triglyceride concentrations with proatherogenic conditions,” Dr. Stanhope and her colleagues explain. Their results add to this existing evidence, even in young adults. “It is [also] important to note,” write the authors, “that for both the current and [a] previous study [by our research group], the differential effects of fructose and [high-fructose corn syrup] compared to complex carbohydrate on the 24-h [triglyceride] profile were most marked in the late evening, approximately 4 and 6 hours after dinner. Studies investigating the relationship between this late-evening peak and proatherogenic changes would be of interest, as would investigations into the sources of the [triglycerides] that contributes to these peaks,” such as diet or fatty acids derived from adipose lipolysis.

According to the researchers, survey data suggest that 13% of the US population consumes 25% or more of their calories from added sugar. The current data provide evidence that this level of sugar consumption in young, healthy, normal, and overweight adults contributes to dyslipidemia after only 2 weeks and contradicts conclusions from recent reviews suggesting that “sugar intakes as high as 25-50% of energy have no adverse long-term effects” in terms of the metabolic syndrome, and “that fructose consumption up to 140 grams/day does not result in a biologically relevant increase of fasting or postprandial [triglycerides] in healthy, normal weight or overweight or obese” individuals.

Furthermore, the researchers conclude, their findings indicate the need for the government to reconsider its recommendations that include a maximal upper limit of 25% of total energy requirements from added sugar.

The study was supported by the National Heart, Lung and Blood Institute and by the National Center for Research Resources, both of the National Institutes of Health. One author has consulted for Denka Seiken Company and for Otsuka Pharmaceutical Company, Ltd, both in Tokyo, Japan. Another author is currently employed by Denka Seiken Co., and a third was formerly employed by this same company. Dr. Stanhope and the remaining 8 authors have disclosed no relevant financial relationships.

High-Fat Diets Won’t Harden Arteries Low-carbohydrate diets that require patients to fill up on fats won’t lead to harder arteries, researchers say June 3, 2011

Posted by ADAM PARTNERS in High Fat Low Carb Diet, Obesity.
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Those who lost 10 pounds after curbing their carb intake had no differences in arterial stiffness than those on a more traditional, low-fat diet, Dr. Kerry Stewart of Johns Hopkins and colleagues reported at the American College of Sports Medicine meeting in Denver. “Losing weight may be more important to [arterial] health than the diet you’re on,” Stewart said. Some researchers have raised concerns that replacing carbs with fats may have adverse effects on blood vessels, especially since promoting consumption of fats runs “counter to what the public has been told [about reducing fat intake] for the last 20 or so years,” Stewart said. Yet studies have shown that a low-carb diet can have positive effects on blood pressure, cholesterol, and other parameters that may reduce the risk of the artery disease atherosclerosis and subsequent heart disease. So to assess what the diets are actually doing to patients’ arteries, Stewart and colleagues enrolled 55 overweight or obese but healthy patients ages 30 to 65 in a lifestyle modification program. None had heart disease or other markers of cardiovascular risk at enrollment. In addition to a supervised exercise program — an hour-long regimen three days per week — patients were randomized to either a low-carb or low-fat diet for six months. The researchers monitored arterial stiffness and other measures of blood vessel health. For this analysis, the researchers had data on 23 of 28 patients who lost 10 pounds on the low-carb diet, and 23 of 27 who did so on the traditional diet. Those on the low-carb diet lost the 10 pounds sooner than the low-fat group did — just 45 days instead of 70 days. There were no changes in arterial stiffness or endothelial function in either diet group, and that didn’t change after the results were adjusted for the time it took to shed 10 pounds, Stewart said. “My theory is that if people can achieve weight loss, it will benefit vasculature in every other system of body,” he told “Weight loss, in the long run, will count more than the specific content of the diet.” Nor were there any acute effects on vascular function after a lone high-fat meal, the researchers found. In a companion study, 66 patients had no changes in endothelial function after eating a 900-calorie, 50-grams-of-fat meal from McDonald’s. In fact, arterial stiffness significantly improved by 16 percent after that feast, the researchers found. “It really seemed to make the arteries relax more, but we’re not entirely sure how,” Stewart said. “We’ll have to look more deeply into that.” Some researchers contacted for outside comment said longer-term follow up may be needed to confirm those benefits. And analyses of the diet study that include the type of fats eaten would be helpful, they said. “It would be nice to know what the fat consisted of, as some may be safer than others — i.e. monounsaturated fats and omega-3 fatty acids and even polyunsaturated fats would be better than saturated fats,” said Dr. Carl Lavie of the University of Queensland in New Orleans, who was not involved in the study. Stewart said that upcoming analyses will break down the type of fats consumed, and that the dieticians involved in the study advised patients to stick to these healthier fats. He added that the work should help allay physicians’ concerns about recommending a low-carbohydrate diet — something the medical community has largely been reluctant to do, he said.

Can You Be Addicted to Foods? May 26, 2011

Posted by ADAM PARTNERS in Possible causes of Obesity Epidemic in USA.

Many people tend to think that all obese people have to do to solve their problems is eat less and move more. Alcoholics, on the other hand, need treatment.

But are the two disorders really all that different? Is it possible that eating in today’s sweet and salty fast-food world is actually somewhat, well, addictive? Could people with a predilection to abusing alcohol and drugs just as easily abuse food?

study published in The Archives of General Psychiatry this week is not the first to examine the neurobiological similarities between behaviors that drive obesity and those that drive substance abuse. The researchers, from Washington University School of Medicine in St. Louis, examined two large surveys of nationally representative samples of American adults questioned about alcoholism in their families. Each included about 40,000 adults; one survey was carried out in 1991 and 1992; the other was done a decade later, in 2001 and 2002.

The people surveyed were asked whether a relative had “been an alcoholic or problem drinker at any time in his/her life,” a question repeated for several types of relative — mother, father, brother, sister, half-sibling and children. Participants also reported their own weight and height, so body mass index could be calculated (B.M.I. is a calculation of weight in kilograms divided by height in meters squared, and a result of 30 or more is considered obese).

The first survey, from the early 1990s, found no link between a family history of alcoholism and obesity. “There was an almost perfect overlap between the B.M.I. distribution of people without a family history of alcoholism and people with a family history of alcoholism,” said Richard A. Grucza, assistant professor of psychiatry at Washington University and lead author of the new paper.

Ten years later the survey told a different story. In 2001 and 2002, adults with a family history of alcoholism were 30 to 40 percent more likely to be obese than those with no alcoholism in the family. Women were at particularly high risk: they were almost 50 percent more likely to be obese if there was family alcoholism than if there wasn’t. (Men were 26 percent more likely to be obese.)

Why the change over time? Dr. Grucza says our so-called obesigenic, or obesity-inducing, food environment has changed in the decade between the two surveys. The most likely culprit, he said, “is the nature of the food we eat, and its tendency to appeal to the sorts of reward systems, which are the parts of the brain implicated in addiction.”

Certain foods — loaded with sugar, salt and fat and specially formulated to appeal to consumers — might be cues that trigger overeating in people with the predisposition for addiction, appealing to the primitive reward centers of the brain, and reinforcing the addictive behavior. These types of foods, which the former Food and Drug Administration commissioner Dr. David Kessler has called “hyperpalatable,” may be more reinforcing of overeating than, say, green vegetables, Dr. Grucza said, and they’re more commonly and easily available than they were in the past.

In his book “The End of Overeating,” Dr. Kessler describes how these highly palatable foods — the kind served at fast-food and chain restaurants — change brain chemistry, triggering a neurological response that stimulates people to crave more food, even if they’re not hungry. The sense some people have that they cannot control their intake may in fact be true, he argues, because these rich, sweet and fatty foods stimulate the brain to release dopamine, a neurotransmitter associated with the pleasure center. In the process, they rewire the brain, so that the dopamine pathways light up even at the thought of eating these foods.

Other explanations for the increased obesity among relatives of alcoholics are possible, however. For example, it may be that people from families with alcoholism are more susceptible to stress generally, or to suffer from underlying depression that leads them to drink or overeat.

No single gene is responsible for making someone obese or alcoholic, Dr. Grucza said. But people who eat or drink excessively may share critical characteristics like lack of impulse control and the inability to stop once they get started, a sort of “missing stop signal,” he said. Stress is also implicated in both behaviors.

“The notion of alcoholism being a disease can be oversimplified,” Dr. Grucza said. “At some point, it’s a behavior and a choice. It’s just that some people are more vulnerable to the effect of that choice than others. I think the same is probably true of overeating — some people just don’t have the predisposition to find certain kinds of food that pleasurable, or to eat that much.”

Central Heating May Be Making Us Fat May 26, 2011

Posted by ADAM PARTNERS in Possible causes of Obesity Epidemic in USA.
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Americans like to crank up the heat in the winter — and some scientists think it’s making us fat. Turn down the thermostat, they say, and you might lose a few pounds.

The link between ambient temperature and weight is not completely far-fetched. When we’re exposed to extreme cold, we shiver, an involuntary reaction that makes our skeletal muscles contract to generate heat, burning extra calories in the process.

And even in mildly cold conditions, like in a chilly room with the thermostat turned down to the lower 60s, people generate extra heat without shivering. The process, called non-shivering thermogenesis, may involve a substance called brown fat that adults carry in certain areas, like the upper back and side of the neck. Unlike regular fat, which stores excess energy and calories, brown fat acts like an internal furnace that consumes lots of calories, but it has to be activated first — and cold temperatures do that.

Now, in a provocative new paper, British researchers argue that rising indoor temperatures are contributing to obesity. The research team included scientists from several disciplines, including health psychologists, biologists and those who specialize in the effects of indoor environments.

The hypothesis was initially put forth several years ago in a paper listing 10 “putative contributors” to obesity, including environmental endocrine disruptors, pharmaceuticals that induce weight gain, sleep debt, older mothers having children and epigenetic changes, or environmental factors that influence the expression of our genes.

The newer paper, published this week in the journal Obesity Reviews, looked specifically at indoor temperatures. The researchers found that since central heating became commonplace in the 1960s, room temperatures have increased slowly but steadily in both the United States and Britain. In both countries, obesity has also been on the rise.

The average temperature of living rooms in Britain, around 64.9 degrees Fahrenheit in 1978, had risen to 70.3 degrees by 2008. Bedrooms, kept at 59 degrees in 1978, were up to 65.3 by 1996, the last year figures were available.

In the United States, living rooms have long been heated to just over 70 degrees in the winter, at least when the house is occupied. Bedroom temperatures continue to rise and were up to 68 as of 2005, from 66.7 in 1987.

“What’s particularly noticeable is that people are heating the whole of their house,” said Fiona Johnson, a research fellow at University College London and the paper’s lead author. “In the past they would heat the main living areas, and the bedrooms might be cold at night.” That means people no longer have to adjust to different temperatures as they move through the house.

In addition, most people get around town in heated cars, instead of walking, and children spend less time playing outdoors.

All this time spent in toasty interiors may be affecting the levels of brown fat we carry, Dr. Johnson said. “It’s kind of ‘use it or lose it,’ ” she said. “If you’re not exposed to cold, you’re going to lose your brown fat, and your ability to burn energy will be affected. But you can get it back.”

While we all start out with substantial amounts of brown fat as babies, “it gradually decreases over the life course,” she said. “But if it is needed — if we’re regularly exposed to cold — the body can actually generate more brown fat.”

That is not to say exposure to cold is a major driver of obesity: overeating and lack of exercise are the main causes.

But could lowering the thermostat make a notable difference in people’s weight?

Dr. C. Ronald Kahn, a Harvard Medical School professor who does research on brown fat, says it might actually help with weight control over time, provided people stick with it.

“When we put people in a 60-degree room, they increase their energy expenditure by 100 or 200 calories a day if they’re in light clothing,” like hospital scrubs, he said. “They’re not shivering. They activate their brown fat.”

Over a period of several weeks, they will have burned an extra 3,500 calories, which translates into the loss of one pound. Wearing a sweater will dilute the effect.

The problem, Dr. Kahn said, is that “most people won’t stay at that temperature for very long.”

Less Active at Work, Americans Have Packed on Pounds May 26, 2011

Posted by ADAM PARTNERS in Possible causes of Obesity Epidemic in USA.
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Getty Images/SuperStockA worker operates a press at the New Orleans Times-Picayune, typical of the physical activity that was common in many workplaces in earlier decades.

Looking beyond poor eating habits and a couch-potato lifestyle, a group of researchers has found a new culprit in the obesity epidemic: the American workplace.

A sweeping review of shifts in the labor force since 1960 suggests that a sizable portion of the national weight gain can be explained by decliningphysical activity during the workday. Jobs requiring moderate physical activity, which accounted for 50 percent of the labor market in 1960, have plummeted to just 20 percent.

The remaining 80 percent of jobs, the researchers report, are sedentary or require only light activity. The shift translates to an average decline of about 120 to 140 calories a day in physical activity, closely matching the nation’s steady weight gain over the past five decades, according to the report, published Wednesday in the journal PLoS One.

Today, an estimated one in three Americans are obese. Researchers caution that workplace physical activity most likely accounts for only one piece of the obesity puzzle, and that diet, lifestyle and genetics all play an important role.

But the new emphasis on declining workplace activity also represents a major shift in thinking, and it suggests that health care professionals and others on the front lines against obesity, who for years have focused primarily on eating habits and physical activity at home and during leisure time, have missed a key contributor to America’s weight problem. The findings also put pressure on employers to step up workplace heath initiatives and pay more attention to physical activity at work.

“If we’re going to try to get to the root of what’s causing the obesity epidemic, work-related physical activity needs to be in the discussion,” said Dr. Timothy S. Church, a noted exercise researcher at the Pennington Biomedical Research Center in Baton Rouge, La., and the study’s lead author. “There are a lot of people who say it’s all about food. But the work environment has changed so much we have to rethink how we’re going to attack this problem.”

The report shows that in 1960, one out of two Americans had a job that was physically active. Now it is estimated that only one in five Americans achieves a relatively high level of physical activity at work. Dr. Church notes that because the research doesn’t factor in technological changes, like increasing reliance on the Internet and e-mail, many people in service and desk jobs that have always involved only light activity are now moving less than ever, meaning the findings probably understate how much physical activity has been lost during work hours.

While it has long been known that Americans are more sedentary at work compared with the farming and manufacturing workers of 50 years ago, the new study is believed to be the first in which anyone has estimated how much daily caloric expenditure has been lost in the workplace.

“It’s a light bulb, ‘aha’ moment,” said Barbara E. Ainsworth, the president-elect of the American College of Sports Medicine and an exercise researcher at Arizona State University. “I think occupational activity is part of that missing puzzle that is so difficult to measure, and is probably contributing to the inactivity and creeping obesity that we’re seeing over time.”

For years, the role that physical activity has played in the obesity problem has been uncertain. Numerous studies suggest there has been little change in the average amount of leisure-time physical activity, posing a conundrum for researchers trying to explain the country’s steady weight gain. As a result, much of the focus has been on the rise of fast-food and soft drink consumption.

Other studies have suggested that changing commuting habits, declining reliance on public transportation and even increased time in front of the television have played a role in the fattening of America. But none of those issues can fully explain the complex changes in nationwide weight-gain patterns.

Some earlier research has hinted at the fact that workplace physical activity is associated with weight and health. One seminal set of studies of London bus drivers and conductors showed that the sedentary bus drivers had higher rates of heart disease than the ticket-takers, who moved around during the workday.

Dr. Church said that during a talk on the country’s obesity patterns, he was struck by the fact that Mississippi and Wisconsin both have high rates of obesity, despite having little in common in terms of demographics, education or even weather. It occurred to him that both states have waning agricultural economies, prompting him to begin exploring the link between changes in the labor force and declines in workplace physical activity.

He quickly discovered that a decline in farming jobs alone could not explain increasing obesity around the country, and began exploring job shifts over several decades. Using computer models, Dr. Church and colleagues assigned metabolic equivalent values to various job categories and then calculated changes in caloric expenditure at work from 1960 to 2008.

“You see the manufacturing jobs plummet and realize that’s a lot of physical activity,” said Dr. Church. “It’s very obvious that the jobs that required a lot of physical activity have gone away.”

Ross C. Brownson, an epidemiologist at Washington University in St. Louis, said that both health professionals and the public needed to broaden the traditional definition of physical activity as something that occurs during planned exercise, like running or working out at the gym.

“We need to think about physical activity as a more robust concept than just recreational physical activity,” said Dr. Brownson, whose 2005 report on declining physical activity in the workplace is cited in the PLoS One report. “In many ways we’ve engineered physical activity out of our lives, so we’ve got to find ways to put it back into our lives, like taking walks during breaks or having opportunities for activity that are more routine to our daily lives, not just going to the health club.”

Researchers said it is unlikely that the lost physical activity can ever be fully restored to the workplace, but employers do have the power to increase the physical activity of their employees by offering subsidized gym memberships or incentives to use public transit. Some companies have set up standing workstations, and marketers now offer treadmill-style desks. Employers can also redesign offices to encourage walking, by placing printers away from desks and encouraging face-to-face communication, rather than e-mail.

“The activity we get at work has to be intentional,” said Dr. Ainsworth. “When people think of obesity they always think of food first, and that’s one side of it, but it’s high time to look at the amount of time we spend inactive at work.”

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