'Office of The Future' Environment Study

Mayo Clinic endocrinologist Dr. James Levine has continued his research in environment-changing innovations with a six-month study of a real-life office that was re-engineered to increase daily physical activity or NEAT (non-exercise activity thermogenesis).

The study began in late 2007 and ended in 2008 at SALO, LLC, a Minneapolis-based financial staffing firm. Of the 45 employee volunteers involved in the scientific study, 18 were studied for weight loss and other changes, according to an announcement of the study.

Re-engineering included:

• Removing chairs and traditional desk seating
• Introducing walking tracks
• Educating and encouraging staff to conduct walking meetings
• Replacing traditional phones with mobile sets
• Adding desks attached to treadmills
• Introducing games in the workplace
• Providing high-tech activity monitors
• Advising staff about nutrition

Results:

• The 18 individuals lost a total of 156 pounds, 143 of that in body fat.
• Individuals lost an average of 8.8 pounds -- 90 percent of that was fat.
• Triglycerides decreased by an average of 37 percent.
• The nine participants who had expressed a desire to lose weight lost an average of 15.4 pounds.

Another key finding -- no productivity was lost due to the new environment. In fact, company officials say revenue rose nearly 10 percent during the first three months of the study, and the company recorded its highest-ever monthly revenue in January 2008 -- the study's midpoint.

Conclusion:

This "office of the future" is a functional environment that can also enhance weight loss and maintain health.

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How We Can Stop Stress From Making Us Obese

Herbert Herzog, Director of the Neuroscience Research Program at the Garvan Institute of Medical Research, together with scientists from the US and Slovakia, have shown that neuropeptide Y (NPY), a molecule the body releases when stressed, can ‘unlock’ Y2 receptors in the body’s fat cells, stimulating the cells to grow in size and number. By blocking those receptors, it may be possible to prevent fat growth, or make fat cells die.

“We have known for over a decade that there is a connection between chronic stress and obesity,” says Herzog. “We also know that NPY plays a major role in other chronic stress-induced conditions, such as susceptibility to infection. Now we have identified the exact pathway, or chain of molecular events, that links chronic stress with obesity.”

“There is not much we can do about the increased levels of NPY caused by stress, but we can do something about the damage it causes. If we can interfere before it causes fat to amass, it could have a major impact on cardiovascular disease, diabetes, and cancer (which all have links with obesity).”

“Basically, when we have a stress reaction, NPY levels rise in our bodies, causing our heart rate and blood pressure to go up, among other things. Stress reactions are normal, unavoidable, and generally serve a useful purpose in life. It’s when stress is chronic that its effects become damaging.”

Scientists at Georgetown University in Washington D.C, part of this collaborative study, have found a direct connection between stress, a high calorie diet and unexpectedly high weight gain. Stressed and unstressed mice were fed normal diets and high calorie (high fat and high sugar, or so called ‘comfort food’) diets. The mice on normal diets did not become obese. However, stressed mice on high calorie diets gained twice as much fat as unstressed mice on the same diet. The novel and unexpected finding was that when stressed and non-stressed animals ate the same high calorie foods, the stressed animals utilised and stored fat differently.

“Our findings suggest that we may be able to reverse or prevent obesity caused by stress and diet, including the worst kind of obesity; the apple-shaped type, which makes people more susceptible to heart disease and diabetes,” says senior author of the Nature Medicine paper, Professor Zofia Zukowska of Georgetown University. “Using animal models, in which we have either blocked the Y2 receptor, or selectively removed the gene from the abdominal fat cells, we have shown that stressed mice on high calorie diets do not become obese. “Even more surprisingly, in addition to having flatter bellies, adverse metabolic changes linked to stress and diet, which include glucose intolerance and fatty liver, became markedly reduced. We do not know yet exactly how that happens, but the effect was remarkable,” she says.

Herzog believes that these research findings will have a profound effect on the way society will deal with the obesity epidemic. “There are millions of people around the world who have lived with high levels of stress for so long their bodies think it’s ‘normal’. If these people also eat a high fat and high sugar diet, which is what many do as a way to reduce their stress, they will become obese.”

“Until now, the pharmaceutical industry has focused on appetite suppressants with only moderate success. Our hope is that in the near future pharmaceutical companies, using the results of our research, will develop antagonists against the Y2 receptor that will bring about a reduction in fat cells.”






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