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Showing posts with label FOOD ADDITIVES. Show all posts
Showing posts with label FOOD ADDITIVES. Show all posts

UA to Serve Up Fresh Approach to Health

The commitment of the Department of Nutritional Sciences to promoting and adapting Mediterranean diet principles will continue through all three areas of the University’s land grant mission: academic programs, research and Cooperative Extension outreach programs. Credit: UA

The Mediterranean diet has seen growing global popularity as researchers find that the dietary pattern can help prevent or reduce obesity, heart disease, type 2 diabetes and certain types of cancer.

Responsive to that popularity, the University of Arizona Department of Nutritional Sciences is hosting a series of events meant to explore and share current research related to the dietary pattern, which focuses on fresh fruits and vegetables, whole grains, beans and nuts, along with lesser amounts of lean fish, meats, dairy, olive oil and red wine.

"We want to emphasize how this pattern of eating has been demonstrated to contribute to disease prevention," said Donato Romagnolo, a professor in the Arizona Cancer Center and the nutritional sciences department, which is housed in the UA College of Agriculture and Life Sciences. 

National Geographic Blue Zones speaker Rudy Maxa, a Washington Post reporter and columnist, and five Tucson-area celebrity chefs will kick off the Jan. 28 opening-night reception, "A Food, Wine and Healthy Living Event," at the Tucson Museum of Art.

The 6-8 p.m. event is open to the public and will feature food prepared by the chefs, award-winning wine provided by the Arizona Wine Growers Association and live flamenco and Spanish guitar.

Then the UA will will host the Jan. 29-30 "Health Benefits of the Mediterranean Diet – Bringing Science to the Plate (With an Arizona Twist!)" scientific conference at the Student Union Memorial Center.

Supported in part by a grant from the U.S. Department of Agriculture, the conference is geared toward public health and nutrition professionals, nurses, physicians, physical therapists and chiropractors, and it is offered for continuing professional credit. The event is also open to students and features a student showcase.

A full agenda and registration for the conference are available online.

Promoting the health benefits of the Mediterranean lifestyle is just one of numerous initiatives sponsored by the UA Department of Nutritional Sciences to advance optimal health and well-being for Arizonans and to focus on ways of preventing and treating chronic diseases. 

After the conference, a four-part, hands-on cooking series will be offered to the public during February and March at the UA Cooperative Extension's Garden Kitchen, "The Many Faces of the Mediterranean Diet: Four Evenings," featuring the cuisines of Spain, France, Morocco and Italy. Information is available online. 

Also, the Mediterranean Diet and Health course will be offered for academic credit during summer 2015 (one week in Tucson and three weeks in Verona, Italy) for students through the UA Global Initiatives Study Abroad Program.

Much of the interest in the Mediterranean diet stems from evidence that it can reduce the risk of death associated with heart disease and cancer. Other research indicates that the diet can reduce the incidence of Parkinson's and Alzheimer's diseases.

Romagnolo, also the program director of the Mediterranean Diet and Health Study Abroad Program, said the benefits are especially important given pervasive health concerns across the nation. He noted that about 60 percent of people in the U.S. are overweight and 30 percent are obese.

"The latter is a risk factor for diabetes, cancer and metabolic syndrome," Romagnolo said.
During the conference, more than 20 presenters from the UA College of Agriculture and Life Sciences, the UA College of Medicine, national and international universities, institutes and organizations will talk. 

Presenters will cover four general areas: the Mediterranean diet and regional trends; obesity, diabetes and healthy aging; cancer prevention and control; and methods for translating science to the plate.

Live demonstrations by Arizona growers, vendors and educators will provide attendees with tasting opportunities, meal preparation ideas and information on where to find local products that help make healthful eating easy in the Southwest.

Also, prominent diet researchers from Spain, France and Greece will present current research on the health benefits of the traditional Mediterranean diet and offer ways to adapt it using local agricultural ingredients and cooking techniques. Speakers include:

Lluis Serra-Majem of the University of Las Palmas de Gran Canaria, Spain, who will present the keynote address on "The Mediterranean Diet as an Intangible and Sustainable Food Culture."

Mariette Gerber of the INSERM-Institut du Cancer de Montpellier, France, who will discuss "Implementing the Mediterranean Diet: The French Perspective." 

Antonia Trichopoulou of the University of Athens, Greece, who will speak on "Mediterranean Diet and Longevity."

"The conference is an opportunity to present ideas and concepts that may be adopted by the food industry, nutritionists, researchers and policymakers to help reduce the burden of these chronic diseases," Romagnolo said. "We want to show people how they can do it on their own and apply the basic tenets of the diet here in Arizona."

Source: University of Arizona

New Weight Loss Device Makes You Feel Full

People who are obese have a new tool in their arsenal for fighting excess weight.

The U.S. Food and Drug Administration approved a medical device called the Maestro Rechargeable System that is implanted in the stomach and, through an external, adjustable controller, helps obese people lose weight. It is approved for patients 18 and older who have a body mass index of 35 to 45, have a condition related to being obese such as type 2 diabetes, and have not been able to lose weight through traditional means. 

The Maestro Rechargeable System targets nerve pathways between the brain and the stomach that are responsible for making a person feel full. In a clinical trial, patients using the device lost 8.5% more weight than people who received an inactive version of it. About 53% of the patients with the device lost at least 20% of their excess weight, and 38% lost at least 25%.

But compared with bariatric surgery, the trial’s results are not as impressive. Eric T. Volckmann, M.D., who specializes in bariatric surgery at University of Utah Health Care, says that after gastric bypass surgery, patients can expect to lose 60% to 80% of their excess body weight.

Bariatric surgery is a highly invasive procedure. But so is implantation of the Maestro Rechargeable System. 

“Any procedure, no matter how small, is still risky,” Volckmann says.

Furthermore, Volckmann says the long-term effects of the device are not as well understood as those of bariatric surgery. He says more research is needed before he would recommend the Maestro Rechargeable System for a severely obese patient.

In the future, the device may make sense for a patient with a BMI between 30 and 35 who is not responding to medical weight loss measures such as lifestyle modifications.

Source: University of Utah

Heart drug may help treat ALS, mouse study shows

In the top image, cells from a mouse model of amyotrophic lateral sclerosis caused normal healthy brain cells (green) to die. But when scientists blocked an enzyme in the cells from the mouse model, more of the normal cells and their branches survived (bottom). Credit: Nature Neuroscience
Digoxin, a medication used in the treatment of heart failure, may be adaptable for the treatment of amyotrophic lateral sclerosis (ALS), a progressive, paralyzing disease, suggests new research at Washington University School of Medicine in St. Louis.

ALS, also known as Lou Gehrig's disease, destroys the nerve cells that control muscles. This leads to loss of mobility, difficulty breathing and swallowing and eventually death. Riluzole, the sole medication approved to treat the disease, has only marginal benefits in patients.
But in a new study conducted in cell cultures and in mice, scientists showed that when they reduced the activity of an enzyme or limited cells' ability to make copies of the enzyme, the disease's destruction of nerve cells stopped. The enzyme maintains the proper balance of sodium and potassium in cells.

"We blocked the enzyme with digoxin," said senior author Azad Bonni, MD, PhD. "This had a very strong effect, preventing the death of nerve cells that are normally killed in a cell culture model of ALS."

The findings appear online Oct. 26 in Nature Neuroscience.

The results stemmed from Bonni's studies of brain cells' stress responses in a mouse model of ALS. The mice have a mutated version of a gene that causes an inherited form of the disease and develop many of the same symptoms seen in humans with ALS, including paralysis and death.

Efforts to monitor the activity of a stress response protein in the mice unexpectedly led the scientists to another protein: sodium-potassium ATPase. This enzyme ejects charged sodium particles from cells and takes in charged potassium particles, allowing cells to maintain an electrical charge across their outer membranes.

Maintenance of this charge is essential for the normal function of cells. The particular sodium-potassium ATPase highlighted by Bonni's studies is found in nervous system cells called astrocytes. In the ALS mice, levels of the enzyme are higher than normal in astrocytes.

Bonni's group found that the increase in sodium-potassium ATPase led the astrocytes to release harmful factors called inflammatory cytokines, which may kill motor neurons.

Recent studies have suggested that astrocytes may be crucial contributors to neurodegenerative disorders such as ALS, and Alzheimer's, Huntington's and Parkinson's diseases. For example, placing astrocytes from ALS mice in culture dishes with healthy motor neurons causes the neurons to degenerate and die.

"Even though the neurons are normal, there's something going on in the astrocytes that is harming the neurons," said Bonni, the Edison Professor of Neurobiology and head of the Department of Anatomy and Neurobiology.

How this happens isn't clear, but Bonni's results suggest the sodium-potassium ATPase plays a key role. When he conducted the same experiment but blocked the enzyme in ALS astrocytes using digoxin, the normal motor nerve cells survived. Digoxin blocks the ability of sodium-potassium ATPase to eject sodium and bring in potassium.

In mice with the mutation for inherited ALS, those with only one copy of the gene for sodium-potassium ATPase survived an average of 20 days longer than those with two copies of the gene. When one copy of the gene is gone, cells make less of the enzyme.

"The mice with only one copy of the sodium-potassium ATPase gene live longer and are more mobile," Bonni said. "They're not normal, but they can walk around and have more motor neurons in their spinal cords."

Many important questions remain about whether and how inhibitors of the sodium-potassium ATPase enzyme might be used to slow progressive paralysis in ALS, but Bonni said the findings offer an exciting starting point for further studies.

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