THURSDAY, June 26 (HealthDay News) -- Older adults with type 2 diabetes are apt to have memory problems after eating a meal loaded with fat, but a new study has found the damage can be undone if they take antioxidant vitamins along with the unhealthy food.
However, the researchers emphasize, it is better to eat healthy foods and not rely on vitamins to undo the cognitive harm.
"What we are aiming for is for people to actually eat healthier meals," said study author Michael Herman Chui, a third-year medical student at the University of Toronto. His report is published in the July issue of Nutrition Research.
"From this study, we could conclude that if people continue to eat this kind of meal long-term, the memory impairment would potentially be long-lasting," he said. His co-author is Dr. Carol E. Greenwood, a senior scientist at Baycrest Centre for Geriatric Care, a research and care facility affiliated with the University of Toronto.
In 2003, Greenwood published a paper finding that memory problems occurred after type 2 diabetics ate a meal of rapidly absorbed carbohydrates -- in this case, half a bagel and white grape juice.
In the recent study, Greenwood and Chui added fat to the meal. They looked at the effects of the meal on the cognitive performance of 16 adults with type 2 diabetes, average age 63. The meal included 3,356 calories and had more than 50 grams of fat, more than 63 grams of carbs and more than 25 grams of protein. It included Danish pastry, cheddar cheese and yogurt with whipped cream.
They tested their cognitive performance on various tests 60 minutes and 105 minutes after eating the meal. On a second occasion, the researchers conducted the same tests after the participants ate the same meal but also took 1,000 milligrams of vitamin C and 800 IUs of vitamin E. On a third occasion, they tested the participants again after they had only water.
Eating the high-fat meal without vitamins caused performance to fall in verbal recall and working memory when tested 105 minutes later, compared to the water-only meal. After eating the high-fat meal, participants showed more forgetfulness of words and paragraph information in recall tests.
But when they ate the high-fat meal and took the vitamins, their performance was as good as after the water-only session, Chui said.
The vitamins are thought to work by reducing oxidative stress, which is triggered when levels of free radicals, unstable molecules that can damage brain and other tissues, are elevated. Eating unhealthy foods induces oxidative stress. Having type 2 diabetes is also associated with oxidative stress, which in turn is associated with vascular problems.
The study produced interesting results, said Lona Sandon, an assistant professor at the University of Texas Southwestern Medical Center at Dallas. But she offered several caveats: The study was small, with only 16 participants. Comparing performance after a meal with vitamins to performance after having only water is not the best idea, she said.
"Of course, they would perform poorly with water only; there is no glucose getting to their brains," she explained.
"Type 2 diabetics are encouraged to avoid high-fat meals and choose plenty of fruits and vegetables high in antioxidants," she said.
More study is definitely needed, said Connie Diekman, director of university nutrition at Washington University in St. Louis. Among the unanswered questions: "The meal consumed was not a typical meal, so would the vitamins have similar effect on a more typical meal?"
If anything, Sandon said, the study reinforces standard advice that those with type 2 diabetes should avoid high-fat, rapidly absorbed carbohydrate meals for heart health, blood sugar control, and possibly brain health.
More information
To learn more about healthy eating with diabetes, visit the American Diabetes Association.
MONDAY, June 30 (HealthDay News) -- Caffeine just might prevent multiple sclerosis, a new animal study suggests.
Giving mice the equivalent of 6 to 8 cups of coffee a day prevented mice from getting the animal model equivalent of MS, said Dr. Linda Thompson, of the Oklahoma Medical Research Foundation, and a member of the team reporting the finding in this week's issue of the Proceedings of the National Academy of Sciences.
Multiple sclerosis, an autoimmune disease, affects about 400,000 Americans, according to the National Multiple Sclerosis Society. The T-cells from the body's immune system attack the myelin, the fatty sheath that normally protects the nerve fibers in the central nervous system. This, in turn, produces scar tissue and triggers the symptoms of MS, which can include numbness, weakness, lack of muscle coordination and problems with bladder control, speech and vision.
Here's why the coffee warded off MS, Thompson explained: It prevented the molecule adenosine, one of the four building blocks of DNA, from binding to the adenosine receptor at the cellular level. When adenosine cannot bind to receptors at the cellular level, this in turn prevents T-cells from reaching the central nervous system and setting off the events that lead to the animal version of MS.
"From a scientific point of view, the bottom line is, adenosine in this mouse model is needed for the disease-causing T-cells to get into the central nervous system," Thompson said. "That was the big, unexpected finding."
The discovery shows how important the adenosine molecule is in allowing immune cells to infiltrate the central nervous system. In the animals, the T-cells were activated, but they couldn't get into the central nervous system, because the caffeine was bound to the adenosine receptors.
Dr. John Richert, executive vice president of research and clinical programs for the National Multiple Sclerosis Society, said the new finding is "potentially big news many years down the road."
But he cautioned that the research is in the early stages, and the whole process needs to be studied in humans.
Thompson agreed.
"First, we have to learn if adenosine plays the same role in people," she said. "In humans, it is not known if adenosine regulates the entry of T-cells into the central nervous system."
If the same findings bear out in humans, she said, the hope is to develop a drug that would degrade adenosine, prevent it from being formed, or prevent T-cells from getting into the central nervous system. She noted that the discovery holds promise for other autoimmune diseases, including lupus and rheumatoid arthritis.
The challenge, she said, is that adenosine receptors "are everywhere in the body." So, the drug would have to be specific enough to only act on the adenosine receptors that control access of the T-cells to the central nervous system.
Even so, Richert said, "it's a potential therapeutic target that needs to be explored."
More information
To learn more about multiple sclerosis, visit the National Multiple Sclerosis Society.
