Gauging Sugar's Effect on the Brain
By Catherine Hamrick
There was once a time when sodas were considered to be a simple treat. In the words of an old Coca-Cola advertisement, they were the “pause that refreshes,” but pausing is definitely out of fashion today. Caffeine-laced, sugar-laden soft drinks are now our energy source of choice—12-ounce power cells to get us going in the morning and keep us moving all day.
Many of us are starting to realize that this rush comes with consequences, however, and not only in caffeinated jitters. Researchers have blamed sodas for everything from epidemic childhood obesity to kidney stones to osteoporosis, and chilling news reports based on their studies may be at least partly responsible for a recent drop in soft-drink consumption in the United States. But a study published in the Journal of Biological Chemistry by UAB’s Ling Li, D.V.M., Ph.D., a specialist in Alzheimer’s disease, produced what may be the most disturbing news of all. Her animal experiments suggest that soft drinks may be damaging our brains.
Scientists know that high fat intake and being overweight are risk factors for the development of Alzheimer’s, Li says. She wondered if excess consumption of simple sugars—such as those found in non-diet soft drinks—could also play a role, so she designed a small study to address the question.
The experiment divided mice into two groups. Both ate a normal, low-fat rodent diet, but while one group drank unsweetened water, the other was allowed free access to liquids made up of 10 percent sucrose, a sugar content similar to that of most non-diet sodas. This drink proved to be as popular with the mice as it is with humans. “They loved it,” says Li. “They drank much more than those given regular water.” In fact, the average mouse in the sweet group chose to consume the human equivalent of five 12-ounce cans of soda per day.
After six months, the mice received a battery of behavioral tests and physical exams. Unsurprisingly, the sugar-drinking mice gained 17 percent more weight than their water-drinking brethren. Their LDL (so-called “bad”) cholesterol also increased, and the sweet solution seemed to induce insulin resistance, a precursor to diabetes. The eye-opening result, however, was that sweet-drinking mice did poorly on learning and memory tasks. Not only that, but beta-amyloid protein plaques—a hallmark of Alzheimer’s disease—had accumulated in their brains.
“Added sweeteners are important components of the modern human diet,” Li says. She feels they deserve more scientific attention, especially in terms of the chain of effects that high-sugar diets produce. “Compelling evidence indicates that overconsumption of sweet foods, particularly calorically sweetened beverages, plays an important role in the epidemic of obesity worldwide,” says Li. Even moderate obesity, she points out, can contribute to chronic metabolic abnormalities that lead to type 2 (adult-onset) diabetes. And recent epidemiological studies have suggested that type 2 diabetes is associated with a higher incidence of Alzheimer’s.
Although her initial study involved only a small group of test subjects, Li is now expanding the research. “It is imperative to assess the potential detrimental effects of long-term excess consumption of dietary sugars—even with an otherwise normal diet—on age-related diseases such as Alzheimer’s.”