Aspartame may have protective effect against cataract formation

Danbury, CT-Cataract onset appears to be delayed among consumers of diet soda relative to their counterparts who drink non-diet beverages, according to a study by Ralph J. Falkenstein, MD, and colleagues.

"Our conclusion that aspartame usage seems to be associated with a later onset of cataract formation [leads] us to think there might be one pathway that can be modified to reduce the incidence of early-onset cataracts," said Dr. Falkenstein, a private practitioner in Danbury, CT.

To investigate any association between diet soda ingestion and cataract development, researchers queried 216 patients with an extensive dietary questionnaire and performed a comprehensive review of their medical records to determine presence of cataract; age of onset; use of other medications; and history of medical illnesses, particularly diabetes.

Findings from an analysis of a dose-response relationship between diet soda ingestion and age of cataract onset and of a literature review to identify potential biologic mechanism(s) to explain the study's findings were consistent with the concept that aspartame ingestion through diet soda consumption might delay cataract development.

Interest in the association between aspartame usage and cataracts arises from appreciation of the popularity of artificially sweetened beverages and recognition of prior reports linking aspartame to cataracts.

"Americans are drinking more soda than ever; in the year 2000, more than 15 billion gallons were sold in the United States," Dr. Falkenstein said. "That statistic translates to daily consumption of at least one 12-ounce can by every man, woman, and child in this country.

"Aspartame has been the most common agent used as an artificial sweetener in diet sodas since it was FDA-approved in 1981," Dr. Falkenstein added. "Information on the Internet links aspartame with a variety of medical diagnoses-including cataracts-and also attributes cataract formation to the effects of methanol and formaldehyde, which are breakdown products of aspartame."

Later cataract onset

Dr. Falkenstein and his colleagues had noted that the age of onset of cataract among patients in their practice seemed to be later than it was 20 years earlier. Therefore, they designed their study to investigate what they postulated might be a possible protective effect of aspartame ingestion.

Due to the relatively low number of diet soda drinkers in their population of cata-ract patients, the study was not sufficiently powered to investigate whether any statistically significant association existed between volume of diet soda consumed and age of cataract onset. A trend in the available data, however, suggested a relationship between increasing amounts of diet soda ingested and later age of cataract onset.

To gather information that would provide biologic plausibility for the observation, Dr. Falkenstein and colleagues turned to the pharmacologic and biochemical literature. Results of one study showing that ingestion of aspartame results in an increase in aspartame and aspartic acid concentrations in the blood but no elevation of formate and methanol levels above the normal range argued against the hypothesis that aspartame ingestion results in exposure to toxic breakdown products that could cause cataract formation.

Further, one group of investigators reported that incubation with aspartic acid decreased the non-enzymatic glycolation of lens protein, and another research group reported that aspartame and other dipeptides inhibit ascorbic acid-induced lens protein modifications by glycolation.

"Glycolation of lens proteins is thought to play a major role in cataract formation," Dr. Falkenstein said.