Grapefruit have strong antioxidant properties that can have healing effects on stomach ulcers

May 17 2005

Extracts of the popular diet item grapefruit have strong antioxidant properties that can have healing effects on stomach ulcers, according to a new study presented today at Digestive Disease Week 2005 (DDW).

In a second study, researchers clarified that while females metabolize alcohol differently in the body, they are more susceptible to alcohol-related liver injury than males. DDW is the largest international gathering of physicians, researchers and academics in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery.

"Choices in food and the amount of alcohol intake can influence a number of bodily systems, most notably the GI and liver tract," said Lee Kaplan, M.D., Ph.D., of Massachusetts General Hospital. "Incorporating healthy eating habits and lifestyle choices can directly benefit digestive and overall health over the long term."

Role of Lipid Peroxidation, Expression, and Activity of Superoxide Dismutase amd Endogenous Prostaglandins in the Acceleration of Ulcer Healing by Grapefruit Seed Extract (Abstract 569)

In addition to being a staple in the United States "5-a-day" fruit intake recommendations, grapefruit seed extract (GSE) contains nutrients with antioxidant properties that maintain digestive health. While grapefruit is often associated with acidity and GI irritation, GSE actually possesses antibacterial and antioxidative properties that calm the gastric tract. Researchers from Jagiellonian University Medical College in Poland examined the beneficial healing effects of GSE on preexisting gastric ulcers.

For the study, investigators induced gastric ulcers in rats and applied graded doses of GSE (2-20 mg/kg) to measure levels of gastric secretion, one the major causes of gastric ulcers. The team tested ulcer healing by using a combination of acetic acid (an acid compound used to induce experimental ulcers) with or without a COX-1 inhibitor (indomethacin, 2 mg/kg) and a COX-2 inhibitor (rofecoxib, 10 mg/kg).

Rats treated with GSE at 10 mg/kg experienced a 50 percent reduction in gastric acid secretion, and a progressive decrease in the area of gastric ulcers by days six and nine of treatment. The treatment also prompted a significant rise in blood flow at the ulcer sites. In addition, the effects were completed abolished by indomethacin, and significantly inhibited by rofecoxib.

Researchers concluded that treatment with GSE does accelerate ulcer healing via a mechanism involving COX-1 and COX-2 activity, combined with effects on gastric acid, gastric blood flow at the ulcer margin and release of gastrin, which promotes ulcer healing.

"Because grapefruit is acidic in nature, people with ulcers might assume that they should not include the fruit in their diet," said Thomas Brzozowski M.D., Ph.D., of the Jagiellonian University Medical College and lead author of the study. "However, this research suggests the exact opposite. The antioxidant properties found in grapefruit and the ability of this fruit extract to limit oxidative stress in the ulcerative gastric mucosa have therapeutic properties that, when combined with additional therapies, can be especially beneficial for healing of gastric ulcers."

Alcohol-Induced Changes in Gut Permeability and Liver Injury are Influenced By Sex and Dietary Fatty Acids (Abstract 182)

Maintaining safe limits of alcohol intake can mean different things, as females are more susceptible to liver injury at much lower doses than their male counterparts and, as a result, may suffer more extensive liver disease if they drink the same amount as a man. In this study, researchers at the University of Pittsburgh School of Medicine and the Veterans Affairs Medical Center used animal models to analyze the differences in liver injury between the sexes due to chronic alcohol ingestion, using two diets that vary in carbohydrate and fatty acid content. One diet contained fish oil while the other contained a mixture of vegetable oils.

Alcohol-induced liver injury (ALI) can involve damage that ranges from mild to quite severe: fatty liver (fat buildup in liver cells), alcoholic hepatitis (an inflammatory condition) or cirrhosis (replacement of normal tissue with fibrous scar tissue).

Male and female rats were divided into groups and given either no alcohol (IC) or alcohol (AF) in a higher carbohydrate diet (LDC) or a low-carb, higher fat diet (NFO) for a total of eight weeks. Researchers determined injury to the intestine by measuring bacterial translocation and blood endotoxin levels, and also the degree of liver injury. Previous reports have shown that endotoxins, which are bacterial products that can escape from the intestine, appear to be a major factor in the development of ALI.

Female rats fed alcohol in the high fat fish oil (NFO) diet had significantly greater bacterial translocation (escape of bacteria from the GI tract to abdominal lymph nodes, in this example), higher blood endotoxin levels and more severe liver injury than male rats on the same diet or rats of either sex on the LDC diet (two-fold increase in total change), based on their intake of unsaturated fatty acids and alcohol. These results indicate that the intestines of the females had become permeable as a result of the alcohol-fish oil combination in the diet.

All rats that ingested alcohol demonstrated some degree of fatty change in their livers, but liver inflammation was evident only in females fed the NFO diet, and both female and male rats on the LDC diet showed fatty liver only, without bacterial translocation nor elevation of endotoxin levels.

"Our research suggests that women should be cautious about the amount of alcohol they consume, since they highly susceptible to more severe liver injury than men and thus to potentially serious complications," said Patricia Eagon, Ph.D., of the University of Pittsburgh and Pittsburgh VA Medical Center and lead author of the study. "Our work also shows that in females, alcohol in the diet along with fish oil injures the intestine, which causes release of factors that contribute to liver injury."