If you have an ulcer, here are things you should discuss with your doctor to promote healing, courtesy of the American Academy of Family Physicians:

• Medications can help ulcers heal. Antibiotics are prescribed to thwart bacteria, and other medications may be taken to help reduce stomach acid.
• Avoid smoking.
• Don't take anti-inflammatory medications such as aspirin or ibuprofen.
• Avoid caffeine and alcohol in your diet. If you do have some, try to make sure it's after you've eaten a meal or snack.
• Don't eat foods that seem to aggravate your ulcer. Examples may include chocolate, coffee, certain herbs and spices, and some spicy foods.
• Eat several small meals throughout the day, rather than one big meal.

FRIDAY, May 2 (HealthDay News) -- Prompt treatment of a common stomach infection reverses the damage that can lead to gastric cancer, according to tests on mice done by researchers at the Massachusetts Institute of Technology (MIT).

The findings should put a stop to any questions about whether, and when, antibiotic treatment of Helicobacter pylori can reduce or eliminate the risk of developing stomach cancer.

"We concluded that H. pylori eradication prevented gastric cancer to the greatest extent when antibiotics were given at an early point of infection, but that eradication therapy given at a later point also delayed the development of severe lesions that can lead to cancer," study author James G. Fox, director of the division of comparative medicine at MIT, said in a prepared statement.

Stomach cancer is the second-leading cause of cancer death worldwide and about half the world's population is infected with H. pylori, which is recognized as a major cause of both peptic ulcers and stomach cancer. It typically takes several decades for stomach cancer to develop in people who are susceptible -- about 3 percent of people infected with H. pylori.

It's been unclear when doctors should screen and treat people with antibiotics -- other than immediate relatives of patients with stomach cancer and peptic ulcer disease -- or when to treat H. pylori infection for maximum benefit, Fox said.

He and his colleagues created mice prone to accelerated H. pylori infection and progression to stomach cancer. The researchers found that mice treated with antibiotics had less severe disease at every stage of advancing infection.

Mice treated eight weeks post-infection had the same risk of cancer as uninfected mice. However, treatment at 12 and 22 weeks post-infection didn't reverse damaging changes, such as inflammation and development of precancerous lesions, to levels seen in uninfected mice.

"Our mouse model mimics the progressive process we know occurs in the development of human gastric cancer. This [study] shows early intervention provides the maximum benefit," Fox said.

The study appears in the May 1 issue of Cancer Research.

More information

The American Cancer Society has more about stomach cancer.

IBS -- with symptoms including cramps, abdominal pain, bloating, constipation and diarrhea -- affects twice as many women as men, the agency said in a statement.

Amitiza's safety and effectiveness were evaluated in two studies involving 1,154 people with IBS-C, more than 90 percent of whom were women. More people treated with the drug said their symptoms were moderately or significantly relieved than those who took a non-medicinal placebo.

The effectiveness of the drug in men wasn't conclusively established during clinical testing, the FDA said.

Common side effects included nausea, diarrhea and abdominal pain. More serious yet rarer adverse reactions could include urinary tract infections, dry mouth, fainting, swelling of the extremities, difficulty breathing and heart palpitations, the agency said.

The 8-microgram dose is meant to be taken twice daily with food and water. Amitiza is produced by Maryland-based Sucampo Pharmaceuticals and Illinois-based Takeda Pharmaceuticals North America.

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The FDA has more about this drug's history.

MONDAY, April 28 (HealthDay News) -- The inflammatory bowel diseases ulcerative colitis and Crohn's disease appear to share several genetic variants and risk factors, two new British studies suggest.

Though similar in many ways, the two diseases are distinct, and scientists have been trying to pinpoint the underlying relationship between them to improve their understanding of and treatment for both. The latest findings, expected to be published online in the April 27 issue of Nature Genetics, may be a significant step forward.

Ulcerative colitis and Crohn's disease affect one in 250 individuals of Northern European descent. Ulcerative colitis is a common inflammatory bowel disease, while Crohn's disease is a related, but chronic disorder of the intestine.

In the first study, researchers identified ECM1, a gene variant that encodes a protein secreted by cells to activate a key immune regulator as tied to the risk of colitis. They also found that five genes previously linked to the probability of developing Crohn's disease are also common to ulcerative colitis, while three others are not.

In the second study, several of 50 previously reported susceptibility loci for Crohn's disease were deemed risk variants for both diseases. Three others were found to be specific to Crohn's disease and three specific to ulcerative colitis.

More information

The American Academy of Family Physicians has more about inflammatory bowel diseases.

In a study done on mice, scientists at the Melbourne Branch of the International Ludwig Institute for Cancer Research (LICR) found that blocking the signaling pathway of the IL-11 protein -- either through genetic manipulation or with medications -- would prevent certain inflammation, hyperplasia (an abnormal increase in the number of cells), and tumor formation in pre-clinical models of stomach cancer.

Stomach cancer, the second most common cause of cancer-related deaths worldwide, has been shown previously to be correlated with chronic inflammation.

The findings were published online April 22 in The Journal of Clinical Investigation.

The study shows that IL-11 promotes chronic inflammation and the formation of tumors in the stomach by increasing activation of the Stat3 protein, a known player in inflammation-associated carcinogenesis. Excessive Stat3 activity is often found in gastric and other types of cancer. The underlying cause of the Stat3 issue had previously been unknown.

"The clear link between inhibition of IL-11/Stat3 activity and suppression of gastric tumorigenesis that we identified supports the further development of pharmacologic agents that target these molecules for the treatment of gastric and potentially other cancers," study author Matthias Ernst, from the LICR Melbourne Branch, said in a prepared statement. "We believe that we have a very relevant model in our hand for the preclinical assessment of such compounds as well as for the identification of potential markers that may ultimately help in the early detection of disease."

More information

The American Cancer Society has more about stomach cancer.