About 10 to 15 percent of children experience recurrent abdominal pain, the researchers said. The pain can be due to irritable bowel syndrome — which is usually relieved by defecation — or can be “functional abdominal pain,” which is not explained by another disease. While LGG has been tested before in children with abdominal pain, the studies were small and showed mixed results. The new study, which involved 141 children with irritable bowel syndrome or functional abdominal pain, was conducted in Italy between 2004 and 2008. Researchers gave the kids either the probiotic or a placebo for eight weeks. Neither the doctors nor the patients were aware which treatment they received.
Following the treatment, the patients were followed up for another 8 weeks. During the treatment and follow-up, the severity and frequency of abdominal pain decreased for both groups, but the probiotic group experienced a more drastic reduction. For instance, after 12 weeks, patients who took the probiotic reported experiencing, on average, 1.1 episodes of pain per week, compared with 3.7 weekly episodes before the treatment. Those who took the placebo reported experiencing 2.2 pain episodes per week, compared with 3.5 episodes initially.
And a greater percentage of parents of children who took the probiotic reported that their children experienced a decline in pain,compared with those whose kids took the placebo. Among kids who took the probiotic, it was mostly children with irritable bowel syndrome who showed improvements, the researchers said.
Why does it work?
The results suggest LGG may be specifically beneficial for those with irritable bowel syndrome, the researchers said. It's possible that children with irritable bowel syndrome have an imbalance of good and bad bacteria in their guts, which contributes to the pain, and the probiotics relieves pain by restoring the proper balance, Francavilla said. Probiotics have also been suggested to reduce inflammation in the gut, as well as stimulate the release of analgesic substances that relieve pain. The researchers noted they cannot be sure whether the beneficial effects will last for more than a few weeks after treatment is stopped.
The results were published in the journal Pediatrics.
For this study, Chenchen Wang, M.D., M.Sc., and colleagues recruited 40 patients from the greater Boston area with confirmed knee OA who were in otherwise good health. The mean age of participants was 65 years with a mean body mass index of 30.0 kg/m2. Patients were randomly selected and 20 were asked to participate in 60-minute Yang style Tai Chi sessions twice weekly for 12 weeks. Each session included: a 10-minute self-massage and a review of Tai Chi principles; 30 minutes of Tai Chi movement; 10 minutes of breathing technique; and 10 minutes of relaxation.
The remaining 20 participants assigned to the control group attended two 60-minute class sessions per week for 12 weeks. Each control session included 40 minutes of instruction covering OA as a disease, diet and nutrition, therapies to treat OA, or physical and mental health education. The final 20 minutes consisted of stretching exercises involving the upper body, trunk, and lower body, with each stretch being held for 10-15 seconds.
At the end of the 12-week period, patients practicing Tai Chi exhibited a significant decrease in knee pain compared with those in the control group. Using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain scale, researchers noted a -118.80 reduction in pain from baseline between the Tai Chi and control group. Researchers also observed improved physical function, self-efficacy, depression, and health status for knee OA in subjects in the Tai Chi group. “Our observations emphasize a need to further evaluate the biologic mechanisms and approaches of Tai Chi to extend its benefits to a broader population,” concluded Dr. Wang.
Curcumin, one of the principal components of the Indian spice turmeric, seems to delay the liver damage that eventually causes cirrhosis, suggests preliminary experimental research in the journal Gut. Curcumin, which gives turmeric its bright yellow pigment, has long been used in Indian Ayurvedic medicine to treat a wide range of gastrointestinal disorders.
Previous research has indicated that it has anti-inflammatory and antioxidant properties which may be helpful in combating disease. The research team wanted to find out if curcumin could delay the damage caused by progressive inflammatory conditions of the liver, including primary sclerosing cholangitis and primary biliary cirrhosis.
Both of these conditions, which can be sparked by genetic faults or autoimmune disease, cause the liver's plumbing system of bile ducts to become inflamed, scarred, and blocked. This leads to extensive tissue damage and irreversible and ultimately fatal liver cirrhosis.
The research team analysed tissue and blood samples from mice with chronic liver inflammation before and after adding curcumin to their diet for a period of four and a period of eight weeks.
The results were compared with the equivalent samples from mice with the same condition, but not fed curcumin.
The findings showed that the curcumin diet significantly reduced bile duct blockage and curbed liver cell (hepatocyte) damage and scarring (fibrosis) by interfering with several chemical signalling pathways involved in the inflammatory process.
These effects were clear at both four and eight weeks. No such effects were seen in mice fed a normal diet.
The authors point out that current treatment for inflammatory liver disease involves ursodeoxycholic acid, the long term effects of which remain unclear. The other alternative is a liver transplant.
Curcumin is a natural product, they say, which seems to target several different parts of the inflammatory process, and as such, may therefore offer a very promising treatment in the future.
Source: Anna Baghdasaryan, Thierry Claudel, Astrid Kosters, Judith Gumhold, Dagmar Silbert, Andrea Thüringer, Katharina Leski, Peter Fickert, Saul J Karpen, Michael Trauner. Curcumin improves sclerosing cholangitis in Mdr2-/- mice by inhibition of cholangiocyte inflammatory response and portal myofibroblast proliferation. Gut, 2010; 59: 521-530