Study in mice links appetite hormone and autoimmune disease.
28 January 2003
Starvation could relieve the symptoms of multiple sclerosis (MS) and other autoimmune diseases, a new study suggests.
Mice with a condition akin to MS that were deprived of food for 48 hours still developed the disease but had fewer brain lesions and performed better on tests of walking, balance, weakness and paralysis.
"Using a nutritional approach together with other drugs might offset the progression of MS," says study leader Giuseppe Matarese of the University of Napoli Federico II in Italy.
MS patients are currently advised to eat heartily. "The general rule of thumb is that eating a healthy, well-balanced diet is the best thing that you can do for treating MS," says Stephen Reingold of the National Multiple Sclerosis Society in New York.
No one is suggesting that patients forgo food to ease their symptoms just yet. Matarese intends to identify which components of diet have the strongest impact on autoimmune disease.
Multiple sclerosis is thought to arise when the immune system turns against the tissues of the brain and the spinal cord, normally between the ages of 20 and 40. Immune cells strip neurons of their protective insulation, making simple actions such as walking and talking more difficult. Fatigue, tremor and paralysis are common. Drugs that suppress or alter immune function can reduce the severity of the symptoms, but none cures the disease.
"The results open up new pathways and targets for treating the disease," says Larry Steinman, who studies the genetics of autoimmune diseases affecting the nervous system at the Stanford University in California.
One of these targets is the hormone leptin, which is normally the focus of obesity research. Fat cells release leptin after a meal to curb the appetite, and it also alters immune function. "Leptin is upregulated during inflammatory or immune responses," explains Graham Lord, an immunologist at Imperial College London, UK.
This is exactly what Matarese's team found in their mouse MS model. Just before the onset of disease, the animals' leptin levels doubled. But in mice that ate nothing for 48 hours - the equivalent of 7 to 10 days for humans - the leptin surge was smaller. Matarese also finds that neurons in the brain lesions of diseased mice produce leptin.
"I am stunned that there are mediators that are produced by the brain, that can influence appetite and have influence on the immune system," says Steinman.
The relationships between nutrition, leptin and MS are intriguing, Lord
agrees, but the study doesn't prove that leptin causes the progression
of the disease, he cautions.
© Nature News Service