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Starvation could relieve multiple sclerosis

Study in mice links appetite hormone and autoimmune disease.

28 January 2003

 

HANNAH HOAG

 

After a meal, fat cells release leptin to curb ap

Starvation could relieve the symptoms of multiple sclerosis (MS) and other

autoimmune diseases, a new study suggests1.

 

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 California2.

 

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.

 

References

 

1. Sanna, V. et al. Leptin surge precedes onset of autoimmune

encephalomyelitis and correlates with development of pathogenic T cell

responses. Journal of Clinical Investigation, 111, 241 - 250, (2003).

|Article|

2. Steinman, L. et al. The intricate interplay among body weight, stress,

and the immune response to friend or foe. Journal of Clinical

Investigation, 111, 183 - 185, (2002). |Article|

 

 

 

© Nature News Service / Macmillan Magazines Ltd 2003

 

 

 

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the more they are condensed,

the deeper they burn.

-Robert Southey (1774-1843)