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 Fatty acid therapy and compositions for the treatment of myalgic encephalomyelitis

Details
Inventors: Horrobin, David F.; Stewart, John C. M.;
Assignee: Efamol Holdings PLC (Surrey, GB)
Primary Examiner: Griffin; Ronald W.
Assistant Examiner: Gitomer; Ralph
Attorney, Agent or Firm: Nixon & Vanderhye

The use of one or more of the 6-desaturated or higher EFAs of each of the n-6 and n-3 series for the manufacture of a medicament for use in the treatment of post-viral fatigue syndrome (otherwise known as myalgic encephalomyelitis (ME)).

DETAILED DESCRIPTION We claim: 1.
A method of treating myalgic encephalomyelitis comprising administering to a person suffering therefrom an effective amount of a mixture of a 6-desaturated essential fatty acid of the n-6 series and a 6-desaturated essential fatty acid of the n-3 series.
2.
The method of claim 1 including also administering an effective amount of alpha, beta or gamma interferon in addition to said fatty acids.
3.
The method of claim 1 wherein each of said n-6 and n-3 series of essential fatty acids is administered in an amount of 50 mg to 20 g per day.
4.
The method of claim 3, wherein each of said essential fatty acids is administered in an amount of 500 mg to 5 g per day.
5.
The method of claim 2, wherein from 5 to 25 million units of interferon are administered per week.




Description:
FIELD OF THE INVENTION The invention relates to fatty acid therapy and compositions.
BACKGROUND Myalgic encephalomyelitis (ME), also known as benign ME, Royal Free disease, Icelandic disease, epidemic neurasthenia, post-viral syndrome, post-viral fatigue syndrome and by various other names, is a common illness for which there is no known treatment.
The characteristic feature of the disease is that a previously healthy person, often a young or middle-aged adult, develops a syndrome characterised by severe fatigue, muscle aching, loss of concentration, headache and palpitations, the last probably indicating an abnormality of cardiac rhythm.
The syndrome persists for months or years.
The cause is unknown, but a careful history often reveals the occurrence of a febrile viral infection prior to the onset of the syndrome.
The majority of patients have some evidence of impaired immune function and of chronic viral infections.
Coxsackle and Epstein-Barr viruses are commonly involved but no single specific viral type has been implicated.
It seems probable that a variety of viruses can initiate the syndrome in individuals who have an impaired immune response which pre-disposes to chronic infections



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