Deficiencies of polyunsaturated fatty acids and replacement by nonessential fatty acids in plasma lipids in multiple sclerosis.

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Abstract
Fatty acid compositions of plasma phospholipids, cholesteryl esters, triacylglycerols, and nonesterified fatty acids of 14 clinically proven and graded cases of multiple sclerosis were determined by capillary gas chromatography and compared with the values obtained for 100 normal, healthy subjects. In phospholipids, linoleic acid (18:2 .omega.6; 18 carbon atoms, 2 double bonds, 6 carbon atoms beyond last double bond) was normal and 18:3 .omega.6 was increased, but all subsequent .omega.6 acids were subnormal (P < 0.001), indicating impairment of chain elongation. All .omega.3 acids were subnormal. The paucity of polyunsaturated fatty acids was compensated mass-wise by an increase in saturated acids. Disproportionate increases in short-chain, saturated, and monounsaturated acids, decreases in long-chain homologs, and increases of branched and odd-chain acids were observed. Loss of polyunsaturated fatty acids and replacement by nonessential acids lowered mean chain length and raised mean melting point significantly, suggesting that lowered membrane fluidity was only partially compensated by endogenous synthesis of lower-melting, nonessential acids. This phenomenon was not observed in cholesteryl esters or triacylglycerols. Nonesterified fatty acids showed significant changes in pattern of possible autacoid precursors. The abnormal profile of fatty acids in multiple sclerosis has features in common with profiles of other syndromes involving viral infections.