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. 1974 Jul;50(585):425-40.
doi: 10.1136/pgmj.50.585.425.

Abnormal fatty acid composition and human atherosclerosis

K J Kingsbury, C Brett, R Stovold, A Chapman, J Anderson, D M Morgan

Abnormal fatty acid composition and human atherosclerosis

K J Kingsbury et al. Postgrad Med J. 1974 Jul.

Abstract

Eighty patients with aorto-iliac / femoro-popliteal atherosclerosis were collected to examine in detail their plasma cholesteryl ester fatty acid compositions and to compare them with the incidence of ischaemic heart disease through a 4-year follow-up. Various other biochemical and rheological parameters were also measured to see if these might explain any association between the abnormal fatty acid pattern and ischaemic heart disease.

The abnormal fatty acid pattern was specifically and generally similar to that found in essential fatty acid (EFA) deficient animals and children as shown by the increase of the specific trienoic acid (C.20: 3ω9) by reduced linoleic acid concentrations, and by an increase of C.18 and C.16 monoenoic acids (oleic and palmitoleic), but not of their corresponding saturated forms, stearic and palmitic. The results suggest that the abnormal fatty acid composition resulted from an increased synthesis of monoenoic acids and monounsaturase activity, coupled with a relative inadequacy of linoleic acid.

The patients with a reduced concentration of linoleic acid (<35%) subsequently had a higher incidence of myocardial infarction. No significant correlations were found between the fatty acid concentration and various other biochemical or rheological parameters except marginally between linoleic acid and platelet adhesiveness. Only the linoleic acid concentration distinguished between the patients with and without myocardial infarction.

A marked inverse correlation was found, however, between the monoenoic and linoleic acid concentration, without parallel changes in other fatty acids. It seems that as in animals, a balance exists between EFA and monoenoic pathways which are known to compete for the same desaturase systems and acyl sites. It appears that human EFA requirements and effects need to be considered not only by their intake and metabolism, but also through individual factors which vary the monoenoic concentrations and monounsaturase activity. Since these factors include several currently associated with human atherosclerosis the question arises of whether the EFA-monoenoic balance is one link between them and the pathology of the arterial occlusions and myocardial infarction.

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