Early studies on the cardioprotective effects of high doses (up to 20 g of
eicosapentaenoic and docosahexaenoic acids, EPA and DHA, per day) of omega-
3 fatty acids (FAs) suggested that these FAs primarily lowered triglyceride
levels. These supraphysiological intake studies soon gave way to trials us
ing lower and lower intakes of omega-3 FAs such that it is now clear that u
p to 45% lowering of serum triglyceride levels can be achieved with 3-4 g o
f EPA+DHA. This is an intake that can hardly be achieved by dietary means;
direct supplementation is required. This is a public health challenge since
implementing wide-scale supplementation programmes would be difficult.
Relatively few investigators have examined the effects of low (<2 g) EPA+DH
A on serum lipid profiles, presumably because until recently there was litt
le expectation that any benefit would be detectable. With the publication o
f the DART study and more recently the GISSI-Prevenzione Study, it is becom
ing clear that small intakes of omega-3 FAs can significantly impact CHD ri
sk.
A review of the studies on the effects of small doses (<2 g.day(-1)) of ome
ga-3 FAs on serum triglyceride levels suggests that serum triglyceride leve
ls decreased in every study (compared with control or placebo treatment). T
he decreases were often not statistically significant, but this is to be ex
pected with small doses given for short time-periods. Four of the five stud
ies that examined postprandial lipids (PPL) reported significant reductions
in thus parameter even when fasting levels were not altered. This suggests
that chronic intake of small amounts of omega-3 FAs may reduce overall (da
y-long) triglyceride-rich lipoprotein levels which could have long-term imp
lications for the reduction of CHD risk.
Whilst the cardioprotective effects of omega-3 FAs are becoming well docume
nted, the question of whether such beneficial effects of omega-3 FAs are at
least partially mediated by changes in serum levels of triglyceride-rich l
ipoproteins or their remnants remains open. Further studies to examine the
effects of this low level of intake are clearly needed to determine the rel
ative contribution of hypolipidaemic mechanisms versus those involving dimi
nished platelet function, altered adhesion molecule expression, improvement
s in endothelial function and antiarrhythmic or hypotensive effects. <(c)>
2001 The European Society of Cardiology.