116 Introduction to Human Nutrition
monounsaturated fat was considered to be neutral
with respect to its effects on lipids and lipoproteins
and was omitted from the predictive formulae of Keys
and Hegsted. However, further studies, prompted by
interest in the role of MUFAs in the Mediterranean
diet, have shown that MUFA-enriched diets may
decrease LDL cholesterol, although possibly to a lesser
extent than linoleic acid, and increase HDL choles-
terol. An additional benefi t of MUFAs is thought to
be conferred by the presence of a single double bond
in MUFAs, which when incorporated into the mem-
brane phospholipids of LDL, protect this lipoprotein
from oxidative modifi cation, an essential prerequisite
step in the deposition of cholesterol in the artery wall.
In this regard, there has been concern that increasing
dietary PUFA will impose additional oxidative stress
on LDL. While this idea forms part of the rationale
for limiting the amount of dietary PUFA to less than
10% of energy intake, there is as yet no convincing
evidence of adverse effects from increasing the level
of PUFA in tissues and circulating lipoproteins.
Trans fatty acids
While saturated fats consist of straight chains of
carbon atoms which pack together tightly in the
phospholipids of cell membranes and lipoproteins, in
contrast, carbon double bonds in the cis confi gura-
tion in MUFAs and PUFAs introduce a bend or kink
into the carbon chain. This alters the physical proper-
ties of the phospholipids containing these fatty acids,
by, for example, increasing their packing volume, a
physical property that contributes to an increase in
membrane fl uidity. The partial hydrogenation of
MUFAs and PUFAs, most notably during the indus-
trial processing of foods for the purpose of solidifying
unsaturated oils, results in a loss of this kink as the
fatty acid assumes a straighter, trans confi guration
that resembles that found in SFAs. This likeness in
chemical structure is thought to account for the SFA-
like effects of trans fatty acids such as elaidic acid
(trans isomer of oleic acid) on serum lipids (see
Figures 6.1 and 6.2). The results of prospective cohort
studies such as the Nurses’ Health Study showed that
high levels of trans fats in excess of 7% energy
increased serum LDLs and reduced HDLs (Willet et
al. 1993). However, despite the continued use of par-
tially hydrogenated fats in food products, the average
intake of trans fatty acids in most Western diets does
not exceed 2% of total energy intake, and at this level
of intake these fats are unlikely to exert adverse effects
on serum lipoproteins.Plant sterols and soluble
nonstarch polysaccharides
These compounds may be grouped together as they
share a similar mode of action on LDL cholesterol,
which is to reduce the availability of dietary and
biliary cholesterol for absorption in the gut. This
action interrupts the enterohepatic circulation and
upregulates the production and activity of LDL recep-
tors (see Section 6.5). Plant sterols and their esters
such as those incorporated into margarines (stanols
and stanol esters), despite being nearly identical in
structure to cholesterol, are poorly absorbed and
interfere with the reabsorption of cholesterol origi-
nating from bile (~1 g/day) and dietary sources
(300 mg/day) by either coprecipitation or competi-
tion. Margarines or spreads (30–40 g/day) containing
plant sterols or their derivatives have been shown to
reduce LDL cholesterol by up to 14% in controlled
trials. Soluble NSPs such as those found in gums and
gelling agents from fruit (gum arabic and pectins) act
in a similar way and have been shown to be equally
effi cacious in reducing LDL cholesterol.Dietary cholesterol
There is a popular misconception that dietary choles-
terol correlates directly with serum cholesterol, when
in fact dietary cholesterol, within a range of normal
dietary consumption (100–400 mg/day), has only a
very small impact on blood cholesterol levels. Eggs
represent the principal source of dietary cholesterol
in most diets (1 egg yolk = 150–250 mg cholesterol);
in their absence, most Western diets would contain
considerably less than 100 mg cholesterol/day. The
classic but extreme egg-feeding studies showed that
feeding of up to six eggs per day (900 mg cholesterol)
increased LDL cholesterol acutely. However, the body
effectively counters this effect with sensitive, compen-
satory mechanisms to deal with an increasing load of
dietary cholesterol, one of which is to reduce the
amount of cholesterol absorbed in the gut. This com-
pensation effectively abolishes any dose–response
relationship between dietary cholesterol, over a prac-
tically realistic range of intakes, and serum choles-
terol. Two factors that may infl uence the variability in
response to dietary cholesterol are dietary saturated
fatty acids, which have been shown to augment the