The SA Journal Diabetes & Vascular Disease Vol 8 No 4 (November 2011) - page 34

176
VOLUME 8 NUMBER 4 • NOVEMBER 2011
REPORT
SA JOURNAL OF DIABETES & VASCULAR DISEASE
also showed increased deposition of sterols
in the central nervous system of these mice,
suggesting that plant sterols may be able to
cross the blood–brain barrier.
14
However, he
acknowledged that the data are not clear,
as other studies have not shown this.
15,16
Whether methodological issues, notably
differences in the cholesterol content of the
diets used in these studies, may explain this
is not clear.
In his rebuttal, Prof Bruckert once again
argued for a cautious approach when con-
sidering data from a single experimental
study. In respect of the effect of plant ster-
ols on endothelial function, he highlighted
evidence from numerous human studies
indicating that consumption of plant sterols
is instead associated with anti-inflammatory
effects, as shown by reduction in levels of
C-reactive protein (CRP).
17
However, he did
agree that there was a need for further
study to better understand how and to what
extent dietary plant sterols might modify
inflammation and the immune system.
In summing up, it was acknowledged
that there was a considerable weight of evi-
dence for the LDL-lowering effects of die-
tary phytosterol supplementation, providing
a firm basis for recommendations made
by the recent joint ESC/EAS dyslipidaemia
guidelines. Beyond LDL cholesterol lower-
ing, there is also some evidence to suggest
that dietary plant sterols may exert benefi-
cial effects on other lipids and biomarkers,
such as CRP. Whether these effects translate
to prevention of CVD requires further analy-
sis. For a definitive answer, long-term, ran-
domised, placebo-controlled studies would
be the ideal, but are probably unlikely from
a practical perspective.
debate was less combative, as both of the
participants agreed that diet is an impor-
tant part of lifestyle intervention to prevent
CVD. The debate therefore hinged on the
word ‘alone’.
Prof Horowitz argued the case that diet
is a major determinant of the risk for CVD,
supported by epidemiologic data. For exam-
ple, he cited the Lyon Diet Heart Study,
18,19
in which adoption of a Mediterranean diet
by myocardial infarction survivors resulted
in
70% reduction in mortality compared
with a comparator group treated with a
prudent diet. These data led to termination
of the trial. This difference in mortality was
evident from three months, was not related
to the extent of LDL cholesterol lowering,
and the benefit persisted at follow up four
years later.
Subsequent studies showed that adher-
ence to a Mediterranean diet was inversely
associated with CHD risk. Specifically, con-
sumption of plant-based foods, and the
ratio of mono-unsaturated to saturated fats
in the diet were linked with lower choles-
terol levels and in turn reduction in the risk
of CHD.
20
Diet, as part of intensive lifestyle
intervention, has also been shown to regress
atherosclerosis and improve risk for CVD, in
part due to beneficial effects on endothe-
lial function and inflammatory markers of
atherosclerosis.
21
In his conclusions, Prof Horowitz said
that these data clearly argue for an early,
proactive approach using diet, as part of
a comprehensive lifestyle-modification
programme, to prevent CVD. Indeed, this
approach is already regarded as a funda-
mental first step in current guidelines.
2
However, as argued by Prof Sleight, long-
term adherence is problematic, even among
highly motivated individuals. As an exam-
ple, he referred to the Nurses’ Health Study
in 84 129 women free of diagnosed CVD,
cancer and diabetes at baseline. Only 3% of
the sample was able to maintain a healthy
lifestyle (i.e. not smoking, moderate alcohol
consumption, at least 30 minutes of mod-
erate physical activity/day, and maintaining
a healthy body weight and diet) over the
long term.
22
Furthermore, he emphasised that in indi-
viduals at high risk of CVD, the magnitude
of LDL cholesterol reduction achieved with
lifestyle is usually insufficient. In such indi-
viduals pharmacotherapy is also clearly indi-
cated, in line with recent guidelines, with
statins the recommended first-line therapy.
2
Prof Sleight concluded his presenta-
tion by highlighting the need for new
approaches in motivating people to adopt
a healthy lifestyle, possibly involving nurse-
led intervention programmes, as well as col-
laborative approaches across the spectrum
of healthcare professionals.
In conclusion, both participants of the
debate agreed that diet, as part of inten-
sive lifestyle modification, is a fundamen-
tal first step in the prevention of CVD. An
early, proactive approach is key to reduc-
ing lifetime cardiovascular risk. However, it
was recognised that motivation and non-
adherence are the most important stum-
bling blocks in the long term. Additionally,
in high-risk patients, diet alone is usually
insufficient to achieve sufficient reduction
in LDL cholesterol levels as recommended
by guidelines.
References
Demonty I, Ras RT, van der Knaap HC, et al.
1.
Continuous dose–response relationship of the LDL-
cholesterol-lowering effect of phytosterol intake.
J
Nutr
2009;
139
: 271–284.
Reiner Z, Catapano A, de Backer G,
2.
et al
, ESC/EAS
guidelines for the management of dyslipidaemias.
TheTaskForceonthemanagementofdyslipidaemias
of the European Society of Cardiology (ESC) and
the European Atherosclerosis Society (EAS).
Eur
Heart J
2011; doi: 10.1093/eurheartj/ehr158.
Law MR, Wald NJ, Rudnicka AR. Quantifying effect
3.
of statins on low-density lipoprotein cholesterol,
ischaemic heart disease, and stroke: systematic
review and meta-analysis.
Br Med J
2003;
326
:
1423.
Benn M, Nordestgaard BG, Grande P, Schnohr
4.
P, Tybjærg-Hansen A. PCSK9 R46L, low-density
lipoprotein cholesterol levels, and risk of ischemic
heart disease.
J Am Coll Cardiol
2010;
55
: 2833–
2842.
Wilund KR, Yu L, Xu F,
5.
et al
. No association between
plasma levels of plant sterols and atherosclerosis in
mice and men.
Arterioscler Thromb Vasc Biol
2004;
24
: 2326–2332.
Fassbender K, Lütjohann D, Dik MG,
6.
et al
.
Moderately elevated plant sterol levels are
associated with reduced cardiovascular risk – the
LASA study.
Atherosclerosis
2008;
196
: 283–288.
Escurriol V, Cofán M, Moreno-Iribas C,
7.
et al
.
Phytosterol plasma concentrations and coronary
heart disease in the prospective Spanish EPIC
cohort.
J Lipid Res
2010;
51
: 618–624.
Trautwein EA, Demonty I, Ras RT. Plant sterols – a
8.
dietary approach for effective blood lipid lowering
as part of a heart healthy diet.
Curr Topics Nutraceut
Res
2010;
8
: 137–148.
März W. Plant sterols and cardiovascular disease: A
9.
systematic review and meta-analysis. Latebreaker
abstract, EAS 2011, Gothenburg, Sweden, June
2011.
Barter PJ, CaulfieldM, ErikssonM,
10.
et al
; ILLUMINATE
investigators. Effects of torcetrapib in patients at
high risk for coronary events.
N Engl J Med
2007;
357
: 2109–2122.
Forrest MJ, Bloomfield D, Briscoe RJ,
11.
et al
.
Torcetrapib-induced blood pressure elevation is
independent of CETP inhibition and is accompanied
by increased circulating levels of aldosterone.
Br J
Pharmacol
2008;
154
: 1465–1473.
Is diet alone sufficient to reduce
cardiovascular risk?
This motion was debated by Prof Steven F
Horowitz, Stamford Hospital, USA (for) and
Prof Peter Sleight, Oxford, UK (against). This
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