Safety evaluation of certain food additives - ipcs inchem

146 PHYTOSTEROLS, PHYTOSTANOLS AND THEIR ESTERS
levels of campesterol was used) and of -sitosterol levels of 16–75% (Kritchevsky
& Chen, 2005).
Results from a post-launch monitoring study in the Netherlands were in
agreement with these observations. Long-time users of food items supplemented
with phytosterols (n = 67) or with phytostanols (n = 13) were investigated and
compared with non-users. Intake of 1.1 g phytosterols/day over 5 years led to an
increase in cholesterol-adjusted serum -sitosterol and campesterol concentrations
by 22% and 103%, respectively. A mean phytostanol intake of 0.6 g/day resulted in
elevations of serum -sitostanol and campestanol levels by 197% and 196%,
respectively (Fransen et al., 2007).
In a study published as a “preliminary report”, a small group of patients
submitted to hospital for artery coronary bypass graft operation was investigated.
The study group was divided in subgroups, which either had (n = 26) or did not have
(n = 27) a family history of coronary heart disease (CHD). Serum campesterol and
-sitosterol levels differed significantly between groups, although absolute
differences were small (patients with CHD family history had about 30% higher sitosterol
and campesterol plasma concentrations). Differences between groups
were also significantly different for campesterol/cholesterol and -sitosterol/
cholesterol ratios. Total, LDL and HDL cholesterol were not different between
groups (Sudhop et al., 2002).
As part of the Prospective Cardiovascular Münster (PROCAM) study, a
nested case–control study was performed in Germany. One hundred and fifty-nine
men with myocardial infarction or sudden coronary death in the last 10 years were
compared with 318 controls matched for age, smoking status and date of
investigation. Baseline plasma samples at the start of the study were obtained,
stored and analysed retrospectively. Plasma -sitosterol, but not campesterol,
concentrations were higher in cases than in controls. Triglycerides, total cholesterol
and LDL cholesterol were also higher and HDL cholesterol was lower in cases than
in controls. When -sitosterol was normalized to cholesterol (-sitosterol/cholesterol
ratio), no significant difference was observed between groups. Only if cases were
further stratified did the -sitosterol/cholesterol ratio show a significant difference
for the high-CHD subgroup, but not for the lower-risk subgroups. No multivariate
analysis was performed to discriminate between the various parameters (Assmann
et al., 2006).
Results of the population-based MONICA/KORA follow-up study were
recently published as a conference contribution. In this prospective cohort study,
1186 male (randomly sampled) residents of southern Germany were followed from
1994 to 2005. Serum concentrations of campesterol and other sterols were
analysed. In the observation period, there were 49 incident cases of (fatal or nonfatal)
CHD. After multivariable adjustment for CHD risk factors (such as cholesterol),
a significant association between campesterol concentration and myocardial
infarction was observed (Thiery et al., 2007).
In a cohort of 2542 subjects (participants of the Dallas Heart Study), the
relationships between phytosterol plasma concentrations and a) a family history of
CHD and b) coronary artery calcium levels were examined. The latter is a marker