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Influence of Soy Lecithin Administration on Hypercholesterolemia

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Recent studies suggest that lecithin-rich diet can modify cholesterol homeostasis and hepatic lipoprotein metabolism. Considering the phytotherapeutic impact of lecithin, this work hypothesizes that lecithin administration in hypercholesterolemic patients may reduce cholesterol concentrations by increasing biliary secretion. Total cholesterol and LDL were evaluated after soy lecithin administration in hypercholesterolemic patients. One soy lecithin capsule (500 mg/RP-Sherer) was administrated daily. One-two months before the treatment beginning, blood samples were collected for total lipids and cholesterol fractions analysis. The results showed a reduction of 40.66% and 42.00% in total cholesterol and of 42.05% and 56.15% in LDL cholesterol after treatment for one and two months, respectively. A significant reduction in total cholesterol and LDL-cholesterol concentrations was observed during the first month of treatment, suggesting that the administration of soy lecithin daily may be used as a supplemental treatment in hypercholesterolemia.
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Hindawi Publishing Corporation
Cholesterol
Volume 2010, Article ID 824813, 4pages
doi:10.1155/2010/824813
Clinical Study
Influence of Soy Lecithin Administration on
Hypercholesterolemia
Amouni Mohamed Mourad,1, 2, 3 Eder de Carvalho Pincinato,3Priscila Gava Mazzola,4
Maricene Sabha,4and Patricia Moriel4
1Department of Pharmacy, Camilo Castelo Branco University, Rua Carolina Fonseca 584-Itaquera, 08230-030 S˜
ao Paulo, SP, Brazil
2Department of Pharmacy, Santo Amaro University, R Isabel Schmidt 339, 04743-030 S˜
ao Paulo, SP, Brazil
3Health and Biological Sciences Department, Mackenzie Presbiterian University, Rua da Consolac¸˜
ao 896, Campus S˜
ao Paulo,
01302-907 S˜
ao Paulo, SP, Brazil
4Department of Clinical Pathology, Faculty of Medical Sciences, State University of Campinas (FCM-Unicamp),
Rua Tess´
alia Vieira de Camargo 126, Campinas-S˜
ao Paulo, P.O. Box 6111, 13083-970 S˜
ao Paulo, SP, Brazil
Correspondence should be addressed to Patricia Moriel, morielpa@fcm.unicamp.br
Received 24 July 2009; Accepted 4 October 2009
Academic Editor: W. Gibson Wood
Copyright © 2010 Amouni Mohamed Mourad et al. This is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
Recent studies suggest that lecithin-rich diet can modify cholesterol homeostasis and hepatic lipoprotein metabolism. Considering
the phytotherapeutic impact of lecithin, this work hypothesizes that lecithin administration in hypercholesterolemic patients
may reduce cholesterol concentrations by increasing biliary secretion. Total cholesterol and LDL were evaluated after soy lecithin
administration in hypercholesterolemic patients. One soy lecithin capsule (500 mg/RP-Sherer) was administrated daily. One-two
months before the treatment beginning, blood samples were collected for total lipids and cholesterol fractions analysis. The results
showed a reduction of 40.66% and 42.00% in total cholesterol and of 42.05% and 56.15% in LDL cholesterol after treatment for one
and two months, respectively. A significant reduction in total cholesterol and LDL-cholesterol concentrations was observed during
the first month of treatment, suggesting that the administration of soy lecithin daily may be used as a supplemental treatment in
hypercholesterolemia.
1. Introduction
Lipid metabolism studies include a vision for the lipoprotein
structure, function, and a description of the lipid metabolism
forms, indicating that the dyslipidemias are important risk
factors in the context of cardiovascular disease and that
appropriate intervention can have a significant impact on
clinical treatment [1].
Atherosclerosis, the most serious cardiovascular disease,
may aect individuals at an early age (20–29 years). One of
the disease symptoms is greasy striations, and its evolution
depends on several factors, such as heredity addition to
the diet, stress, and aging resulting from vascular serious
imbalances. The relationship between hypercholesterolemia
and coronary atherosclerosis disease has been demonstrated
in many clinical trials [2,3]. Moreover, the reduction in
the number of events and mortality or coronary disease,
interruption, or even the decline in atherosclerotic disease by
plasma cholesterol-lowering drugs has also been reported by
numerous studies [4,5].
One of dietary risk factors for dyslipidemias and athero-
genesis is the deficiency in the antioxidant intake, such
as selenium [6], vitamin E [7], in addition to the low
consumption of unsaturated fats [8,9]andfiber[10]. More
recently, it has been suggested that antioxidant substances
are capable of reversing endothelial dysfunction caused by
hypercholesterolemia [1113] and also reduce the number of
coronary events [14], although their use in medical practice
still needs more conclusive information.
Considering the high cost of drugs to reduce the plasma
cholesterol and the prospect of their prolonged use, patients
have relied on alternative treatments for the control of
2Cholesterol
hypercholesterolemia [15,16]. These treatments have been
used in an empirical way by the population in general
due to the lack of methodologies that allows more reliable
conclusions.
Recent studies suggest that a lecithin enriched diet
can modify the cholesterol homeostasis and lipoprotein
metabolism. Lecithin diet modifies the cholesterol home-
ostasis in the liver, increasing the activity of HMG-CoA
reductase and cholesterol 7 alpha-hydroxylase, and decreas-
ing the microsomal ACAT activity [17].
One of the most spectacular properties of lecithin is
its ability to reduce the excess of LDL cholesterol. It also
promotes the synthesis in the liver of great amount of HDL,
the beneficial cholesterol [18].
Bile acid secretion with high levels of cholesterol and
phospholipids is encouraged by lecithin-rich diets when
compared with diets without lecithin [17]. Therefore, this
study evaluates hypercholesterolemic eect of soy lecithin on
patients with pure or combined hypercholesterolemia.
2. Materials and Methods
Volun t e e rs (n=30) were chosen from a group previ-
ously diagnosed with hypercholesterolemia. Placebo cap-
sules, containing 500 mg of soy oil and 500 mg soy lecithin
capsules (22% phospholipid (phosphatidiletanolamine), 10%
triacylglycerol, and 68% phosphatidylcholine), were kindly
donated by RP-Sherer (Brazil). Blood was collected using
Vacuttainer System (Bd, Brazil). Analytical determinations
were performed using commercial enzymatic kits donated by
Labtest (Brazil). Statistical analysis were done using Sigma
Stat and the graphs were built in Microsoft Excel software.
2.1. Patients. Thirty volunteers (58–70 years old) were
selected for administration of lecithin. The groups were
chosen from patients diagnosed with hypercholesterolemia,
participants of a project at the University Camilo Castelo
Branco (Unicastelo, SP, Brazil). These voluntary patients
were previously informed about the use of biological material
to carry out the work. The project was approved by the
Ethics Committee of the Faculty of Medical Sciences, State
University of Campinas under the protocol number 792/08.
Every volunteer was given one capsule (n=20) of
500 mg soy lecithin daily and placebo group received one
capsule placebo. One and two months after treatment with
beginning, the blood samples were withdrawn and the lipid
profile was performed.
This was a double-blind study, in which only one person
in the group knew the patients who received placebo or soy
leciythin capsule; after the data analysis, it was allowed access
to the primary research groups.
Blood was collected in tubes for serum obtention;
serum was separated by centrifugation at 2500 rpm for 10
minutes. Serum samples were stored in a freezer (20C)
until the determination completion. The volume of blood
required to perform the analysis was 10 mL per withdrawn.
For placebo influence determination blood was withdrawn
before and two months after administration. Patients taking
0
40
80
120
160
200
240
280
Cholestrol (mg/dl)
CH
total
VLDL LDL HDL
Before
CH
total
VLDL LDL HDL
After two months
Figure 1: Total cholesterol (CH, mg/dL) and cholesterol concen-
tration in lipoproteins (mg/dL) before and 2 months after placebo
administration. The error bars represent statistical significance (P<
.001).
soy lecithin capsules had blood withdrawn before and after
the administration (one and two months).
2.2. Lipid Determination. Total cholesterol and triglyceride
concentrations in the plasma were determined by enzymatic
methods, using commercial reagents (Labtest diagnostics,
Brazil).
The HDL cholesterol level was also determined by an
enzymatic method (Labtest diagnostics, Brazil), after the
precipitation of LDL and VLDL fractions. The Friedewald
equation (1), below, was used to obtain the concentration of
LDL cholesterol [19]:
ChLDL =ChTota l (ChVLDL +Ch
HDL),(1)
where Ch stands for cholesterol and ChVLDL represents
triglycerides divided by five.
2.3. Statistical Analysis. Results were calculated using average
±standard deviation. The statistical analysis, which was
considered significant, used the paired t-test of the Sigma Stat
software (P<.001). The graphs were built in Microsoft Excel
software.
3. Results and Discussion
Patients who took placebo capsules showed no dierences in
lipid profile after two months of administration (Figure 1),
total cholesterol was reduced in 11.4%, but this decrease is
not statically significant.
For patients taking soy lecithin capsules significant
decrease in the total cholesterol concentration and in HDL
cholesterol during the first and the second months of
administration suggests that the administration time did not
influence the results (Figure 2). Also, triglyceride concentra-
tion did not change as seen in relation to cholesterol (data
not shown).
Figure 2 also shows the concentration of lipoprotein
cholesterol, showing a significant reduction in the LDL
cholesterol concentration after administration of soy lecithin
capsules, which was not dependent on the administration
time.
Cholesterol 3
0
100
200
300
400
(mg/dl)
CH
total
VLDL
LDL
HDL
Before
CH
total
VLDL
LDL
HDL
1st month
CH
total
VLDL
LDL
HDL
2nd month
Figure 2: Total cholesterol (CH, mg/dL) and cholesterol concen-
tration in lipoproteins (mg/dL) in serum before and after the first
and the second months of lecithin administration. Significant in
relation to the period before treatment.
Scientific community believes that the cholesterol con-
centration is a risk factor of cardiovascular disease. It
was observed that a decrease of 10% in cholesterol is
associated with a 27% reduction in cardiovascular disease
risk [20]. The main determinants of plasma cholesterol are
saturated fatty acids polyunsaturated and dietary cholesterol.
Plasma cholesterol can be further reduced by specific dietary
supplements, such as fiber, garlic, and fish oils [21].
Thus, many scientists have explored the possibility of
increasing hypocholesterolemic components of foods; recent
studies have shown that soy protein and soy sterols have
hypocholesterolemic eect [22,23].
In this work, soy lecithin eect on the serum cholesterol
concentration was evaluated. The results showed a decrease
of 40.65% and 42.60% in total cholesterol and 42.65%
and 56.11% in LDL cholesterol, one and two months after
administration, respectively. The results of this study are in
line with studies of soy protein as a whole; there is no work
in literature on the isolated eect of lecithin.
Soybean presents a number of advantages compared with
other sources of vegetable protein [24]. It has high-protein
content (38%–42%) of low cost and high quality as well as
isoflavones that help in reducing blood cholesterol. The daily
intake of 25 grams of soy protein dramatically reduced the
total cholesterol over a period of approximately three weeks,
that is, one month after treatment beginning. It was also
shown that this eect was not dependent on time, since there
was no increase two months after the treatment end. The
daily intake of soy protein may reduce the LDL concentration
by 30%, while occurs a stimulus for the HDL production
[25,26].
Soybean protein increases the cholesterol-lowering
eects of plant sterols on rats fed cholesterol; the
combination of plant sterols and soy protein increases
fecal neutral sterols and bile acid excretion compared with
the sterol and soy protein alone; therefore, the combination
of sterol and soy protein shows a more ostensible decrease in
plasma lipids than the isolated ingredients [27].
A decrease in the cholesterol intestinal absorption and
an increase in the bile acid excretion have been suggested as
possible mechanisms for the eects in the reduction of lipids
by soy protein [28].
Jiang et al. [29] demonstrated the inhibition of choles-
terol absorption in diets rich in phosphatidylcholine. This
study suggests that the high degree of saturation of acyl
groups of the soybean phosphatidylcholine decreases the
cholesterol intestinal absorption.
Lecithin is one of the nature elements that have dispers-
ing properties. That is why it can emulsify fat, avoiding its
absorption. Lecithin is capable of reducing LDL-cholesterol.
It also promotes the HDL-cholesterolsynthesis [27]. In addi-
tion to be used to help reduce cholesterol and triglycerides
and protect the liver in the prevention of kidney stone
formation, it is used as a tonic for the nervous system and
brain activities. The Food and Drug Administration-(FDA)
USA, and the World Federation of Cardiology recommended
the use of 25 grams per day of soy protein, which corresponds
to approximately 60g of soybeans for cardiovascular disease
prevention. However, it is not yet clear which components of
soy are responsible for their antiatherogenic purposes.
Recent studies suggest that a lecithin-rich diet can modify
the cholesterol homeostasis and lipoprotein metabolism in
liver. Lecithin diet modifies the cholesterol homeostasis in
the liver, increasing the HMG-CoA reductase and alpha 7
hydroxylase cholesterol activities and decreasing the micro-
somal ACAT activity. The LDL concentration and size are
also significantly reduced and the bile acid pool and bile lipid
secretion are increased [17].
4. Conclusion
This work suggests that soy lecithin-rich diets can be used
as an adjunct in the treatment of hypercholesterolemia;
however, further works with a large number of patients
should be carried out towards finding the ideal dose-
response.
Lecithin-rich diets can stimulate the fatty acid secretion
with high levels of cholesterol and phospholipids when com-
pared with diets without lecithin, considering the lecithin
performance as phytotherapic, with a large spectrum of
activity. The results showed significant reduction in the con-
centration of total cholesterol and LDL-cholesterol during
the first month, suggesting that the daily administration
of lecithin capsule could be used as an adjuvant treatment
in hypercholesterolemia, possibly by reducing the intestinal
absorption or by the increased secretion of bile acids with
high levels of cholesterol and phospholipids.
Acknowledgment
The authors acknowledge Scherer (Brazil) and Labtest
(Brazil).
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The use of additives in food products has become an important public health concern. In recent reports, dietary emulsifiers have been shown to affect the gut microbiota, contributing to a pro-inflammatory phenotype and metabolic syndrome. So far, it is not yet known whether similar microbiome shifts are observable for a more diverse set of emulsifier types and to what extent these effects vary with the unique features of an individual's microbiome. To bridge this gap, we investigated the effect of five dietary emulsifiers on the fecal microbiota from 10 human individuals upon a 48 hour exposure. Community structure was assessed with quantative microbial profiling, functionality was evaluated by measuring fermentation metabolites and pro-inflammatory properties were assessed with the phylogenetic prediction algorythm PICRUSt, together with a TLR5 reporter cell assay for flagellin. A comparison was made between two mainstream chemical emulsifiers (carboxymethylcellulose and P80), a natural extract (soy lecithin) and biotechnological emulsifiers (sophorolipids and rhamnolipids). While fecal microbiota responded in a donor-dependent manner to the different emulsifiers, profound differences between emulsifier were observed. Rhamnolipids, sophorolipids and soy lecithin eliminated 91% ± 0%, 89% ± 1% and 87% ± 1% of the viable bacterial population after 48 hours, yet they all selectively increased the proportional abundance of putative pathogens. Moreover, profound shifts in butyrate (-96% ± 6 %, -73% ± 24% and -34 ± 25% respectively) and propionate (+13% ± 24 %, +88% ± 50% and +29% ± 16% respectively) production were observed for these emulsifiers. Phylogenetic prediction indicated higher motility, which was, however, not confirmed by increased flagellin levels using the TLR5 reporter cell assay. We conclude that dietary emulsifiers can severely impact the gut microbiota and this seems to be proportional to their emulsifying strength, rather than emulsifier type or origin. As biotechnological emulsifiers were especially more impactful than chemical emulsifiers, caution is warranted when considering them as more natural alternatives for clean label strategies.
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Prospective data at Framingham and elsewhere have shown conclusively that risk of coronary heart disease in persons younger than age 50 is strikingly related to the serum total cholesterol level. Within so-called normal limits risk has been found to mount over a five-fold range. The impact has been found to be augmented by other risk factors. The contribution of the serum total cholesterol to risk has also been found to be determined by its partition in the various lipoprotein fractions. A relatively large amount of cholesterol in the low-density lipoprotein fraction is atherogenic, whereas that in the high-density fraction appears protective. The independent contribution of very-low density lipoprotein and its triglyceride or cholesterol content has, on the other hand, not been established. The previous position that virtually all of the lipid information pertaining to coronary heart disease resided in the serum total cholesterol must be accordingly modified.
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Soybean protein was exhaustively digested with endo- and exo-type microbial proteases and the effect of the digestible low molecular fraction (LMF) and the undigested high molecular fraction (HMF) on the serum cholesterol level was compared to that of the intact protein in rats given a cholesterol-enriched diet. The HMF, peptides relatively abundant in hydrophobic amino acids, was found to be substantially hypocholesterolemic when fed at the nitrogen level equivalent to that of the 20% soybean protein diet, and not only serum but also liver cholesterol levels were similar to those usually encountered in rats given diets free of cholesterol. There was a dose-dependent reduction of serum and liver cholesterol when casein was replaced stepwise with HMF. The cholesterol-lowering action could be attributable to an increased fecal steroid excretion.
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A method for estimating the cholesterol content of the serum low-density lipoprotein fraction (Sf- 0.20)is presented. The method involves measure- ments of fasting plasma total cholesterol, tri- glyceride, and high-density lipoprotein cholesterol concentrations, none of which requires the use of the preparative ultracentrifuge. Cornparison of this suggested procedure with the more direct procedure, in which the ultracentrifuge is used, yielded correlation coefficients of .94 to .99, de- pending on the patient population compared. Additional Keyph rases hyperlipoproteinemia classifi- cation #{149} determination of plasma total cholesterol, tri- glyceride, high-density lipoprotein cholesterol #{149} beta lipo proteins
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The causal role of an elevated serum cholesterol level in the genesis of atherosclerosis and its clinical sequelae, particularly ischemic heart disease, is now well established. The recognition of this role has been the impetus for numerous trials designed to test the hypothesis that a reduction in the cholesterol level will lead to a reduction in morbidity and mortality from cardiovascular disease. Most of these studies have indeed demonstrated a reduction in the incidence of ischemic cardiac events, and some have also shown a reduction in mortality from cardiovascular disease. Despite this intensive investigation, however, the mechanism (or mechanisms) responsible . . .
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To estimate by how much and how quickly a given reduction in serum cholesterol concentration will reduce the risk of ischaemic heart disease. Data on the incidence of ischaemic heart disease and serum cholesterol concentration were analysed from 10 prospective (cohort) studies, three international studies in different communities, and 28 randomised controlled trials (with mortality data analysed according to allocated treatment to ensure the avoidance of bias). Decrease in incidence of ischaemic heart disease or mortality for a 0.6 mmol/l (about 10%) decrease in serum cholesterol concentration. For men results from the cohort studies showed that a decrease of serum cholesterol concentration of 0.6 mmol/l (about 10%) was associated with a decrease in incidence of ischaemic heart disease of 54% at age 40 years, 39% at age 50, 27% at 60, 20% at 70, and 19% at 80. The combined estimate from the three international studies (for ages 55-64 years) was 38% (95% confidence interval 33% to 42%), somewhat greater than the cohort study estimate of 27%. The reductions in incidence of ischaemic heart disease in the randomised trials (for ages 55-64 years) were 7% (0 to 14%) in the first two years, 22% (15% to 28%) from 2.1-5 years, and 25% (15% to 35%) after five years, the last estimate being close to the estimate of 27% for the long term reduction from the cohort studies. The data for women are limited but indicate a similar effect. The results from the cohort studies, international comparisons, and clinical trials are remarkably consistent. The cohort studies, based on half a million men and 18,000 ischaemic heart disease events, estimate that a long term reduction in serum cholesterol concentration of 0.6 mmol/l (10%), which can be achieved by moderate dietary change, lowers the risk of ischaemic heart disease by 50% at age 40, falling to 20% at age 70. The randomised trials, based on 45,000 men and 4000 ischaemic heart disease events show that the full effect of the reduction in risk is achieved by five years.
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The vascular effects of dietary vitamin E were investigated in isolated carotid artery preparations from cholesterol-fed New Zealand White rabbits. Rabbits were fed either a control, 1% cholesterol, or 1% cholesterol plus 0.2% vitamin E diet for 4 weeks. In raised-tone preparations, relaxant responses to acetylcholine were enhanced in rabbits fed cholesterol plus vitamin E, reversing the reduction in responses measured in preparations from cholesterol-fed rabbits. Relaxant responses to the calcium ionophore A23187 were significantly enhanced in cholesterol plus vitamin E-fed rabbits compared with those fed cholesterol alone, with no difference between control and cholesterol-fed rabbits. Relaxant responses to sodium nitroprusside were not different between the three dietary groups. Constrictor responses to noradrenaline and serotonin in isolated carotid artery preparations at basal tone were unaltered after cholesterol and cholesterol plus vitamin E diets. The copper-induced oxidation of beta-very-low-density lipoproteins (beta VLDL) isolated from plasma of rabbits fed a cholesterol plus vitamin E diet was almost completely inhibited compared with the oxidation of beta VLDL from rabbits fed cholesterol alone. These results show that vitamin E prevents endothelial dysfunction associated with cholesterol feeding and suggests that vitamin E may be beneficial in preventing functional impairment associated with atherosclerosis.