ArticlePDF Available

Effect of natural honey on human platelets and blood coagulation proteins

Authors:

Abstract and Figures

Present study was conducted to determine the effects of honey on blood hemostasis, in-vitro effect of honey was observed on platelet aggregation and blood coagulation employing, activated partial prothrombin time (aPTT), prothrombin time (PT), thrombin time (TT) and fibrinogen levels in blood. Honey samples showed moderate inhibition of platelet aggregation with IC(50) 5-7.5%. The coagulation assays showed that at higher concentrations (>15%) honey samples increased whole blood clotting time. When assayed in platelet poor plasma (PPP), honey samples significantly (P>0.005) prolonged aPTT, PT, and TT. The honey samples (at 3.75% and 7.5% concentrations) cause mean increment of aPTT = 19±10% and 62±10%; PT 6±5% and 40±5%; TT 35±15% and 112±30% respectively. Moreover, PPP isolated from whole blood pre-incubated with honey samples (9.0% for 10 minutes) showed mean prolongation of aPTT, PT and TT of 45±21%, 26±9% and 105±24% respectively. Interestingly, incubation of honey at 6.25% and 11.75% concentrations in PPP considerably (P≥0.005) reduced fibrinogen levels i.e. 13±4% and 86±30% respectively. The present study outlines the inhibitory effect of natural honey on platelet aggregation and blood coagulation. These observations provide first line data for modulatory role(s) of honey on process of hemostasis.
Content may be subject to copyright.
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397 389
REPORT
EFFECT OF NATURAL HONEY ON HUMAN PLATELETS
AND BLOOD COAGULATION PROTEINS
ASIF AHMED1, RAFEEQ ALAM KHAN2*, M. KAMRAN AZIM3, S. ARSHAD SAEED3,
M. AHMED MESAIK3, SHAKIL AHMED4 AND IMRAN IMRAN3
1Department of Pharmacology, Baqai Medical University, Karachi, Pakistan
2Department of Pharmacology, Faculty of Pharmacy, University of Karachi, Karachi, Pakistan
3Dr. Panjwani Center for Molecular Medicine and Drug Research, ICCBS,
University of Karachi, Karachi, Pakistan
4Industrial Analytical Centre, International Center for Chemical and Biological Sciences
University of Karachi, Karachi, Pakistan
ABSTRACT
Present study was conducted to determine the effects of honey on blood hemostasis, in-vitro effect of honey was
observed on platelet aggregation and blood coagulation employing, activated partial prothrombin time (aPTT),
prothrombin time (PT), thrombin time (TT) and fibrinogen levels in blood.
Honey samples showed moderate inhibition of platelet aggregation with IC50 5-7.5%. The coagulation assays
showed that at higher concentrations (15%) honey samples increased whole blood clotting time. When assayed
in platelet poor plasma (PPP), honey samples significantly (P0.005) prolonged aPTT, PT, and TT. The honey
samples (at 3.75% and 7.5% concentrations) cause mean increment of aPTT = 19±10% and 62±10%; PT 6±5%
and 40±5%; TT 35±15% and 112±30% respectively. Moreover, PPP isolated from whole blood pre-incubated
with honey samples (9.0% for 10 minutes) showed mean prolongation of aPTT, PT and TT of 45±21%, 26±9%
and 105±24% respectively. Interestingly, incubation of honey at 6.25% and 11.75% concentrations in PPP
considerably (P0.005) reduced fibrinogen levels i.e. 13±4% and 86±30% respectively.
The present study outlines the inhibitory effect of natural honey on platelet aggregation and blood coagulation.
These observations provide first line data for modulatory role(s) of honey on process of hemostasis.
Keywords: Nutraceuticals; cardiovascular diseases and cerebro-vascular accident; thrombosis; anti-platelet;
anticoagulation.
INTRODUCTION
Vascular diseases contribute a major fraction in human
diseases. All over the world, major vascular diseases such
as cardiovascular diseases (CVD) and cerebro-vascular
accident (CVA) accounts for high mortality and morbidity
(Kumar and Clark, 2005). Atherosclerotic lesion is the
primary pathology found in CVA and CVD (Steinberg,
1992; Wegge et al., 2004).
In the established atherosclerotic disease; disturbed
platelet aggregation and blood coagulation complicates
the silent atherosclerotic lesion, by the formation of
superimposed thrombus (Escandon et al., 1999; Meigs et
al., 2000; Carr, 2001; Sobel, 2002). This thrombus
formation leads to a variety of acute clinical events such
as unstable angina, myocardial infarction or
cerebrovascular accidents (Franco et al., 2000; Libby et
al., 2002; Levi et al., 2004).
Unhealthy diet is a major cause of high mortality and
morbidity of vascular diseases (Pearson, 1999;
Kuulasmaa et al., 2000; Kelly, 2003). Therefore, it could
be prudent to consume a diet that is supplemented with
the food that may interfere physiologically with platelet
aggregation and blood coagulation; thus interrupts the
thrombotic progress of atherosclerotic disease. As part of
normal healthy diet, people around the world use natural
honey as a sweetener as well as due to its medicinal
benefits (Amy and Carlos, 1996). Honey is a
supersaturated sugar solution mainly comprises of D-
fructose, D-glucose, sucrose, maltose and higher sugars
(~80% of solid mass); while other natural products
includes alkaloids, flavonoids / isoflavones, glycosides,
phenolics, peptides/proteins are present in minor amounts
(White et al., 1962). Health benefits of honey have been
reported in a variety of conditions including microbial
infections (Cooper et al., 2002), wound healing (Molan,
2001a,b), anti-inflammation and inhibition of reactive
oxygen species (Mesaik et al., 2008; Ahmad et al., 2009),
glucose tolerance (Ahmad et al., 2008) and analgesia
(Azim et al., 2007).
In continuation of our studies, on medicinal attributes of
honey, we hypothesized that honey might have effects on
blood hemostasis. This effect of honey was assessed in
vitro, on platelet aggregation and blood coagulation.
*Corresponding author: e-mail: rkhan1959@gmail.com
Effect of natural honey on human platelets
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397
390
MATERIALS AND METHODS
Honey Samples
Six commercially available unifloral and multifloral
honey samples were used in this study. Pakistani honey
samples were collected from colonies of Apis mellifera
bees foraged on Acacia modesta (Sha), Plectranthus spp.
(Swa) and Ziziphus spp. (Sid). For comparison, Clover
honey (Clo), Eucalyptus honey (Cap) and LangneseTM
honey (Lan) from USA, Australia and Germany
respectively were included in the study. Information
regarding the floral origin of these commercial honeys
was obtained as detailed on the packing labels. The honey
samples were diluted with sterile phosphate buffered
saline pH 7.4.
Estimation of predominant sugars, water content, pH,
ash, viscosity and specific gravity of honey samples
In the present study, determination of amount of simple
sugars present in honey samples were done by using high
performance liquid chromatography. Simple sugars in
honey samples were separated isocratically by reversed
phase HPLC on a Prevail Carbohydrate ES, 5µm, 250 x
4.6mm column with acetonitrile/water. Karl Fischer
titration method was used to estimate the water content in
honey samples (Cedergren, 1974; Hoffmann, 1998),
where as estimation of pH in honey samples were carried
out by using pH meter. Ash content of honey samples
was determined by dry ashing, through Furnace method
(Milne et al., 1992). Viscosity was measured using a
Brookfield Viscometer (Cheng, 1990) and specific gravity
of honey samples was determined by Pycnometer -
density bottle method (Wattiaux et al., 1991; Wattiaux et
al., 1992; Bailoni and Bittante, 1994).
Determination of anti platelet activity of honey
Human platelets were isolated from blood samples
collected from healthy subjects (n=6), aged 35-48, who
did not consumed any medication in the last two weeks.
Blood was taken by clean vein puncture and immediately
mixed with 3.8% (w/v) sodium citrate solution (9:1) and
centrifuged at 260×g for 15 minutes at 20°C to obtain
platelet rich plasma (PRP).
Platelet count was determined by phase contrast
microscopy and all aggregation studies were carried out at
37°C with PRP having counts between 2.5-3.0×108/ml of
plasma (Shah and Saeed, 1995). All experiments were
performed within 2 h of PRP preparation. Platelet
aggregation was monitored using Dual-channel lumi-
aggregometer (Model 400 Chronolog Corporation,
Chicago, USA) using 0.425-0.49 ml aliquots of PRP
(Shah and Saeed, 1995, Shah et al., 1996). The final
volume was made up to 0.5 ml with the honey samples,
dissolved in sterile phosphate buffer saline pH 7.4.
Aggregation was induced with 10 µl of adenosine 5’-
diphosphate (ADP) solution (4 µM). The time of addition
of inducer was defined as 0 time. Various concentrations
(2.5, 5, 6 and 7.5%) of honey samples were added
following addition of the aggregation agent. Percentage of
aggregation inhibition was calculated comparing with the
control (no honey).
Determination of effects of honey on blood coagulation
Blood was taken by clean vein puncture from normal
human healthy volunteers; who did not consumed any
medication in the last two weeks. Platelet poor Plasma
(PPP) was obtained by centrifugation at 1500×g for 10
min at 4°C. Effects of honey samples on blood
coagulation were carried out by using HemoStat-aPTT-
EL, HemoStat Thromboplastin-SI, HemoStat-Thrombin
time and HemoStat-Fibrinogen. All reagents were
prepared, maintained and performed as directed by the
manufacturer (Human Diagonista-Germany GmbH) with
some modifications (Posta et al., 2002; Nilsson et al.,
1997; Berry et al., 2002; Valeria et al., 2000). Clotting
time for all coagulation assays was measured by taking
the average of 2-5 measurements using Coagulometer
(Human Diagonista-Germany GmbH).
Effect of honey on whole blood coagulation
The extracted blood from the healthy human volunteer
(male) was equally distributed (0.3ml) into glass tubes
(without anticoagulant) containing diluted honey samples
(Lan and Swa) at the final concentrations of 15, 24 and
30%. Upon addition of blood into tubes, whole blood
clotting time was noted by optical method. Whole blood
(no honey) was taken as control. For the validity of
coagulation test results, sterile phosphate buffer saline
was also tested.
Effect of honey on coagulation parameters tested in
platelet poor plasma
Blood was collected from 30 healthy human volunteers
(20 males, 10 females; aged 32±6). Whole blood was
mixed with anticoagulant (sodium citrate) and platelet
poor plasma (PPP) was removed by using plastic pipette
and kept in covered plastic tube to avoid pH changes.
Diluted honey samples were mixed with PPP in pre-
warmed tubes and clotting was timed, after addition of
reagents for aPTT, PT, TT and Fibrinogen level. For
aPTT, PT, TT assays the final concentrations of honey
samples were 3.75 and 7.5%; whereas for fibrinogen
assays, final concentrations were 6.25 and 11.76%.
Platelet free plasma (no honey) was taken as control. For
the validity of coagulation test results, sterile phosphate
buffer saline and Dextran solution (Clinical grade, M.W.
=200,000-300,000) were also tested.
Effect of honey mixed in whole blood and coagulation
parameters tested on extracted platelet poor plasma
Blood samples collected from 7 healthy male human
volunteers (aged, 25.8±8.2) were taken and placed into
two tubes in equal amounts (containing sodium citrate as
Asif Ahmed et al.
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397 391
anticoagulant). Diluted honey samples (9.0%) were added
to one of the tube (T1) and incubated for 10 minutes.
After incubation, PPP was removed and aPTT, PT and TT
assays were carried out. Platelet free plasma (tube-T2,
with no honey) was taken as control. For the validity of
coagulation test results, sterile phosphate buffer saline and
dextran solution (Clinical grade, M.W. =200,000-
300,000) were also tested.
Statistical analysis
Results are mentioned as mean with standard deviation.
The mean values were calculated from 2-5 observations.
One-way analysis of variance (ANOVA), two-way
analysis of variance (ANOVA), test for homogeneity of
variance, and post-hoc tests (Tukey HSD and Games-
Howell) were all performed wherever applied. All
analyses were carried out using Excel (Microsoft Corp.,
Redmond, Wash., U.S.A.) and SPSS version 12 (Aspire
Software Intl., Ashburn, Va., U.S.A.).
RESULTS
Estimation of predominant sugars, water content, pH,
ash, viscosity and specific gravity of honey samples
Table 1 shows percentage composition of honey sugars
analyzed by HPLC (see methods). During the study, first
glucose, fructose, maltose and sucrose separately and then
a mixture of four sugars were standardized and considered
as control. Later all honey samples were analyzed against
the control. Table 2 shows the results of Ash content (%),
Viscosity (Poise), pH, Sp. Gravity (20oC) and Water
content (% w/w basis) of honey samples.
Effect of honey on blood hemostasis
The results of present study show honey-mediated (a)
inhibition of platelet aggregation, (b) prolongation of
aPTT, PT, and TT and (c) reduction in Fibrinogen levels.
Platelet aggregation activity of honey
In this study, effect of different honey samples on platelet
aggregation assay was carried out. Fig. 1 shows, that
addition of honey in the reaction mixture, inhibited ADP-
induced platelet aggregation. Table 3 shows IC50 dose of
honey samples that remained between 5.0-6.5 %. Among
the honey samples studied in this experiment,
Plectranthus (Swa) and Euclayptus honeys (Cap) showed
maximum inhibition of platelet aggregation with IC50~5.0
%. PRP without honey was taken as control. In order to
eliminate the false positive effect due to the viscosity of
honey, Dextran (9.0 %) was also tested. However, no
significant effect was observed supporting the inhibitory
activity of honey.
Effect of honey on blood clotting time
Fig. 2 shows, effect of honey on whole blood coagulation.
In this study, Lan and Swa honey samples were tested in
15, 24 and 30% concentrations. Honey at less than 15%
concentration (results not shown) did not show any effect
on clotting time. However, after addition of 15% honey in
whole blood resulted 2.5 and 5% increase in clotting time.
With 24% honey, mean clotting time was increased to 18
and 27% and finally honey at dose of 30% increased the
mean clotting time by 38%. Whole blood (no honey) was
taken as control.
Table 1: Percentage composition of honey sugars (in %).
Honey Samples Glucose Fructose Sucrose Maltose Total sugar %
Reference Ranges
28-36% 36-50% 0.8-5.0% 1.7-11.8% *
Cap 30.09 38.45 5.17 2.1 75.84
Clo 33.33 37.33 3.03 1.83 75.52
Lan 26.78 33.91 6.4 2.59 69.73
Swa 25.09 23.54 4.38 3.67 56.69
Sid 24.3 31.66 9.4 3.79 69.15
Sha 33.63 36.9 2.59 1.87 74.99
Table 2: Composition of honey samples
Ash
( % )
Viscosity
(Poise) pH Sp. Gravity
(20o C)
Water content
(% w/w basis)
Reference Ranges
Honey Samples
0.04-0.93% 150 3.3-5.6 1.423 15-18
Cap 0.06 130 4.098 1.4335 20.412
Clo 0.07 140 3.859 1.4277 20.364
Lan 0.07 114 4.09 1.4203 21.237
Swa 0.06 140 3.701 1.429 21.814
Sid 0.05 145 5.057 1.422 23.931
Sha 0.06 130 5.216 1.4293 22.798
Effect of natural honey on human platelets
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397
392
Table 3: Effect of honey on platelet aggregation
No. Honey Samples IC50 (%)
1. Plectranthus honey (Swa) 5.0±0.1
2. Ziziphus honey (Sid) 5.5±0.15
3. Acacia modesta honey (Sha) 5.5±0.09
4. Euclayptus honey (Cap) 5.0±0.2
5. Clover honey (Clo) 6.5±0.1
6. LangneseTM honey (Lan) 6.0±0.17
Effect of honey on coagulation parameters tested in
platelet poor plasma
In this study, six honey samples were tested in platelet
poor plasma using aPTT, PT, TT and Fibrinogen level
assays. Results clearly indicate that addition of honey
significantly increased measured aPTT, PT, TT and
decreased the Fibrinogen levels.
Fig. 2: Effect of honey samples on whole blood clotting
time.
Fig. 1: Effect of honey samples on human platelet aggregation
Asif Ahmed et al.
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397 393
Effect of honey on aPTT tested in platelet poor plasma
Fig. 3 shows effect of different honey samples on aPTT.
Incubation of natural honey at different concentrations
i.e., 3.75 and 7.5% showed progressive prolongation in
aPTT. Results shows, the mean increase in aPTT by
incubation of 3.75 and 7.5% honey in PPP determined as
19±10% (Swa honey response not included) and 62±10%
respectively. PPP (without honey) was taken as control.
Effect of honey on pt tested in platelet poor plasma
Fig. 3 shows, effect of different honey samples on PT.
Incubation of natural honey at concentration 3.75 and
7.5% caused progressive prolongation in PT and
determined as 6.0±5.0% and 40±5.0% respectively. PPP
(no honey) was taken as control.
Fig. 3: Effect of honey on activated partial prothrombin
time in platelet poor plasma.
Effect of honey on TT tested in platelet poor plasma
Similar to above results, fig. 4, show that incubation of
natural honey at concentration 3.75 and 7.5% caused
progressive prolongation in TT and determined as
35±15% and 112±30% respectively. PPP (no honey) was
taken as control.
Fig. 4: Effect of honey on prothrombin time in platelet
poor plasma.
Effect of honey on fibrinogen level tested in platelet
poor plasma
Fig. 5 shows results of honey samples with natural honey
at concentrations 6.25 and 11.75% that shows decrease in
Fibrinogen level and determined as, as 13±4% (Sha honey
response not included) and 86±30% respectively. PPP (no
honey) was taken as control.
Fig. 5: Effect of honey on thrombin time in platelet poor
plasma.
Effect of honey mixed in whole blood and coagulation
parameters tested on extracted platelet poor plasma
Fig. 6 shows the results of different honey samples at 9%
concentration that were initially incubated in whole
blood; later PPP was isolated and assayed for aPTT, TT,
PT. This experiment showed that honey treatment of
whole blood caused significant prolongation of tested
assays. The mean increase in aPTT, PT and TT in
extracted PPP determined as 45±21%, 26±9% (Sid honey
response not included) and 105±24%, respectively. PPP
(no honey) was taken as control.
Fig. 6: Effect of honey on fibrinogen level in platelet poor
plasma.
Effect of natural honey on human platelets
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397
394
DISCUSSION
The present study is the first report about the effect of
honey on blood hemostasis. Previously, only
anticoagulant properties of honey bee venom were known
(Ouyang et al., 1979; Kini et al., 1994; Gowlik et al.,
2004; Franco et al., 1994). During the pathogenesis of the
vascular disorder, the formation of unwanted thrombus on
the pre-existing atherosclerotic plaques can cause partial
or complete occlusion of the blood vessel, which leads to
sinister clinical events such as acute myocardial infarction
or cerebrovascular accidents (Victor et al., 2002; Thomas,
2008). More over independent, abnormal and
uncontrolled coagulation termed as hypercoagulability
leads to serious clinical events such as deep vein
thrombosis (Libby, 2002; Kannel, 2005). The formation
of thrombus is initiated by the platelet aggregation
(platelet plug); that follows the activation of blood
coagulation proteins to further reinforcement platelet plug
by forming a mesh work of insoluble fibrin (Kannel,
2005; Rauch et al., 2001; Furie and Furie, 2005).
Platelets play a key role in primary hemostasis,
thrombosis and inflammation (Ahmad, 2003). Therefore,
the importance of anti-platelet therapy in the prevention
of vascular disorder is unquestionable. The results of the
present study indicate that addition of natural honey into
the reaction mixture; causes the inhibition of platelet
aggregation.
The mechanism by which honey inhibits the platelet
aggregation can be explained by many factors such as,
honey contains hydrogen peroxide (Molan, 2001a, b);
studies shows that exogenous exposure to hydrogen
peroxide result in platelet inhibition (Ferroni et al.,
2004a), therefore it can be assumed that the presence of
hydrogen peroxide might be the underlying basis of honey
induced inhibition of platelet aggregation. Moreover, it
can be suggested that honey is competitively antagonizing
ADP receptor mediated aggregation. Natural honey is
known to have suppressive effects on reactive oxygen
species (Ahmad et al., 2009). Here it would be
meaningful to mention, that activated platelets during and
after the platelet aggregation release different cytokines
which in turn activates phagocytes. Thus platelet activated
phagocytes results in increase production of free oxygen
radicals (Pervushina et al., 2004; Kazemi et al., 2008).
Since honey inhibits the aggregation of platelets therefore
it can be assumed that it indirectly inhibits the production
of free oxygen radicals. Interestingly free oxygen radicals
indirectly act on platelet function via oxidative
modification of low-density lipoproteins or oxidation of
lipids and their derivatives (Ferroni et al., 2004a). Hence
it can be assumed that honey can influence the platelet
function by inhibition of LDL oxidation (Hegazi and El-
Hady, 2007) that indirectly affects platelets function.
Natural honey causes physiological euglycemia (Ahmad
et al., 2008) and it has been reported that hyperglycemia
causes redox activation of platelets (Ferroni et al., 2004b).
The honey induced physiological euglycemia might be
additional factor, affecting the functions of platelets.
After the process of primary hemostasis induced by
platelets; secondary hemostasis is achieved by the
activation of blood coagulation that resulted in the
formation of fibrin mesh work. Therefore, the importance
of anti-coagulant therapy in the prevention of vascular
disorder is also without a shred of doubt.
Results of present study demonstrate that honey inhibited
the coagulation proteins of all three coagulation pathways
i.e., intrinsic pathway (assayed by aPTT); extrinsic
pathway (assayed by PT) and final common pathway
(assayed by TT). Moreover, during this study honey-
induced decrease in fibrinogen levels that is in agreement
with the prolongation of aPTT, PT and TT observed.
There could be several reasons for natural honey to have
anticoagulant attributes such as, honey contains variety of
flavonoids that may affect the activity of coagulation
factors like fibrinogen and factor VII (Cazenave, 1988;
Middleton and Kandaswami, 1992; Beretz and Cazenave
1991). Similarly different types of sugars affect the
process of blood coagulation. Honey contains glucose
(28-36%) and it has been suggested that high level of
glucose interferes with coagulation through different
mechanisms such as, non-enzymatic glycation, the
development of increased oxidative stress, and a decrease
in the levels of subendothelial heparin sulphate (Carr,
1996; Bakaltcheva and Reid, 2003). Moreover, honey
contains maltose (1.7-11.8%) that also reported to
interfere with blood coagulation (Carr and Carr 1995;
Carr et al., 1996; Bakaltcheva and Reid, 2003).
The results of present study, provides clear evidence for
multi-dimensional anti-haemostatic properties of honey;
that encompasses interference with the intrinsic, extrinsic,
common coagulation cascades as well as platelet
aggregation. It can be assumed that observation of median
levels of efficacy in honeys originated from different
floral sources and geographical regions indicated that
anti-platelets / anticoagulant activity might be a general
property of honey. These observations provide first line
evidence for modulatory role(s) of honey on process of
hemostasis.
Medicinal properties of honey, encompass various
mechanisms that might play a role in the prevention of
atherosclerotic vascular disorders e.g., cardiovascular and
cerebrovascular disorders. Honey has reported to inhibit
thrombin (main enzyme of blood coagulation) induce
formation of reactive oxygen species from phagocytes; as
Asif Ahmed et al.
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397 395
free oxygen radicals particularly superoxide and
hypochlorous acid provides the nidus for the development
of atherosclerotic plaque, thus honey might interrupts the
nidus formation of atherosclerotic plaque (Ahmad et al.,
2009). Honey independently inhibits LDL oxidation that
also prevents the development of primary atherosclerotic
lesion (Hegazi and El-Hady 2004). It is reported that
fasting blood sugar is an independent predictor of platelet
dependent thrombosis in patients with coronary artery
(Shechter et al., 2000). Honey has reported to have
physiological euglycemia in fasted human subjects
(Ahmad et al., 2008). This effect also possibly interferes
with the process of thrombosis.
On the basis of present and previous results, it can
assumed that honey might interferes at several steps in the
formation of atherosclerotic disease this effect finally
translates into the prevention of vascular disorders such as
cardiovascular and cerebrovascular disorders.
REFERENCES
Ahmad A, Azim MK, Mesaik MA, Nazimuddin and Khan
RA (2008). Natural honey modulates physiological
glycemic response compared to simulated honey and
D-Glucose. J. Food Sci., 73: 165-167.
Ahmad A, Khan RA and Mesaik MA (2009). Anti-
inflammatory effect of natural honey on bovine
thrombin induced oxidative burst in phagocytes.
Phytother. Res., 23: 801-808.
Ahmad SS, London FS and Walsh PN (2003). The
assembly of the factor X-activating complex on
activated human platelets. J. Thromb. Haemost., 1: 48-
59.
Amy EJ and Carlos ME (1996). Medical uses of honey.
Biomedica, 7: 43-49.
Azim MK, Perveen H, Mesaik MA and Simjee SU
(2007). Antinociceptive activity of natural honey in
thermal-nociception models in mice. Phytother. Res.,
21: 194-197.
Bailoni ML and Bittante G (1994). Solubility, water-
holding capacity, and specific gravity of different
concentrates. J. Dairy Sci., 77: 774-781.
Bakaltcheva I and Reid T (2003). Effects of blood product
storage protectants on blood coagulation. Transfus.
Med. Rev., 17: 263-271.
Beretz A and Cazenave JP (1991). Old and new natural
products as the source of modern antithrombotic drugs.
Planta Med., 57: 68-72.
Berry CN, Lassalle G and Lunven C (2002).
SSR182289A, a novel, orally active thrombin inhibitor:
In vitro Profile and ex vivo anticoagulant activity. J.
Pharmacol. Exp. Ther., 303: 1189-1198.
Carr M and Carr S (1995). Fibrin structure and
concentration alter clot elastic modulus but do not alter
platelet mediated force development. Blood Coag.
Fibrin 6: 79-86.
Carr M, Dent M and Carr S (1996). Abnormal fibrin
structure and inhibition of fibrinolysis in patients with
multiple myeloma. J. Lab. Clin. Med., 128: 83-88.
Carr ME (2001). Diabetes Mellitus: A Hypercoagulable
State. J. Diabetes Complications, 15: 44-54.
Cazenave AJP (1988). The effect of flavonoids on blood-
vessel wall interactions. In: Cody V, Middleton E,
Harborne JB, Beretz A (eds.) Plant flavonoids in
biology and medicine II: Biochemical, cellular, and
medicinal properties. Alan R Liss, New York, pp. 187-
200.
Cedergren A (1974). Reaction rates between water and
Karl Fischer Reagent. Talanta, 21: 265.
Cheng DCH (1990). A review of on-line rheological
measurement. Food Science Technology Today, 4: 242-
249.
Cooper RA, Molan PC and Harding KG (2002). The
sensitivity to honey of Gram-positive cocci of clinical
significance isolated from wounds. J. Appl. Microbiol.
93: 857-863.
Escandon CJ, Garcia-Rubi E, Mirza S and Mortensen A
(1999). Type 2 diabetes: One disease, multiple
cardiovascular risk factors. Coron. Artery Dis., 10: 23-
30.
Ferroni P, Basili S, Falco A and Davi G (2004a). Oxidant
stress and platelet activation in hypercholesterolemia.
Antioxid. Redox. Signal, 6: 747-756.
Ferroni P, Basili S, Falco A and Davi G (2004b). Platelet
activation in type 2 diabetes mellitus. J. Thromb.
Haemost. 2: 1282-1291.
Franco FO, Benvenuti LA and Fan HW (1994). Severe
and fatal mass attacks by killer bees (Africanized
honey bee-Apis mellifera Scutellata) in Brazil:
Clinicopathological studies with measurement of serum
venom concentrations. Q. J. Med., 87: 269-282.
Franco RF, De Jonge E, Dekkers PE, Timmerman JJ,
Spek CA, Deventer SJV, Deursen PV, Kerkhoff LV,
Gemen BV, Cate HT, Poll TVD and Reitsma PH
(2000). The in vivo kinetics of tissue factor messenger
RNA expression during human endotoxemia:
Relationship with activation of coagulation. Blood, 96:
554-559.
Furie B and Furie BC (2005). Thrombus formation in
vivo. J. Clin. Invest. 115: 3355-3362.
Gowlik R, Rymarczyk B and Rogala B (2004). A rare
case of intravascular coagulation after honey bee sting.
J. Investig. Allergol. Clin. Immunol., 14: 250-252.
Hegazi AG and El-Hady FK (2007). Influence of honey
on the suppression of human low density lipoprotein
(LDL) peroxidation (in vitro). doi:10.1093/ecam/
nem071. e CAM, pp.1-9.
Hoffmann H (1998). Karl-Fischer-Reagenz enthaltend
Ethanol als alkoholische Komponente, European Patent
Application, 98121169.1.
Effect of natural honey on human platelets
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397
396
Jain S, Palmer M and Chen Y (1999). Effect of vitamin E
and N-acetylcysteine on phosphatidylserine externa-
lizetion and induction of coagulation by high-glucose-
treated human erythrocytes. Metabolism, 48: 957-959.
Kannel WB (2005). Overview of hemostatic factors
involved in atherosclerotic cardiovascular disease.
Lipids, 40: 1215-1220.
Kazemi A, Singh AK and Slater NGP (2008). An in vitro
direct chemiluminescence assay for assessment of
platelet-bound antibody in thrombocytopenic patients.
Br. J. Haematol., 79: 624-627.
Kelly C (2003). Diet and cardiovascular disease. Institut
National de la Recherche Agronomique 147, rue de
l'Université 75338 PARIS cedex 07 - France N.
Kini PG, Baliga M and Bhaskaranand N (1994). Severe
derangement of the coagulation profile following
multiple bee stings in a 2 year-old boy. Ann. Trop.
Paediatr., 14: 153-155.
Kumar P. Clark M (2005). Cardiovascular disease in
Clinical Medicine 6th ed. p 725-750.
Kuulasmaa K, Tunstall PH, Dobson A, Fortmann S, Sans
S, Tolonen H, Evans A, Ferrario M and Tuomilehto J
(2000). Estimation of contribution of changes in classic
risk factors to trends in coronary-event rates across the
WHO MONICA Project populations. The Lancet, 355:
675-687.
Levi M, Poll TV and Büller HR (2004). Bidirectional
relation between inflammation and coagulation.
Circulation, 109: 2698-2704.
Libby P, Ridker PM and Maseri A (2002). Inflammation
and Atherosclerosis. Circulation, 105: 1135-1143.
Libby P (2002). Inflammation in Atherosclerosis. Nature,
420: 868-874.
Meigs JB, Mittleman MA, Nathan DM, Tofler GH, Singer
DE, Murphy-Sheehy PM, Lipinska I, D'Agostino RB
and Wilson PW (2000). Hyperinsulinemia,
Hyperglycemia, and Impaired Hemostasis: The
Framingham Offspring Study. JAMA, 283: 221-228.
Mesaik MA, Azim MA and Mohiuddin S (2008). Honey
modulates oxidative burst of professional phagocytes.
Phytother. Res., 22: 1404-1408.
Middleton EJ and Kandaswami C (1992). Effects of
flavonoids on immune andinflammatory cell functions.
Biochem. Pharmacol., 43: 1167-1179.
Milne TA, Chum HL, Agblevor FA and Johnson DK
(1992). Standardized analytical methods. biomass and
bioenergy. Proceedings of International Energy
Agency Bioenergy Agreement Seminar, 2: 341-366.
Molan PC (2001a). Potential of honey in the treatment of
wounds and burns. Am. J. Clin. Dermatol. 2: 13-19.
Molan PC (2001b). The potential of honey to promote
oral wellness. Gen. Dent., 49: 584-589.
Nilsson ACT, Bylund R and Gustafsson D (1997). In
vitro effect of Inogatran, a selective low molecular
weight thrombin inhibitor. Thromb. Res., 85: 133-145.
Ouyang C, Lin SC and Teng CM (1979). Anticoagulant
properties of Apis mellifera (honey bee) venom.
Toxicon., 17: 179-201.
Pearson TA (1999). Cardiovascular disease in developing
countries: Myths, realities, and opportunities.
Cardiovasc. Drugs Ther., 13: 95-104.
Pervushina O, Scheuerer B, Reiling N, Behnke L,
Schröderjm, Kasper B, Brandt E, Bulfone-Paus S and
Petersen F (2004). Platelet factor 4/CXCL4 induces
phagocytosis and the generation of reactive oxygen
metabolites in mononuclear phagocytes independently
of Gi protein activation or intracellular calcium
transients. J. Immunol., 173: 2060-2067.
Posta JM, Sullivan ME, Abendschein D, Ewing J,
Hinchman JW and Light DR (2002). Human in vitro
pharmacodynamic profile of the selective Factor Xa
inhibitor ZK-807834 (CI-1031). Thromb. Res., 105:
347-352.
Rauch U, Osende JI, Fuster V, Badimon JJ, Fayad Z and
Chesebro JH (2001). Thrombus formation on
atherosclerotic plaques: Pathogenesis and clinical
consequences. Ann. Intern. Med., 134: 224-238.
Shah BH and Saeed SA (1995). Phosphatidylinositol 3-
Kinase Inhibitor, Wortmannin, Inhibits 5-
hydroxytryptamine-mediated potentiation of platelet
aggregation induced by epinephrine. Res. Commun.
Mol. Pathol. Pharmacol., 89: 157-164.
Shah BH, Shamim G, Khan S and Saeed SA (1996).
Protein kinase C inhibitor, chelerythrine, potentiates
the adrenaline-mediated aggregation of human platelets
through calcium influx. Biochem. Mol. Biol. Int., 38:
1135-1141.
Shechter MC, Merz NB, Maura J Labrador P and Kaul S
(2000). Blood glucose and platelet-dependent
thrombosis in patients with coronary artery disease. J.
Am. Coll. Cardiol., 35: 300-307.
Sobel BE (2002). Effects of glycemic control and other
determinants on vascular disease in type 2 diabetes.
Am. J. Med., 113: 12-22.
Steinberg D (1992). Antioxidants in the prevention of
human atherosclerosis. Circulation, 85: 2338-2344.
Thomas JW (2008). New cardiovascular risk factors exist,
but are they clinically useful. Eur. Heart J., 29: 441-
444.
Valeria C, Karen B, Dennis C, Yong-MC, Dan G, Henry
WP, Alfred P, Spada MHP, Robert JL and Christopher
TD (2000). In vitro characterization of a novel factor
Xa Inhibitor, RPR 130737. Thromb. Res., 99: 71-82.
Victor JD, Ruediger C, Dullaeus B and Sedding DG
(2002). Vascular proliferation and atherosclerosis: New
perspectives and therapeutic strategies. Nat. Med., 8:
1249-1256.
Wattiaux MA, Mertens DR and Satter LD (1992).
Kinetics of hydration and effect of liquid uptake on
specific gravity of small hay and silage particles. J.
Anim. Sci., 70: 3597-3606.
Asif Ahmed et al.
Pak. J. Pharm. Sci., Vol.24, No.3, July 2011, pp.389-397 397
Wattiaux MA, Satter LD and Mertens DR (1991). Effect
of source and amount of fiber on kinetics of digestion
and specific gravity of forage particles in the rumen. J.
Dairy Sci., 74: 3872-3883.
Wegge JK, Roberts CK, Ngo TH and Barnard RJ (2004).
Effect of diet and exercise intervention on
inflammatory and adhesion molecules in
postmenopausal women on hormone replacement
therapy and at risk for coronary artery disease.
Metabolism, 53: 377-381.
White JW Jr., Reithof ML, Subers MH and Kushnir I
(1962). Composition of american honeys. U.S.
Department of Agriculture Technical Bulletin 1261,
Washington DC. USA
(http://www.libraries.psu.edu/digital/speccolls/FindingAids/whitePD
F/Composition%20Of%20American%20Honeys.pdf)
... 12. Haemostasis property [70,71] The inhibitory effect on the blood coagulation and platelets aggregation was described by the study done by Ahmed, et al. 2011. These findings give the preliminary evidence on the modulatory role(s) of honey on haemostasis process. ...
... 12. Haemostasis property [70,71] The inhibitory effect on the blood coagulation and platelets aggregation was described by the study done by Ahmed, et al. 2011. These findings give the preliminary evidence on the modulatory role(s) of honey on haemostasis process. ...
Article
Full-text available
Since the dawn of time, honey has been one of the most prized and cherished natural goods available to humans and also being used as a medicine in the traditional medicine systems due to its marvellous medicinal effects in various ailments. It has carbohydrate in the form of glucose, fructose, maltose, sucrose, trisaccharide and other constituents such as water, minerals, proteins, vitamins and enzymes because of the same it serves as a nutritional, preservative and potent therapeutic agent. As mentioned in the Unani system of Medicine, it can be used as nutritive agent and medicinally it has antibacterial, anti-inflammatory, detergent, deobstruent, lithotryptic and wound healing properties. As the bee collects the nectar from flowers to make the honey therefore a significant variation in the properties and looks may occur. Many in vitro studies have revealed that it has many pharmacological properties like antibacterial, anti-inflammatory, antioxidant, antiviral, antifungal, and anticancer etc. Present study provides a brief review of medicinal exploration of honey in relation nutrition value, pharmacology, and Therapeutic potential.
... Many epidemiological studies have shown that regular intake of phenolic compounds is associated with reduced risk of heart disease. Many such phenolic and flavonoid compounds e.g; Chrysinhave antioxidant and anti-platelet potential, and hence may ameliorate cardiovascular diseases (CVDs) through various mechanisms, such as by decreasing oxidative stress and inhibiting blood platelet activation [3]. Studies have found flavonoids to exert beneficial action son the cardiovascular system via inhibition of blood platelet activation, reduction of LDL cholesterol level, honey phenolic compounds such as apigenin, quercetin, catechin, and luteolin inhibit blood platelet aggregation though binding to the thromboxane A2 receptor in an in vitro model [4]. ...
Article
Full-text available
Background: The most serious and common adverse side effect associated with anticoagulant is increased risk of bleeding, both non-major and major bleeding events. Risk of bleeding is dependent on the class of anticoagulant agent used, patient's age, and pre-existing health conditions. Drugs derived from plants as green medicine is believed to be safe and dependable, compared with costly synthetic drugs that have adverse effects. Honey has been used since ancient times for its nutritional and therapeutic value, Acacia honey is available worldwide and it is inexpensive in compare to anti-thrombotic and thrombolytic agent. And has anticoagulant activity for treatment these problems. Materials and Methods: In this study 100 normal blood samples from normal individuals with age range (18-30) years, 50% male and 50% female. PT and APTT tests were done before adding acacia honey by mixture patient plasma with normal plasma (as controls) and after adding acacia honey with different concentrations (10% and 25%). Results: the results were analyzed by using SPSS and showed that the acacia honey has a strong statistically significant (p= 0.000) in all concentrations in both PT and APTT tests. Conclusion: this study approved that acacia honey has a strong anticoagulant effect; so acacia honey can be used as a supplementary anticoagulant agent to improve and/ or prevent thrombosis and cardiovascular diseases. Keywords: Natural Acacia Honey; Coagulation; PT and APTT; Sudanese healthy individuals List of abbreviations: PT: Prothrombin Time; APTT: Activated Partial Thromboplastin Time; DVT: Deep Vein Thrombosis; PPP: Platelet poor plasma; BV: Blood Vessel; VWD: Von willebrand disease
... Studies show that regular intake of phenolic compounds, such as those found in honey, is associated with reduced cardiovascular risk [43]. Honey enhances low-density lipoprotein (LDL) resistance to oxidation and contributes to coronary vasodilation, anti-thrombotic effects, and antioxidant activity [44,25]. These properties make honey a powerful tool against atherosclerotic plaque formation and related cardiac disorders. ...
Article
Full-text available
Honey, often referred to as "liquid gold," has captivated humanity for millennia, serving as a completely natural food devoid of additives and preservatives, significant medicinal value and a symbol of cultural and spiritual significance. With over 300 varieties recognized globally, honey's composition, flavor, and therapeutic properties vary significantly based on its botanical and geographical origins. Historically, honey has been revered by ancient cultures, from its symbolic role in Egyptian, Greek, and Indian traditions to its central place in Christianity, Islam, Hinduism and Judaism. Its mention in holy texts emphasizes its sanctity and wholesome potential. Scientifically, honey is a complex supersaturated solution containing sugars, amino acids, vitamins, and antioxidants, with demonstrated antimicrobial, anti-inflammatory, and anticancer properties. Modern research highlights its prebiotic activity, cardiovascular benefits, and role in managing diabetes and promoting wound healing. Despite its remarkable medicinal value, honey is classified as food rather than a drug by regulatory authorities, underscoring the need for further research to standardize its therapeutic use. This manuscript explores the multifaceted nature of honey, examining its historical, religious, nutritional, and medicinal roles across civilizations.
... The mechanism by which honey inhibits the aggregation of platelets can be explained by several factors such as, honey contains hydrogen peroxide. 16 On the other hand, Ahmed et al., 2011 showed Eucalyptus honey increased platelet inhibition aggregation compared to control as a guide. 17 The hypothesis that honey dose not have a high effect on platelets count as a result of honey containing antioxidant preventing LDL oxidation and thus reducing platelet aggregation. ...
Article
Full-text available
Introduction and Aim: Natural honey has many biological activities including increase Hematology (Red Blood Cell (RBC), Packed Cell Volume (PCV), Hemoglobin (Hb), Platelets (PLT) and Prothrombin time (PT)) and serum of testosterone and Luteinizing hormone. The aim of these study to know the effect of honey intake on some blood profile and to know the extent of honey impact on testosterone level. Material and Methods: About 20 healthy men were selected aged 45-60 years in Baghdad, given 50 gram Eucalyptus honey daily orally for 30 days and tested blood samples were collecting to measure the previous parameters before and after treatment. Results: The study found that there was a significant increase in all hematology parameters and testosterone hormone after eat the honey.
... The critical role of Apis mellifera honey in addressing immunodeficiency is substantiated by a corpus of sophisticated clinical and experimental research, as evident in different studies (1,4,6,7,8,9,11,14,15,22,24,26). ...
Article
Full-text available
Aims and objectives: This study systematically investigates Apis Mellifera honey as an integral component within the beekeeping value chain, specifically emphasizing its role in apicultural mountain production. Methods: The research delves into multifaceted dimensions, encompassing agronomical and territorial profiles, generated through the utilization of the Paintmap online software. Additionally, the investigation employs experimental and statistical perspectives, utilizing SPSS and Excel software for analysis. Important observations and results: The outcomes of this comprehensive analysis reveal a noteworthy evolution in the Apis Mellifera honey market, particularly during the prevailing pandemic circumstances. The findings elucidate a discernible surge in market development over recent years. Ultimately, the paper posits that the value chain associated with Apis Mellifera mountain honey originating from European Romania substantiates a substantial foundation for mountain production and agricultural practices. In summation, this exploration contributes to the scholarly understanding of the intricate dynamics within the apicultural sector, shedding light on the pivotal role of Apis Mellifera honey in sustaining robust mountain production and farming activities.
... Several studies demonstrated that honey consumption has beneficial effects on cardiovascular disease indicators [1,16,19]. The reduction in platelet activity was proved by Ahmed et al. [2], who studied the effects of different types of honey on platelet aggregation and coagulation. Recently, in order to increase the biological activity of honey, plant additives have been introduced to it. ...
Article
Full-text available
Background. The Melilotus plants are highly valued in herbal medicine, recommended for the prevention and treatment of thrombotic vein inflammation and varicose veins. Their health-promoting properties primarily result from the presence of coumarin and its derivatives. The aim of the study was to determine whether honey enriched with dried Melilotus albus flowers has the ability to inhibit platelet aggregation. The inhibitory activity of rapeseed honey (control sample), rapeseed honey enriched with 1 % w/w of M. albus dried flowers and pure coumarin were evaluated against ADP (5 µМ) and collagen (2 µg/ml) in duced aggregation of rat platelets. Platelet aggregation was measured by the turbidimetric method. Moreo ver, the quantitative polyphenolic profile determined using HPLC-PDA and volatile compounds profiles obtained by GC-MS methods for rapeseed and M. albus enriched honey were compared to identify the chemical factors that limit platelet aggregation. Results and conclusions. A beneficial, dose-dependent effect of enriched honey on the inhibition of the aggregation process was demonstrated, and for the highest concentration used (20 %), the inhibition of aggregation induced by ADP and collagen amounted to 75 % and 90%, respectively. A weaker inhibitory effect was found for pure rapeseed honey at 20 % concentration – 40 % and 55 % of inhibition, respective ly and pure coumarin (0.5 mg/ml) – 44 % and 20 %, respectively. The results obtained demonstrated that rapeseed honey enriched with M. albus flowers possesses antiplatelet activity resulting from the synergistic effect of coumarin and other bioactive compounds occurred in dried M. albus flowers, including phe nolic and volatile components.. However, the mechanism of this action needs further study.
... Many epidemiological studies have shown that regular intake of phenolic compounds is associated with reduced risk of heart disease. Many such phenolic and flavonoid compounds e.g; Chrysinhave antioxidant and anti-platelet potential, and hence may ameliorate cardiovascular diseases (CVDs) through various mechanisms, such as by decreasing oxidative stress and inhibiting blood platelet activation [3]. Studies have found flavonoids to exert beneficial action son the cardiovascular system via inhibition of blood platelet activation, reduction of LDL cholesterol level, honey phenolic compounds such as apigenin, quercetin, catechin, and luteolin inhibit blood platelet aggregation though binding to the thromboxane A2 receptor in an in vitro model [4]. ...
... Prostacyclin increases the formation cAMP which blocks GPIIb/ IIIa receptors 26 . Flavonoids also interfere with coagulation factors like fibrinogen and factor VII 27 . Fermented garlic has highest effect on the inhibition of platelet aggregation than unfermented garlic 13 . ...
Conference Paper
Full-text available
Sri Lankans consume garlic as raw, cooked and honey-fermented. Anticoagulant properties of garlic vary with different preparations. Here we analysed the in vitro anticoagulant activity of aqueous extracts of raw, boiled and honey-fermented garlic to determine the anticoagulant activity. Aqueous extracts of raw, boiled, and honey-fermented garlic preparations at different concentrations (10, 50, 250 and 500 mg ml-1 ) were prepared. In vitro anticoagulant activity was analysed by replicating prothrombin time (PT) of pooled plasma diluted with different garlic extracts four times. Independent sample t-test and Mann Whitney U test compared the PT values among each preparation. Mean PT values with aqueous extract of honey fermented garlic (25.8 ± 0.5, 27.8 ± 0.5, 30 ± 0.0 and 30 ± 0.0 s) were significantly higher compared to control (24 ± 0.0 s) at all concentrations (p < 0.05). The mean PT values with aqueous extract of raw garlic (25 ± 0.0 and 28.3 ± 0.5 s) and boiled garlic (25.3 ± 0.5 and 26 ± 0.0 s) were significantly higher compared to control only at high concentrations (250 & 500 mg mL-1 ; p < 0.05). The PT values increased with an increasing concentration of garlic extract. Honey fermented garlic had significantly higher PT values than the other two preparations (p < 0.05). Raw garlic had significantly high PT values than boiled garlic at high concentrations (p < 0.05). The boiling of garlic prevented the formation of organosulfur compounds, which are major compounds responsible for its anticoagulant activity. Honey has an effect on platelet aggregation. All three preparations of garlic have inhibitory effects on blood coagulation. Honey-fermented garlic has higher anticoagulant activity than the other two preparations. The anticoagulant activity increased with an increasing concentration of garlic extract. Keywords: Boiled garlic, Honey fermented garlic, In vitro anticoagulant activity, Raw garlic
Conference Paper
Full-text available
The aim of this study was to investigate the effects of exposure cigarette smoke on the cardiac tissues in male rats and the improvement role of Sidr honey. Twenty eight male rats were divided into four groups; Group 1: control rats; group 2: rats were given Libyan Sidr honey (100 mg/kg b.w./d.) orally for 4 weeks.; group 3: rats were exposed to the five lit from sidestream of the Karelia red cigarettes (5 times/d.) by a machine smoking for 4 weeks.; and group 4: rats were received the Sidr honey (100 mg/kg b.w./d.) orally for 2 weeks, then the rats were exposed to the Karelia cigarettes generated by a machine smoking with given the Sidr honey for 4 weeks. The X-Ray radiography of rats showing, heart mildly enlarged size in the KC-exposed rats as compared with the NC rats. While, the POR rats showed normal heart size when compared with KC rats. Moreover, the KC group showed a significant increase (P < 0.05) in CK, CK-MB, and LHD as compared to the NC group, whereas the POR group showed a significant decrease (P < 0.05) in the CK, CK-MB, and LHD when compared with the KC group. Histological investigation of the heart tissues of the KC group showed different histopathological changes as compared to the NC group. Nevertheless, the POR group showed the marked improvement in the heart tissues as compared to the KC rats. Conclusion, results demonstrated that Libyan Sidr honey significantly reduced the toxic effects of KC-exposed on the heart structures.
Article
Full-text available
The effects of solubility and water-holding capacity on functional and unit specific gravity were evaluated in samples of fish, soybean, linseed, corn gluten, corn gluten feed, corn, barley, and dehydrated alfalfa meals and in wheat bran, raw flaked soybeans, cottonseeds, and dried sugar beet pulp. Solubility was estimated by washing the samples in nylon bags in a washing machine. Functional specific gravity was estimated in a pycnometer for unwashed and washed samples after 0 and 15 h of soaking in distilled water. Water-holding capacity was measured by a centrifugation method and by a filtration method. Unit specific gravity was estimated as the weighted mean of the functional specific gravity of insoluble DM and the specific gravity of water held by the particles. Solubility and functional specific gravity of insoluble DM varied significantly among feedstuffs from 5.0 to 53.2% of DM and from 1.31 to 1.62, respectively. The increase in functional specific gravity from soaking was small. Water-holding capacity was lower with filtration than with centrifugation methods and varied from .94 to 6.44 g of H2O/g of DM. Unit specific gravity varied significantly from 1.07 to 1.24. Soluble fractions and water-holding capacity can markedly influence the functional and unit specific gravity of concentrate particles.
Article
Full-text available
This article reviews reports on the use of honey in the treatment of human disorders which are supported by clinical tests and published in medical journals. Firstly, the composition of honey is described, followed by a revision of its effect on the growth of several strains of pathogenic bacteria in laboratory tests. Finally, the influence of honey on gastroenteritis, gastric ulcers, wounds and other disorders is reviewed.
Chapter
When Ancil Keys demonstrated many years ago that saturated fat intake was related to elevated cholesterol levels and coronary artery disease death rates around the world [1], he ignited a debate which has not yet been fully settled. There is a direct linear relationship between saturated fat intake, cholesterol levels, and coronary artery disease. It is less clear whether changing saturated fat intake changes blood cholesterol levels in adults to a sufficient degree to significantly reduce coronary disease. The implications of these relationships are of great economic as well as health importance in those countries in which saturated fat intake is high. The outcome of this debate is not only of significance to physicians and their patients, but also to farmers, livestock producers, food distributors, and the governments which represent and oversee them.
Article
Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.
Article
This document is the methodological appendix to the paper titled "Estimating the contribution of changes in classical risk factors to trends in coronary-event rates across the WHO MONICA Project populations" published in Lancet, 2000;355:675-687. It covers three topics: - brief description of the regression analysis and the output statistics used in the paper; - justification for the age-standardization used for calculating risk factor trends for the regression analysis; and - derivation of the quality score which was used to weight the populations in the regression analysis.
Article
The ever-increasing demand for blood products challenges scientists to develop new and more effective techniques for their preservation. The progress of these novel preservation technologies uses a wide variety of cryoprotectant, lyoprotectant, and other preservatives, which will need to be explored and assessed for their biological effects during blood product formulation. The leading factor in protectant selection is for their ability to provide superior preservation for a particular blood product. We believe that such protectants used in blood product development should also be evaluated for their ability to preserve normal hemostasic mechanisms. In this review, high-molecular-weight cryoprotectants, lyoprotectants, polyols, amino acids, antioxidants, and surfactants, used because of their protective properties, were evaluated for their possible role in relation to their effect on normal hemostatic mechanisms.