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TilE EFFECT OF OLEA EUROPAEA ANI> JUNIPERUS COMMUNIS
ON HYPERCHOLESTEROLAEMIA
By
SANDRA SQUARA
ABSTRACT
Thepurpose of this study was to evaluate the effect of the gemmoiherapeutic substances:
Olea europaea and Juniperus communis in the treatment ofhypercholesterolaemia. This
was evaluated in terms ofchanges in blood cholesterol levels in order to determine the
extent to which gemmothempeutic medicine could be used in the treatment ofthis
condition. It was hoped that there would be a drop inthe total cholesterol levels and an
increase inthe ratioof high density flow density lipoprotein.
Foracceptance into thetrial, participants had to have an elevated total cholesterol level of
~5,t7 mmol/L, and bewithin an age brocket of25 to75 years.
Drawing of blood was performed at the Technikon Pathology Laboratory following an

overnight fast. Of those participants meeting the above criteria thirty were chosen to
participate in the three- month trial. Half constituted the control group and were given a
placebo, theother halfconstituted the trial group and were treated with a combination
preparation ofO/ea europaea and Juniperus communis both in a 01 potency, in a
glycerine base.
This was a double blind study with the division ofthe trial group being done on a random
basis by an independent person from the study.
After commencement ofthe trial venous blood was collected once a month for three
consecutive months from both the control and experimental groups.
The participants were asked to make no changesto their normal lifestyles with regard to
diet and exercise.
Analysis of the dataobtained from the trial study revealed no statistical significant
results. However results showed that the greates! change occurred in the last month of
treatment, warranting further investigation into a longer trial period to vcrify the trend.
iii
TABLE OF CONTENTS Page
ACKNOWLEDGEMENTS ii
ABSTRACf 111
TAULEOFCONTENTS iv
LISfOFTABLES vi
LISf OFGRAPIIS vii
DEFINITION OF TERMS viii
CHAPTER ONE 1
1.1 THE PROBLEM 2

1.2 THE AIM 2
1.3 JUSTIFICATION FOR THE STUDY 2
1.4 THE USE OF GEMMOTHERAPY 2
1.5 DELIMITATIONS 3
1.6 THE ASSUMPTIONS 4
CHAPTER TWO - LITERATURE REVIEW 5
2.1 ATHEROSCLEROSIS, CHOLESTEROL

AND CORONARY HEART DISEASE (CHD) 5
2.2 ATHEROSCLEROSIS AND INFLAMMATORY
MARKERS OF CORONARY RISK 7
2.3 THE LIPOPROTEINS 10
2.4 ASSOCIATED RISK FACTORS FOR CHD 12
2.5 INFLUENCE OF RACE AND GENDER ONLIPOPROTEINS 17
2.6 TREATMENT 20
2.7 DRUG TREATMENT . 21
2.8 GEMMOTHERAPEUTIC TREATMENT 25
iv
CHAPTER THREE - MATERIALS AND METHODOLOGY 34
3.1 STUDY DESIGN 34

3.2 THE RESEARCH METHODOLOGY 34
CHAPTER FOUR 40
4.1 RESULTS 40
CHAPTER FIVE - DISCUSSION 49
5.1 EVALUATIONOFTHERESULTS 49
5.2 DECREASING VALUES FORTC, LDL·C AND TRIGLYCERIDES 49
5.3 HDL·CHOLESTEROL 50
CHAPTER SIX-CONCLUSIONS AND RECOMMENDATIONS
6.1 CONCLUSION 51
6.2 RECOMMENDATIONS 51
REFERENCES 53
APPENDIX A
CONFIRMATION REPORT FOR MEDICATION

APPENDlXB
RAW DATA
v
usr OF TABLES
Table one: Standards for CHO risk factors. 5
Table two: Selected lipid and lipoprotein measures (mg/dl.) 23

from young adults (18- 24 years) in the CARDIA study
bysex and race.
Table three: Effects ofOlea europaea leaves and shoots and 31

oleuropein on cholesterol, total lipids and triglycerides in
hypercholesterolaemic diet-fed rats.
vi
.
usr OF GRAPHS page
GraphOne: Represents the changes in TC (Total cholesterol)

levels for the medication and placebo groups. 41
GraphTwo: Represents the decrease in values for TC betweenthe

medication and placebo groups. 42
GraphThree: Represents the average values ofLDL-C for placebo

and medication groups. 43
Graph Four: Represents the decrease in values for the LDL-e levels
between the placebo and medication groups. 44
Graph Five: Represents the average values forHDL-e levels taken

for both the placebo and medication groups. 45
Graph Six: Represents the increase in HDL-C levels,

compared betweentheplacebo and medication groups. 46
Graph Seven: Represents the average triglyceride values for placebo 47

andmedication groups.
Graph Ei.:ht: Represents the decrease in values for Triglyceride levels, between the
placebo and medication groups. 48
vii
DEFINITION OF TERMS
Ilypercholesterolaemia
Atype of lipid disorder that is associated with an increased risk for coronary heart
disease. The risk is particularly steep after serum cholesterol rises above 5.17mmol/L
(Lee et al., 1993).
CliO
Coronary Heart Disease, acondition that results from an obstruction ofblood flow to the
heart (Cataldo, 1998).
Atherosclerosis
Thickening and narrowing ofarteries due tothe infiltration of fatty streaks. impairing the
functioning and circulation of blood supply(Oberman et al., 1992).
IIDL
High- Density Lipoprotein, a lipid- transporting lipoprotein thatcarries lipids from the
blood stream to theliver, itis the "good" cholesterol (Lee et aI., 1993).
LDL
Low-Density Lipoprotein carries lipids to various cells in the body, and itconsidered the
most atherosclerosis-producing lipoprotein (Lee etal., 1993).
VLDL
Very Low Density Lipoproteins
Gemmothcrapcutic treatment
Atherapeutic method that uses plant bud extracts orother vegetable tissue, freshly
harvested from thegrowing plant (Tetau, 1998).
viii
Chylomicrons
Agroup of lipid-transporting lipoproteins that carry lipids todifferent sites in the body
(Lee et al., 1993).
Dl Potency
The first decimal dilution
be
CHAPTER ONE
1.1 The Problem
In a recent CNN article discussing a new study based on the data from the Framingham
Study concludes: The study "reaffirms" the notion that coronary heart disease is the 800
pound gorilla ofdisease, now and for the foreseeable future", says Dr. Stuart Seides.
Heart attacks were virtually unknown before the tum of the century. Our diets, especially
in "developed" countries, have gone through dmmatic changes in this period.
Elevated serum cholesterol is a major contributory factor for Coronary Heart Disease
(CHO) (Wang, et al., 1998).
Primary prevention through behavioural modification has been designated as a first-line

treatment for patients with elevated cholesterol (Wang, et al., 1998).
However it is not always easy to change people's lifestyle and diets without proper
nutritional and exercise education and advice. The problem still remains that people are at
risk ofCHD due to elevated cholesterol levels and have no option but to resort to drugs,
which do have undesirable side effects.
These drugs are not suitable for everyone, and with a growing interest in living a more
"natural" lifestyle, moving away from contemporary medication, a possible alternative to
drugs would be beneficial.
The problem arises in that people need an available alternative approach for treating
hypercholesterolaemia. Interest in alternative medicine is on the increase and could be the
possible bridge, connecting behavioural modification with a natural medicine in order to
lower cholesterol and in tum decreasing the risk ofCHD.
Very little scientific research has been carried out in investigating the effectiveness of an
alternative treatment for hypercholesterolaemia.
1.2 The Aim
This study looks at linking analternative approach, namely the use ofgemmothempeutic
substances Olea europaea and Juniperus communls for the treatment of
hypercholesterolaernia, with aclinical trial in order toestablish scientific data with regard
to the effectiveness ofsuchtreatment.
1.3 Justification for the study
Research Into the effectiveness of using plant-based substances for the treatment of
hypercholesterolaemia has not been scientifically proven before. These substances have
no known side effects, are inexpensive and natural and would prove to expand the field of
knowledge in this regard, Such a study would add to the scientific data for further
research. This will help find relevant answers to the problem of contemporary drug
treatment programmes being the main mode of treatment offered.
1.4 The use of Gemmotherapy
Gemmothempy is a form ofPhytothempy (plant medicine), using fresh plant buds. It is

currently experiencing rapid development in France and elsewhere asaneffective form of
treatment. It is used as an adjunct to other forms of therapy, such as homeopathy and
provides the unique ability of clearing toxins from the system, thereby helping the body
to repair, and reachbalance (Tetau, 1998).
Gemmothempy has been used successfully for the treatment of four major metabolic
ailments: Adult-onset diabetes, Hypcrcholcstcrolaemla, Hyperuricemia and Excessive
weight. (Tetau. 1998).
2
Olea europaea and Juniperus communis are the two recommended lipid lowering
gernmotherapeutic remedies (Tetau, 1998).
1.5 Delimitations
1.5.1 Delimitation One
The emphasis of this study was on the effectiveness of the two gemmotherapeutic
substances on the total cholesterol and the ratio between the low-density lipoprotein and
high-density lipoprotein levels. It did not attemptto explain the following:
a) The effectofdietorexercise on hypercholesterolaemia,
b) The role played by triglycerides in hyperchoplesterolaemia,
c) The type ofhypercholesterolaemia e.g. familial hypercholesterolaemia.
1.5.2 Delimitation Two
People on alternate medication fur hypercholesteroaemia were not permitted to
participate in this trial.
1.5.3 Delimitation Three
Pregnant women were not permitted to participate inthis trial.
1.5.4 Delimitation Four
People who did not fall within the nge bracket of25 to 7S years were not considered fur
this trial.
3
1.6 The Assumptions
1.6.1 Assumption One
It is assumed that the patients took the medicationas prescribed.
1.6.2 Assumption Two
It was assumed thatthe medication wns prepared by Natura Laboratories as set out in the
French Pharmacopoeia
1.6.3 Assumption Three
It is assumed that the participants in the trial made no significant changes to their diet,
exercise programme or medication during the three-month trial.
1.6.4 Assumption Four
It is assumed that the readings of the lipid profiles for each participant, obtained from the
pathology laboratory, were accurate,
4
,,
CHAPTER TWO - LITERATURE REVIEW
2.1 Atherosclerosis, Cholesterol and Coronary Heart Disease (CHD)
Increased concentration of cholesterol in plasma is associated with a higher risk of

atherosclerosis. Low-density lipoprotein (LOL) is the major cholesterol carrying particle
in plasma. High-density lipoprotein (HDL) is responsible for transporting cholesterol
back from the tissues to the liver. High blood levels of LOL·C (low-density lipoprotein
cholesterol) and lowconcentmtions of HDL·C (high-density lipoprotein cholesterol) are
widely accepted as independent risk factors for coronary heart disease (Loughrey. et 01..
1999).
CHD (Coronary Heart Disease) risk steadily increases as serum cholesterol rises. The
increase in CHD risk is particularly steep after serum cholesterol rises above 200 mg/dL
(5.17 mmol/L). The cutotTpoint that defines high blood cholesterol (total cholesterol of
240 rng/dl, or a LDL·C of 160 mg/dL) is the value above which risk ofCHD rises steeply
(Lee, et al., 1993).
Table I belowshowsthe varying cholesterol levels and their significance associated with
CHD (Cataldo, et al., 1998).
TABLE 1: STANDARDS FOR CnD RISK FACTORS

(I mgldL = 0.02mmoVL)
LDL Cholesterol Total Cholesterol
<130mgldL (3.36 mmol/L) = desirable <200 rng/dl, (5.2mmol/L)= desirable
130-159mgldL(3.36mmol/L-4.lmmol/L)= 200-239 mg/dL (5.2mmollL- 6.2mmol/L)=
borderline high borderline high
~160 mgldL (4.2 mmollLO = high ~240 mgldL (6.3mmol/L) = high
IIDL Cholesterol Tri~l)'cerides (Fasting)
HOL~35 mgldL (0.92mmol/L) indicates risk <200 mg/dl, (5.2 mmollL) = desirable
LOLtoHDL ratio: 200-400 mg/dL (5.2 mmoVL- 10.SmmollL) =
Men: >5.0 indicates risk high
Women: >4.5 indicates risk >1000 mg/dl, (26.3 mmol/L}» very high
s
2.2 Atherosclerosis and Innammatory Markers of Coronary Risk
2.2.1 Dtfinition and causes of Atherosclerosis
Atherosclerosis refers to the underlying disorder involving the intima (the inner wall) of
medium and large arteries, which can result in a compromised circulation to the brain, heart,
kidneys, and extremities. In addition to producing narrowing of the lumen of the arteries, the
atheroma also affects function and impairs endothelium-dependent relaxation in isolated
human coronary arteries (Oberman, et al., 1992).
Early theories of tho pathogenesis of atherosclerosis emphasised the role of injury, or low-
grade inflammation, which was conceived as tissue reaction to filtration of plasma proteins
and lipids. This evolved into the lipid infiltration hypothesis. A second theory postulated that
small thrombi collected at the foci of endothelial injury and organized into plaques. Critical
events in atherogenesis centre on focal accumulation of lipids in the vessel wall. Most
investigators believe that low-density lipoprotein (LDL) is the most atherogenic of the lipids
(Harper, et al., 1999).
Controversy remains over the precise mechanisms by which the lipid enters the arterial wall.
Increased blood levels of LOL or other lipoprotein components may accelerate the rate of
lipid influx into the arterial wall by mass action. The LOL particle is too large to penetrate
endothelial cell junctions but can permeate through specialized receptors on endothelial
surfaces, which recognize LOL and modified forms of LDL. The LOL transport also may
occurthrough nonspecific uptake by macropinocytic channels. It is also possible that lipid is
ingested by circulating monocytes or macrophages that transport it into the vessel wall
(Harper, et el., 1999).
6
2.2.2 Atherosclerosis and Inflammatory Marken orCoronary Risk
The past decade has been characterised by growing interest in the idea that
atherosclerosis is an inflammatory disease and by the finding that serum levels of
markers of inflammation can be used to predict the risk of cardiovascular events (Rader,
2000).
In the October. 2000 issue of The New England Journal of Medicine, are two reports -
one by Lindahl et al. and one by Packard et aI.- that advance our knowledge of these
areas. Both studies made use of clinical trials to address whether levels of serum-based
inflammatory markers were predictive of cardiovascular events (Rader, 2000).
Lindahl et al. addressed whether serum levels of cardiac tropin T, C-reactive protein, and
fibrinogen at the time of presentation 0 f an acute coronary syndrome were predictive of
the long- term risk of death from cardiac causes. Blood levels of tropin T are a well-
established marker of myocardial damage and the short- term risk ofdeath. Lidahl et al,
demonstrated that levels of tropin T were also predictors of the long -term risk of death
from cardiac causes (at a mean of three years). The levels of both C-reactive protein and
fibrinogen were alsopredictive of the long-term risk ofdeath from cardiac causes, though
only C-reactive protein levels remained an independent predictor on a multivariate
analysis. There was only a weak correlation between tropin T levels and C-reactive
protein levels, and both were independently predictive, suggesting that they may reflect
different processes associated with the long- term risk of cardiovascular events (Rader,
2000).
Packard et al. evaluated whether the levels of certain markers were predictive of the risk
of coronary events among men with hypercholesterolaemia but not pre-existing coronary
disease. Levels of C-reactive protein and fibrinogen were both predictive of the risk of
coronary events; however, the strength of this association was significantly reduced when
other, traditional cardiovascular risk factors were considered in the analysis. The most
interesting finding in this study is related to lipoprotein-associated phospholipase A2, an
7
enzyme that is also known as platelet-activating factor acetyl-hydrolase. Lipoprotein-
associated phospholipase A2 circulates in the blood in association with both low-density
lipoprotein (LOL) andhigh-density lipoprotein (HDL), and its levels are correlated with
the levels of LOL cholesterol. Interestingly, Packard et al. found that increased serum
levels of lipoprotein-asscciated phospholipase A2 were associated with an increased risk
of a coronary event. The results may have been confounded by the fact that lipoprotein-
associated phospholipase A2 levels were also significantly correlated with LOL
~ cholesterol levels, although this variable remained an independent risk factor after the
inclusion ofLOL cholesterol levels in the analysis. Lipoprotein-associated phospholipase
A2 hydrolyses the proinflammatory phospholipid platelet-activating factor, as well as
structurally related oxidised phospholipids, and injection of this enzyme into mice
reduced local inflammation. As a result, lipoprotein-associated phospholipase A2 has
been thought to inhibit inflammation and, by extension, possibly atherogenesis. However,
Packard et al, found that lipoprotein- associated phospholipase A2 levels were positively
associated with the risk ofcoronary events (Rader, 2000).
This study therefore raises the important question of whether lipoprotein-associated

phospholipase A2 is simply a marker of risk, perhaps an inflammatory marker, or directly
promotes atherogenesis. Lipoprotein-associated phospholipase A2 appears tobe a marker
of systemic inflammation, since levels in animals are substantially increased by an
injection of endotoxin, its transcription is regulated by mediators of inflammation, and
plasma levels are moderately increased in a variety of inflammatory conditions.
Interestingly, Packard etat found no correlation between levels of C-reactive protein and
levels offipoprotein-associated phospholipase A2 (Rader, 2000).
Lipoprotein-associated phospholipase A2 may promote atherogenesis, perhaps by

hydrolysing oxidised phospholipids into fragments that arc more atherogenic than their
parent compounds or bygenerating lysolecithin, which has a variety ofproinflammatory
properties (Rader, 2000).
8
What are the clinical implications of the finding of increasing numbers of serum-based
inflammatory markers whose levels are predictive of the risk ofcardiovascular events?
It is now generally recognised that although the use of traditional risk factors produces
reasonably accurate estimates of risk in populations, this approach allows clinicians to
predict only about SO to 60 percent of the variation in the absolute risk of an event in
individual patients. Therefore, the addition of other factors that would increase the
predictive ability would also improve the accuracy of decisions regarding the use of
proven preventative therapies (Rader, 2000).
In direct comparison of the usefulness of levels of various serum-based markers, Ridker

et al, found that the effects of inflammatory markers and those of lipids were clearly
additive with respect to the ability to predict the risk of cardiovascular events. The
measurement of certain highly validated inflammatory markers, such as C-reactive
protein, in selected patients may increase the accuracy of assessments of cardiovascular
risk. Whether the levels of additional markers, such as soluble adhesion molecules or
lipoprotein- associated phospholipase A2 should also be used clinically as predictors of
the long- term risk ofcardiovascular eventsawaits further study (Rader, 2000).
There is still much to be learned about themechanisms that link inflammatory markers to
the risk of cardiovascular events, as well as the effect of treatments that reduce the levels
of these markers. Progress in this field enhances our ability to predict the risk of such
events, allows clinicians to administer preventative therapies to those most likely to
benefit, provides potential new targets for the treatment of atherosclerosis, and promises
tocontribute to a new emofpreventative cardiovascular medicine (Rader, 2000).
9
2.3 The Lipoproteins
Because lipids such as cholesterol and triglycerides are fat soluble, they must be
transported within the bloodstream from sites of absorption or synthesis to sites of
storage or metabolism by lipoproteins. The m~or lipid-transporting lipoproteins are
chylomicrons, very-low-density lipoproteins (VLDL), low-density lipoproteins (LOL),
and high-density lipoproteins (IIDL) (Lee, et al., 1993).
Low-density lipoprotein (LDL) is the mnjor cholesterol-carrying particle in plasma.

High-density lipoprotein (IIDL) is responsible for transporting cholesterol back from the
tissues to the liver. High blood levels of LDL-C (low-density cholesterol) and low
concentrations of IIDL-C (high-density lipoprotein cholesterol) are widely accepted as
independent risk factors for coronary disease (Loughrey, et 01., 1999).
HDL is involved in the reverse transport of cholesterol. It is currently thought that HOL
picks up cholesterol from the blood stream and various cells of the body and transports it
to the liver where it is excreted in the bile, converted to bile acids, or reprocessed into
VLDL (Very-low-density lipoprotein). It is hypothesised that this reverse tmnsport
process is responsible, in part, for the strong inverse relationship between serum HDL-C
and the CHO risk, although itis likely that other mechanisms are involved as well (Lee,
et al, 1993),
A low serum HOL-C level is a potent predictor of premature coronary heart disease
(CIID). There nrc numerous epidemiological and interventional studies that substantiate
I'IDL-C as a major independent risk factor for CHD. Isolated lowHDL-C (ILHOH·C)'has
been defined as HDL-C levels less than 35mgldL (0.91 mmollL), low-density lipoprotein
cholesterol levels less than 160mgldL (4.14 mmollL), and triglyceride levels less than
250 mgldL (2.82 mmollL). The National Cholesterol Education Program II (NCEP II)
guidelines focus on using LDL-C levels and the number of ClIO risk factors to treat
patients with dyslipidemia (Harper, et al., 1999).
\0
Although there is strong epidemiological evidence that HDL-C protects against CHD, a
cause-and-effect relationship has not been proven. The Frarnington Heart Study was one
of the first epidemiological studies to show the relationship between CHD and low HOL-
e levels. An aggregate analysis of four of the largest US epidemiological studies
(Framington Heart Study, Lipid Research Clinics Prevalence Mortality Follow-up Study,
Lipid Research Clinics Primary Prevention Trial, and Multiple Risk Factor Intervention
Trial) suggested that for each l-mg/dl, (O.02-mmollL) increase in HOL-C, a 2% decrease
in CliO risk in men and a 3%decrense in women may occur (Harper, et al., 1999).
In addition to epidemiological evidence, rodent studies suggest raising HDL-C levels

may inhibit atherosclerosis. Mice that arc genetically manipulated tooverproduce HDL-C
apo1ipoprotcin A-I were protected against diet-induced atherosclerosis. In a second
experiment, a different strain of mice with premature atherosclerosis, were genetically
altered to express the "human" HDL-C apolipoprotein A-I gene. These mice had a
marked decrease in the development of atherosclerosis. Finally, in another animal model,
rabbits intmvenously infused with HDL-C exhibited regression ofatherosclerotic lesions
(Harper, et al., 1999)
In addition to the data in animal studies, there is clinical trial evidence in humans that
therapy directed at raising HOL-C levels may decrease CHD risk. The Helsinki Heart
Study was a mndomised, placebo-controlled primary prevention trial using gemfibrozil
thempy in more than 4000 high-risk men with dyslipidemia. The treatment group
received gernfibrozil, 600mg twice daily. During a five-year interval, the intervention
group demonstrated a decrease in LDL-C and triglyceride levels by II % and 35%
respectively, while the HDL-C levels increased by 11%. The studydemonstmted that for
every l-mg/dl, (0.02-mmollL) increase in HOL-C, there was a 2% to 3% decrease in
CflO risk. independent ofchanges in LDL-C level (Harper, et aI., 1999).
The primary role of LDL is to transport cholesterol to the various cells in the body. LDL
contains approximately 70% of the serum '5 total cholesterol, is considered the most
atherogenic (atherosclerosis-producing) lipoprotein, and is the prime target of attempts to
lower serum cholesterol (Lee, et al., 1993).
II
•
Modifying the concentration of blood lipids may lower the risk of coronary heart disease
(CHD). Based on the results of epidemiologic and clinical studies. even a 10% reduction
in serum cholesterol levels through dietary and other nonphannacologic means ought to
reduce CUD mtes byabout 200/c) (Oberman, et al., 1992).
2.4 Associated Risk Faetors for enD
The risk factors most directly associated with CHD are elevated serum cholesterol. high
blood pressure. cigarette smoking. and diabetes mellitus. Other potential risk factors
include physical inactivity and emotional stress. Risk factors vary in the extent that they
can be modified. Family history. sex. and advancing ages are recognised risk factors over
which we have no control (Lee. et al., 1993).
2.4.1 Diet and Obesity
Theamount and composition of dietary fat affects plasma cholesterol. In particular. those
fats containing mainly polyunsaturated fatty acids, such as those in fish and vegetable
oils, tend to lower plasma cholesterol, whereas those fats containing mainly saturated
fatty acids, such as animal fat and butter, tend to raise plasma cholesterol (Smith, et al.,
1998).
The Framingham Offspring Study demonstmted that even modest weight loss could have
significant impact on HDL-C levels. The most important consideration in diet is energy
(caloric) restriction with subsequent weight loss. Also. certain types of fats, called trans-
fatty acids. have been shown to lower HDL-C levels. whereas monounsaturated fats are
thought to have a neutral effect in HDL-C. In recommending a diet to a patient with
isolated low HDL-C (ILHDL·C) not only should the total energy be restricted if the
patient is overweight but so should the consumption of energy-dense saturated and
polyunsaturated fats. Saturated fats and trans fatty acids may be substituted with
unhydrogenated monounsaturated fats. such as olive oil or canola oil (Harper. et al.,
1999).
12
These recommendations are based on studies that show that saturated fat raises LDL-C
levels. whereas trans -fatty acids lower HDL-C levels. Although some studies have shown
that low fat diets may lower HDL-C levels. total fat reduction is stilt thought to be
overwhelmingly cardioprotective through mechanisms involving the lowering of LDL-C
and its oxidation as well as possible effects on thrombosis (Harper, etal., 1999).
Obesity is the only factor that consistently shows a positive relation with LOL-C and
VLDL·C and a negative association with HDL-e. An increase in body fat is largely
responsible for the increment in total cholesterol and the fait in HDL·C that occur from
the age of 19 to 29 years. The high VLOL levels associated with obesity promote the
transfer of apo A-I from HOL to VLDL. lowering the numberof available HOL particles.
Genetic regulation of lipoproteins, body habits. and increasing age alt influence the
association ofobesity with VLOL, LOL. and HOL (Oberman, et al., 1992).
The fact that body fat is largely responsible for the suppression ofHOL can be inferred
from the equivalent increases in HOL with fat loss, whether from diet or exercise.
Lipoprotein lipase increases with loss of body fat, a possible explanation for the increased
HOL. It appears that HDL-C can be restored in overweight persons iflower body weight
can be maintained foraprolonged period (Oberman, etal., 1992).
2.4.2 Exercise
When regular, this tends to cause a rise in plasma HOL cholesterol and a small full in
plasma total cholesterol (Smith, et al., 1998).
In general, a minimal energy expenditure of8oo·to 1000 kcal/ week, appears necessary
for these metabolic changes; IIDL-C appears to increase linearly with training, up to
4500 kcal or more perweek. Often, plasma volume is increased with tmining: generally,
there are 20 to 50% more circulating HOL panicles because of both a higher HOL
concentration and plasma volume. Induction of lipoprotein changes requires a period of
months, often a yearormore for older or overweight person (Smith, ctal., 1998).
13
To maintain these exercise-induced lipid changes. exercise must be continued on a
regular basis. Whcn physical activity stops. lipid levels revert to fanner values within
several weeks. It has been demonstrated that exercise combined with diet results in better
weight loss and maintenance. as well as more favourable lipid changes. than with diet
alone (Smith. et al., 1998).
Exercise in sedentary men increases BOL-C levels. but there is a threshold effect. It
appears that moderate exercise is needed to result in a significant increase in BOL-C
levels. Joggers who mn 16 km per week for 10 months showed a 10% increase in BOL-C
levels. Exercise may not have as large an impact on HDL-C levels in women. Although a
mechanism of BDL-C modulation has been proposed. it is still difficult to ascertain how
much of the BOL-C response to exercise is derived from weight loss (Harper. et al.,
1999).
Physical activity increases insulin sensitivity and improves glucose tolerance. Weight
loss by diet combined with physical activity appears to be the best non-pharmacological
approach to improve lipoprotein levels, glucose tolerance, and insulin sensitivity
(Oberman, et al., 1992).
2.4.3 Stress
Severe occupational stress increases the blood cholesterol level, with increments of blood
cholesterol ranging from 8% to 65% having been noted during stressful periods. These
lipid alterations apparently relate to changes in neurohormonal activity, such as the
release of epinephrine. norepinephrine. growth hormone, and ACTH and their influence
on fatty acid release and lipoprotein production (Oberman, et al., 1992).
14
2....4 OIood Pressure
Preliminary findings from severnl studies indicate that dyslipidemia occurs with a greater
frequency than expected among hypertensives. especially in the younger age groups. The
proportion of hypertensive women who also have lipid abnormalities exceeds that of
hypertensive men (Oberman. et al., 1992).
In the Framington Offspring Study, hypertensives aged 20 to 44 years had higher levels
of total cholesterol and LOL-C and lower levels of I·IDL-C. Familial dyslipidemic-
hypertension, has been defined as hypertension in two or more siblings before age 60
associated with abnormal lipids (LDL-C or triglycerides above the 90th percentile or
HOL-C below the 10111 percentile). In the usual sequence ofevents,dyslipidemia develops
10 to 20 years before the onset of hypertension, with subsequent predisposition to CHD
(Oberman. et al., 1992).
2.4.5 Alcohol and smoking
In addition to exercise and weight loss, cigarette and alcohol use significantly affect
HOL-C levels. Cigarette smoking has a "dose-dependent' negative effect on HDL-C even
with consumption of less than I pack per day. After adjusting for other variables,
including alcohol intake, cigarette smoking caused a 5-t09-mg/dL (0.13-to 0.23 mmollL)
reduction in HDL-C when compared with matched controls (Harper, etal., 1992).
Moderate use of alcohol can increase HDL-C levels. Multiple epidemiological studies
have demonstrated that CHO is lower in moderate daily drinkers. Fifty percent of the
cardoiprotective effect of alcohol may be attributed to HDL-C. Other contributors to the
cardioprotective effect of alcohol include LDL-C lowering, inhibition of platelet
aggregation, decrease in fibrinogen, and enhancement of prostacyclin formation. It
appears that men whoconsume I drink per day (12 oz of beer, S oz ofwine, or I.S oz of
80-proofliquor) or lessdo not experience an increase in I·IDL-C level. Women, however,
can consume I drink per day or less and still experience an increase in HDL-e level
(Harper, et 01., 1999).
2.4.6 Coffee
A strong relationship between consumption ofcoffee and bloodcholesterol concentrntion

has been reported in some cross-sectional studies. Coffee consumption of six or more
cups per day is reportedly associated with higher blood cholesterol and apoprotein B
levels, In most studies, tea or caffeine-containing beverages did not affect blood
cholesterol levels (Oberman, et al., 1992).
Thedose and method ofbrewing coffee appear tobe primary determinants of this effect.
Populations from Scandinavian countries, who drink mainly boiled coffee, have
demonstmted the strongest correlation between cholesterol levels and coffee intake.
Apparently, the length of time the coffee grounds remain in hot water determines the
extent of the effect. This suggests that coffee contains one or more substances that affect
the metabolism of cholesterol; however, the precise mechanism is not known. Abstention
from coffee in a small trial of healthy male coffee drinkers resulted insmall decreases in
HDL·C and apolipoprotein-I (A-I) but did not affect LDL-C (Oberman, et at, 1992).
2.4.7 Seasonal Variation
Cholesterol levels are higher in winter than summer. The placebo group in the Coronary
Primary PreventionTrial (CPPT) offered 8 unique opportunity to study this phenomenon
because carefully standardised lipid profiles were obtained at bi-monthly intervals over 8
6.S-year period at twelve United States centres. These analyses demonstrated a clear
seasonal variation of cholesterol levels, higher in winter, lower in summer, with the
increase amounting to ± 3% of mean plasma cholesterol levels, or 7.4 mgldL (0.19
mmolJL). These findings could not be explained by seasonal variations in diet or weight.
Similar patterns emerged for LDL-C and I·IDL-C levels but were of lesser magnitude
(Oberman, et al., 1992).
The seasonal variation could have epidemiological implications if lipid comparisons are
made between studies conducted in different seasons. Such seasonal variation most likely
16
2.4.6 Coffee
A strong relationship between consumption of coffee and bloodcholesterol concentration

has been reported in some cross-sectional studies. Coffee consumption of six or more
cups per day is reportedly associated with higher blood cholesterol and apoprotein B
levels. In most studies. tca or caffeine-containing beverages did not affect blood
cholesterol levels (Oberman. etnl., 1992).
Thedose and method ofbrewing coffee appeartobe primary determinants of this effect.
Populations from Scandinavian countries. who drink mainly boiled coffee. have
demonstrnted the strongest correlation between cholesterol levels and coffee intake.
Apparently. the length of time the coffee grounds remain in hot water determines the
extent of the effect.This suggests that coffee contains one or more substances that affect
the metabolism ofcholesterol; however, the precise mechanism is not known. Abstention
from coffee in a small trial of healthy male coffee drinkers resulted in small decreases in
HDL·C and apolipoprotein-l (A-I) but did not affect LDL-C (Oberman, et aI., 1992).
2.4.7 Seasonal Variation
Cholesterol levels are higher in winter than summer. The placebo group in the Coronary
Primary Prevention Trial (CPPT) offered a unique opportunity to study this phenomenon
because carefullystandardised lipid profiles were obtained at bi-monthly intervals over a
6.S-year period at twelve United States centres. These analyses demonstrated a clear
seasonal variation of cholesterol levels, higher in winter. lower in summer. with the
increase amounting to ± 3% of mean plasma cholesterol levels, or 7.4 mgldL (0.19
mmollL). These findings could not be explained by seasonal variations in diet or weight.
Similar patterns emerged for LDL-C and HDL-C levels but were of lesser magnitude
The seasonal variation could have epidemiological implications if lipid comparisons are
made between studies conducted in different seasons. Such seasonal variation most likely
16
will not create any difficulty in assessing anyone who has repeated measurements over
time; however there is the potential to misclassify individual trends when only two data
points, winter versus summer, are available (Oberman, et at, 1992).
2.5 The Influence ofRace and Gender on Lipoproteins
Race and gender differences in lipoproteins and apolipoproteins have repeatedly been
demonstrated in adults, most recently by the NHANESIII study (National Health and
Nutrition Examination Survey 111). Black men and women have lower LDL-C and higher
HDL-C than white men and women. Women have higher HDL-C than men do. These
differences have also been noted in children, supporting the concept that the variance is
due to genetic influences rather than environmental factors (Loughrey, et al., 1999).
2.5.1 Race
A population-based study, CARDIA, has provided fasting lipoprotein data on 4858 black
and white men and women, aged 18 to 30. The age-adjusted means and standard
deviations for total cholesterol, LDL-C, HDL-C, triglyceride, and apoproteins A-I and B
for the 18 to 24 years sub-group are given below in the Table 2.1. (Oberman, et al.,
1992).
Black men had higher HDL-C and apoprotein A-I levels and lower triglyceride
concentrations than white men. Higher HDL-C levels in black men aged 20 through 74
also were found in the Second National Health and Nutrition Examination Survey
(NHANES II). In CARDIA, black women had higher LDL-C and apoprotein B levels but
similar HDL-C and lower triglyceride concentrations than white women (Loughrey, et
al., 1999).
Racial differences in lipoprotein levels, especially lower VLDL-C and higher HDL-C
concentrations among black children, are established by 9 years of age and are not
attributable to environmental factors, although HDL·C levels in blacks seem to be more
17
responsive to physical activity and alcohol than in whites. The levels are greater in men
than in women and persist even after stmtification for various socio-economic and
behavioural parameters. Age differences in lipoproteins generally are more pronounced
among whites than among blacks. To the extent that apo A-I is indicative ofHDL particle
number. the higher HDL values among blacks also may indicate increased numbers of
HDL particles. The higher ratio of cholesterol to apoprotein B in LDL among blacks
indicates the presence oflarger. less dense. and more cholesterol-enriched LDL particles.
This type LOL particle is thought to be less atherogenic than smaller. dense LDL
particles (Loughrey, et al., 1999).
Overall, blacks have more desirable lipoprotein levels than whites, but because of the
higher prevalence and increased severity of non-lipid risk factors. the percentage of
persons who require lipoprotein modi fication is smaller among blacks and whites
Table 2 Selected Lipidand Lipoprotein Measures (mgldL) From Young Adults (18-
24 years) in the CARDIA Study by Sex and Race
LipidlApoprotein White Men White Women Black Men Black Women

Total Cholesterol 168 (32) 174 (30) 168 (32) 176(34)
LDU 105(29) 105 (28) 102 (30) 109(32)
HDU 46(10) 54 (13) 53 (13) 55(12)
Triglycerides 86(56) 73 (36) 64 (39) 61 (28)
Apo A-I 130 (19) 138 (22) 140 (22) 140(22)
AIlOR 89(23) 88 (22) 85 (23) 89(26)
(Adapted from Donahue RP. Jacobs J:?R. Sidney S. Wagenknecht Le, Albers J1, Hulley
SB. Distribution of lipoproteins and apoprotcins in young adults: the CARDIA study.
Arteriosclerosis 1989; 9:656-654.)
18
2.5.2 Gender
Cardiovascular disease is recognised as the leading cause of death in men and women in
the United States. with similar morbidity in both sexes. The published mortality data
support this observation: deaths in women accounted for 52% of all cardiovascular
deaths. or a total of almost 480.000 women in 1992. Each year more women die of
cardiovascular disease than ofall cancers combined. Coronary artery disease remains the
primary cause of death among women in the United States, resulting in over 250, 000
deaths per year (roughly 28% of all deaths). Despite the similarity in mortality in both
sexes, a substantial number of gender-related differences in cardiac disease present
unique challenges to the detection of'hcart disease inwomen (Zaret, et al., 1999).
Several classic studies detail the differences in the presentation of heart disease between
men and women. The Framingham Study data revealed that women present with their
first anginal symptoms 10 years later and sustain their first myocardial infarction 20 years
laterthan their male counterparts (Zaret, et al., 1999).
Women and men share the major cardiac risk factors of hypertension, diabetes, high
cholesterol levels, smoking, and family history: however, their risk factor profiles differ.
In women, the risk of hypertension is lower at an early age, but by the age of 55, the
prevalence is essentially thesame as that ofmen. Diabetes is more prevalent in women at
all ages, and several studies have found that it imparts a twofold higher risk of heart
disease in women compared with men. The lipid profiles of women generally remain
favourable before menopause, however, after menopause levels of both low-density
lipoprotein and total cholesterol are higher than those in men in a similar age group.
Obesity and physical inactivity have each been independently associated with an
increased risk for heart disease in women. In general, women have more risk factors and
conditions associated with the initial presentation ofheart disease (larct, et at, 1999).
Oestrogen plays a cardioprotective role in women in the prevention of coronary hean

disease. Recent non-randornised trials have shown risk reduction of 50% in
19
postmenopausal women receiving oestrogen replacement therapy. The beneficial effect of
oestrogen on lipid profiles have been described, as have several other theories about the
possible mechanisms by which oestrogen imparts a cardioprotective effect. The gradual
age-related increase incoronal)' disease without an abrupt change at menopause may be
viewed as support of oestrogen's protective role, because menopause represents the result
of 8 gradual rather than abrupt loss of ovarian function over many years. Despite the late
appearance of coronal)' heart disease in women. the risk of disease in postmenopausal
women remains substantial and should not be disregarded (Zaret, et el., 1999).
2.6 Treatment
Numerous studies have documented the value of lifestyle modification in improving

HDL-C levels. The patient's weight, diet, exercise habits. and the useofcigarettes should
be addressed. Weight loss inobese men has been found to increase HDL-C levels. This is
clearly depicted in a Dutch study of 315 men followed up for 10years. Thedata from this
study revealed that HDL·C increased 0.8 mg/dL (0.02 mmol/L) for every unit decrease in
body mass index (a measure of weight in kilograms divided by the square of height in
meters) (Wang, et al., 1998).
A number of studies have reported the lack of physician involvement inadvising patients
on making positive behavioural changes. Patient observations have demonstrated that
physicians have a lowtendency even to recommend dietary therapy orto provide a high
level of dietary advice. When counselling is given, it is often stated in a manner that is
confusing to the patient, or instructions are vague (e.g., "improve your diet" or"eat a low
cholesterol diet" without an explanation of which foods are high in cholesterol). leaving
the patient with few concrete tools with which to face the recommended lifestyle
changes. Only 13% of sedentary individuals reponed that their physician gave them
advice about increasing their physical activity. Fewer than half of the smokers reponed
that their physicians had ever advised them to quit smoking. Numerous studies have
indicated. however, that a clinician's professional attitude, enthusiasm, and involvement
are important determinants of patient adherence to recommended lifestyle changes. For
20
example, Barnes et aI. Found that the attitudes of dieticians toward the therapeutic diets
they are promoting, strongly impacted patient compliance. Other research has
demonstrated that even brief physician advice alone more than doubles the f-year
smoking abstinence rates compared with unadvised controls. These studies indicate that
physicians who take the time to perform motivational interviews and who take pains to
assist patients in behavioural changes may have better results in influencing change. This
suggests that health care intervention must be even more aggressive and creative in order
to cause significant behaviour change (Wang, etal., 1998).
2.7 Drug Treatment
Decisions to use drug therapy for hyperlipidemia must be based on the specific
physiologic defect and its potential for causing atherosclerosis or pancreatitis (Katzung,
1992). In view of the fact that any drug regimen may have undesirable side effects in
some patients and because treatment must be pursued for a lifetime if risk factor
reduction is to be maintained, drugs are not recommended except for patients whose lipid
profile level remains abnormal in spite of an adequate trial of diet therapy and weight
reduction (Council on Scientific Affairs, 1993).
Many patients will not achieve an adequate HDL-C level with nonpharmacologic
therapy. There areseveral classes of drugs available for physicians to use in patients who
do not respond to nonpharmacologic therapy. These classes include niacin. 3-hydroxt-3-
methylglutaryl co-enzyme A (HMO-CoA) reductase inhibitors. fibric acids. and
estrogens (Harper, et aI., 1999).
2.7.1 Niacin
Niacin (Vitamin 83) is the most efficacious drug for raising HDL-C levels. Its
mechanism of action is not completely understood, but it is thought that niacin decreases
hepatic production of very low-density lipoprotein levels and leads to an increase in
HDt.C levels. Significantly lower doses of niacin arc required to mise HDL-C levels
21
than those required to lower LDL-C levels. Studies have shown that an increase in HOL-
e of greater than 20% can be expected from doses of 1000 to 1500 mgldL. At higher
doses niacin has been shown to lower triglyceride, LDL-C, and lipoprotein (0) levels.
Full-dose niacin has been shown to decrease LDL-C levels 10% to 25%, increase HDL-C
levels 15% to 35%, and decrease triglyceride levels 20% to 50%. The crystalline niacin is
less expensive and appears to be more effective at increasing HDL-e levels than the
sustained-release niacin. Sustained-release niacin is well tolerated and more effective at
lowering LDL-C levels. An increased frequency of hepatotoxicity has been reported with
sustained-released preparations (Harper, et al., 1999).
Although niacin has a desirable effect on several lipoprotein sub-fractions, it has several
unpleasant but benign side effects. Flushingand vasomotor symptoms were common and
the most frequent reason for discontinuance. Gastrointestinal complaints include
dyspepsia, nausea, abdominal pain, and activation of peptic ulcer. Niacin can result in
dose-dependent hyperuricaemia and hyperglycaemia and should be used with greater
caution or not at all in patients with uncontrolled diabetes, gout, or peptic ulcer disease.
Niacin is absolutely contraindicated in patients with chronic active liver disease. Dose-
dependent hepatotoxicity has occurred but is more common with sustained- release
preparations. Less common adverse effects include acanthosis nigricans and retinal
oedema. These adverse effects are less severe and less common at doses needed to
increase HDL-C (Harper, etal., 1999).
2.7.2 Fibrates
Gemfibrozil, 600mg twice a day, increases HDL-C levels by an average of II %. This

drug is generally well tolerated; however, reported adverse effects include cholesterol
gallstones, myopathy.Iiver enzyme elevations, dyspepsia. and leukopenia (Harper, et al.,
1999).
Examples include Bezolip, Lipaten, Ltpstn, Lopid, Rolab-Bezaftbrate. Side-effects

include gastro-intestinal disorders, muscular weakness, impotency, hair loss, allergic
22
reactions. mass gain. CNS effects. skin rash, alopecia. anaemia andleucopenia. diarrhoea.
vomiting. dyspepsia. decreased libido. headache and jaundice (MIMS. August 1999).
2.7.3 Hormone Replacement Therapy
Oestrogen is thought to reduce coronary risk by a variety of mechanisms. including

raising HDL-C levels. lowering LDL-C levels, decreasing lipoprotein (a) levels. and
decreasing fibrinogen levels and through beneficial effects on the arterial wall.
Progestogens, however, typically decrease HDL-C levels (Harper, etal., 1999).
Arecent, small. rnndomised crossover trial demonstmted that in postmenopausal women

treatment with the combination ofoestrogen and medroxyprogesterone acetate resulted in
a 7% increase in HDL-C, a decrease in Iipoprotcin (a) levels. and a reduction in LDL-C.
Inthe Coronary Drug Project. which used conjugated oestrogen in men who had survived
myocardial infarctions, the oestrogen arm was discontinued because of unacceptable
thrombotic complications. The doses ofoestrogen used in this study were 2.5 and 5.0 mg.
which are much higher than those used for hormone replacement therapy today (0.625
rng) (Harper. et al., 1999).
The recent Heart and Oestrogen/Progestin Replacement Study (HERS) trial in

postmenopausal women with CHD found that conjugated equine oestrogen, 0.625 mg,
combined with medroxyprogesterone acetate, 2.5 mg, had no effect on CHO end points
nnd resulted in nn increased incidence of thromboembolic complications, (Harper et al.,
1999).
2.7.4 Competiti,·c Inhibitors or IIMG-CoA Reductase
IIMO-CoA reductase inhibitors. or statins, have been shown to decrease overall mortality
in hypercholcsterolncmic patients with CliO (Lindbloom, 1999).
23
Examples include Baycol, Lescot, LiIHJ/or. Pram, Zocor. Side effects include gastro-
intestinal disorders,headache, fatigue, rash, myopathy. musculo-skeletal pain. chest pain,
insomnia. peripheral neuropathy. pancreatitis. hepatitis. impotence and urinary tract
infections (MIMS. August 1999).
A multicentre trial recruited patients aged 31 to 75 years in Australia and New Zealand,
all of whom had acute Ml or discharge diagnosis of unstable angina between 3 and 36
months before study entry. Total cholesterol levels were between ISS and 271 mg/dl.,
and fasting triglyceride levels were <445 mg/dl., The median cholesterol level was 218
mg/dl., the median age 62 years, and only 17% were women. Patients were excluded if
they were already taking any cholesterol-lowering agents or if they had cardiac failure,
renal impairment, or hepatic disease.This was a mndomiscd double-blind trial comparing
pmvastin40mg daily to placebo. Patients were followed for a mean of6.1 years. There
was a 1.9% absolute risk reduction in CHD death in the pravastin group compared with
placebo (6.4% \'5 8.3%) and a 3.1 % absolute risk reduction in overall mortality
(Lindbloom, 1999).
The HMG-CoA reductase inhibitors act by inhibiting the conversion of HMG-CoA to

mevalonic acid. This conversion is the rotc-limiting step in cholesterol production and
requires the enzyme HMG-CoA reductase. The HMG-CoA reductase inhibitors act in the
liver by inhibiting HMG-CoA reductase. which reduces the cholesterol level in the liver
cell. The reduced hepatocyte cholesterol levels result in an increase in the synthesis of
LOL-C receptors. The HMG-CoA reductase inhibitors act predominantly by reducing
LOL-C, but also have moderate effects on HOL-C and endothelial function. A study with
lovastin in patients with ILHDL-C revealed a 6% increase in HDL-C levels. The HMG-
CoA reductase inhibitor drugs are well tolerated by patients. Adverse effects include
increased liver enzyme levels, dyspepsia. and myopathy (Harper, et al, 1999).
24
2.8 Gemmothcrapy as a treatment
2.8.1 Definition
Gemmothempy is a thempeutic method. which, prompted by principles of homeopathic

drainage, uses plant bud extracts or other embryonic vegetable tissue, freshly harvested
from the growing plant (Tetau, 1998).
2.8.2 Precise Therapeutic Properties
Using the embryonic part of the plant has made it possible to isolate the precise
therapeutic effects, beyond those known for the adult plant. With gemmotherapy, it has
been possible to demonstrate. through scientific investigation. the pharmacological
superiority of the bud versus the fully developed plant. as well as specific clinical
indications (Tetao, 1998).
2.8.3 A Homeopathic Drainage
Gemmothempy. a Biotherapy that is studied in depth and taught at the Society Medicate
Biotherapy, is chiefly of interest to homeopathic physicians and was created and
developed by the homeopathic physicians Dr. Pol Henry and Dr. Max Tetau (Tetau,
1998).
Gemmothempy is a super-active and well-defined type of Phytotherapy (plant therapy).

popular with a large number ofpmctising phytotherapists and homeopaths. who prescribe
itextensively, as part ofo treatment programme used in theirpractices (Tetau, 1998).
According to Stof1berg (2000). Olea eumpea and Juniper«... communis are used
commonly by homeopathic practitioners for the treatment ofhypercholesterolacmin.
25
According to Dr. R. Moiloa (2000), Olea europaea and Juniperus communis are
commonly used in his homeopathic practice, as port of his treatment programme for
hypercholesterolaemia.
Many homeopathic physicians, in combination with other homeopathic prescrrpuons,

prescribe Gemmothempy as it provides a modem fonn of drainage, perfectly adopted to
the illness being treated. The concept of drainage was perfected by Dr. Nebel from
Lausanne, Switzerland, developed in France by Dr. Leon Vannier and Dr. ROllY, and is
one of the most original aspects ofthe homeopathic technique (Tetau, 1998).
If people nrc considered as a whole, the ailments to which they fall prey develop on a
terrain weakened by theslowing down of'the elimination organs and the growth ofa pool
of toxic immune complexes related to badly eliminated auto-antibodies. There is also a
decrease in the defense system. Vannier called this toxic pool "toxins", a word that has
come to be used throughout the world. Ourpredecessor's spoke of "intoxication", a term
that is somewhat ambiguous in light of the products manufactured by different bacteria.
However, the hypothesis of a progressive internal clogging of the body related to the
aging process is still valid, since it facilitates the development of a pathology (Tetau,
1998).
One way to aid the return to health is to decrease this endogenous toxic charge by
stimulating the functions of the various elimination organs. This is the role of drainage
(Tetau, 1998).
Draining is a technique aimed at acting internally on the eliminatory organs. Draining

works in a gentle and prolonged manner to aid the functioning ofthe body's eliminatory
organs in order to gently detoxify it. The homeopathic remedy customised to the Law of
Similars, is more likely to work on a terrain that has been improved, with no risk of
aggravation. Gemmothempy acts through plants rich in growth substences-gibberllins-
auxins that act strongly onorgans to be stimulated (Tetau, 1998).
26
Eliminator organs are extremely varied and include organs usually classified as purifiers,
such as the kidneys, intestines, liver and gallbladder. The concept of an eliminator is
extended to include the less obvious: skin, lungs, heart, blood vessels, and nervous
system. This concept is easily explained and fits in with our overall view of the human
body. For the liver or kidney to function properly, the heart, arteries and nervous system
must be in good condition. Metabolic disorders, for instance, can be caused by cardiac
weakness (Tetau, 1998).
For the homeopath, drainage has become even more important, as our patients have
changed considerably from those consulted by Hahnernan, or Kent and Hering. The
patients of today are consuming tmnquillisers and sleeping pills. Patients with diverse
conditions and drug histories come to the homeopath with blocking antibodies, diuretics
and calcium deposits. Hormone therapy and progesterone flourish among menopausal
women. Antibodies, anti-lnflammatories, analgesics, and anti-histamines arc widely used.
As these medications are often necessary, there is no question of stopping them
immediately, but rather we seek an eventual reduction (Tetau, 1998).
Such medications deeply modify the homeopathic case, making the consultation difficult
because the patients manifest poorly the chamcteristic clear symptoms needed for
diagnosis. Gemmotherapy is therefore necessary as the patient can then reach a state that
permits a more precise homeopathic analysis, facilitating the intervention of the main
basic homeopathic remedies (Tetau, 1998).
2.8.4 Method of Preparation
Gcmmotherapy uses freshly harvested buds macerated in a glycerine mixture. As parts of

the growing plants, the rootlets. young shoots and leaves. the inner membrane of the stem
and roots are rich in embryonic ingredients. The glycerinated macerates are prepared in
accordance with the official method for homeopathic preparations in the French
Pharmacopoeia (Tetau. 1998).
27
As soon as they are harvested. bud and embryonic plant tissue are soaked in a mixture of
glycerine and alcohol. in a rntio where the basic mediumcorresponds to 1120th of the dry
weight of the fresh plant used. Glycerine is selected as an excipient as it allows for better
extraction of the embryonic ingredients. After three weeks, the macerate is filtered and
diluted to a I/lOth with a mixture of water, alcohol and glycerine. It is thus a 1/i0th
solution. Hahneman's First Decimal (01). which is the medicinal form ofgemmothernpy
remedies. This is the only potency prescribed since it is the formula that provides the
maximum and. above all, the most constant effect. Obviously. all the glycerinated
macerates are subjected to the controls in the French Pharmacopoela (Tetau, 1998).
2.8.S Clinical Gcmmothcrnpy
Gemmothempy isvery useful in the treatment of major metabolic ailments:

• Adult-onset (non- insulin dependent)diabetes
• Hypercholesterolemia and hypertriglyceridernia
• Hyperuricemia
• Excessive weight
These four afflictions are more nutritional than metabolic in origin. With our over-fed
lifestyle eating. they are more often associated with a rich diet. Medical treatment is
insufficient in itself An appropriate diet must be followed, although even that is not
always enough (Tetau, 1998).
For the purposes ofthis research trial only Hypercholesterolemia will be discussed:
Prescribe 20-50 drops twice per day. morning and evening, of Olea europaea and
Juniperus communis both in Dl potencies. These arc the selected gemmothempeutic
lipid-lowering remedies (Tetau, 1998).
28
2.8.6Olea europaea (Olive Leaf Extract)
Olea europeae: Has hypotensive and arterial anti-sclerotic action, normalises blood
cholesterol levels and is indicated in arteriosclerosis and in hypertension (Tetau, 1998).
The extract from the olive leaf is a potent fighter against disease. Olive leaf contains a
compound called oleuropein acid. a natural microbe catabolist, which is effective against
numerous viruses. bacteria, and fungi. Physicians report success in treating a wide variety
of ailments with olive leaf extract. Notably, it helps bolster the immune system, giving
the body more ammunition to fight infection. Olive leafextract helps to destroy viruses in
two important ways. First, it interferes with ability of the virus to replicate, which
prevents the virus from spreading. Second, it stimulates the immune system to produce
more disease-fighting cells. In particular, olive leaf extract seems to be good for patients
who have suffered through chronic illness, and need an extra boost to regain their health
(Mindell, 2000).
The effects of glycero-alcoholic extracts of shoots and leaves of Olea europaea L. and
olcuropein on diet and triton hypercholesterolemia were studied in Wistar rats. It was
found that the hypocholesterolcmic effects of the Olea extracts could be ascribed to a
synergistic action ofoleuropcin and polyunsatumted fatty acids contained in the drugs,
(De Pasquale, etal., 1991).
In cholesterol fed rats, administration of both olive and sunflower oil decreases the serum
cholesterol level; however olive oil produces a decrease incholesterol levels for a longer
duration than sunflower oil. Since olive oil contains 8-10% of polyunsaturated fatty acid
respect to 50-60% of sunflower oil, obviously in olive oil there are some other factors
responsible for hypolipidaemic activity (De Pasquale, et al., 1991).
In viewof these hypotheses the effects ofglyco-alcoholic extracts ofshoots and leaves of
Olea curopaea (used as a hypocholcsterolemic drug in traditional medicine) and one of
29
its active principles, the oleuropein Iridoid, were studied an experimental
hypercholesterolemia (De Pasquale, et 01.,1991).
Adult male wistar rats (200-254 g) were used in all experiments. They were kept in
standardised conditions (Temperature22'C :t.2'C; Humidity 60:!: 4%; natural lighting),
Glycero-alcoholic extracts of fresh shoots and leavesof the Olea europaea were supplied
from Laboratoire Dolisos, France (De Pasquale, et al., 1991).
The rats were fed with a high cholesterol diet (cholesterol 2%, sodium chelate 2%,
vitamin mixture 2%, oligoelemcnts 0.2%, salt mixture 5.8%, coconut oil 20%, cellulose
4%, sucrose 44%, casein 5%, dmkettprotein 15%) for two weeks. Laboratory diet-fed rats
were used as the non- cholcstcrolemic control groups. The extracts (250mg and
SOOmglkg) and oleuropein (0.2, 0.5 and IOmg/kg) were orally administered once a day
for the duration of the experiment. On the 15 th day the animals, were killed under light
anaesthesia. The blood, collected in heparinized tubes, was immediately centrifuged and
the plasmakept at -20'C until assayed (De Pasquale, et al., 1991).
The results showed that in the hypercholesterolaemic diet-fed rots 250 and 500mg!kg of
glycero-alcoholic extracts of Olea europaea leaves and shoots reduce, though not
significantly, the serum cholesterol levels. Leaf extract, at dose of 500mg!kg,
significantly reduces triglycerides and total lipids, the latter decrease also with250mglkg
of extract. The shoot extract reduces triglycerides and total lipids only at a lower dose,
while at a dose of 500mglkg the decrease is not significant. Oleuropein shows a
remarkable hypocholesterolaemic effect ata dose of 0.5 and IOmglkg, but is inactive at a
dose of0.2mglkg (De Pasquale, et al., 1991).
30
Table 3: Effects of Olea europaea leaves and shoots and oleuropein on baematic
cholesterol, total lipids and triglycerides in bypercholesterolaemic diet-fed rats.
Mean ±,S.E often animals. P is less than 0.05 compared with hypercholesterolaemlc
diet. 250mg ofthe extract = 12.5 mg ofdry drug (De Pasquale; et al., 1991).
Treatment Cholesterol Total Lipids Triglycerides

mg% mg% mg%
Standard diet 105.3± 4.9 249.9 ±38.6 120.9 ± 11.3
Ilypcrcol. Diet 520.0 ± 88.8 430.6 ±66.7 139.9 ±36.2
Ilypcrcol. Diet + Olea leaves 250mglkg 450.2 ± 52.8 183.7 ±,17.7 111.9 ± 17.0
Hypcrcol. Diet + Olea leaves 500mglkg 366.8 ± 39.3 200.9 ±25.1 51.9 ±9.5
Hypercol. Diet + Olea shoots 250mglkg 370.2 ± 23.4 212.1 ±.28.7 36.8 ±9.4
Hypcrcol. Diet +Olea shoots 500mglkg 437.7 ± 47.9 306.4 ± 16.4 137.9 ± 36.3
Hypercol. Diet +Oleuropein 0.2 mg/kg 485.2 ± 31.7 328.6 ± 14.1 105.4 ±22.1
Hypercol, Diet +Oleuropein 0.5mglkg 279.3 ± 44.6 160.9 ±27.S 38.3 ± 10.2
Hypercol. Diet + Oleuropein 10mglkg 305.2 ± 25.5 146.9 ±25.8 44.9 ± 6.1
The present study shows that the glycero-alcoholic extracts of the leaves and shoots of
Olea europaea and oleuropein reduce hypercholesterolaemia and hyperlipemia in
hypercholesterolaemic diet-fed rats (DePasquale, et aI., 1991).
Oleuropein, at adose about ten times higher than that contained in leaves and shoots has
no effect on hypercholesterolaemic diet-fed rats, Leaves and shoots of Olea therefore
seem to contain some other factors responsible for the hypocholesterolaemic effects (De
Pasquale, et 01.,1991).
Oleuropein reduces the total lipid level, the leafextract increases them. This can be due
to a presence in the drug of polyunsatumted fatty acids that, binding cholesterol in
31
2.8.7 Juniperus communis (Juniper Berry)
The Juniper is a small shrub, 4 to 6 feet high, widely distributed throughout the Northern
hemisphere. It is a common shrub where bands of limestoneoccur and on siliceous soils.
Juniper berries take two or three years to ripen, so that blue and green berries occur on
the same plant. Only blue, ripe berries are picked. They are then laid out onto shelves to
dry a little, during which they lose some of the blue bloom and then develop a blackish
colour (Grieve, 1984).
The principle constituents is the volatile oil which contains monoterpenes and
sesquiterpenes; invert sugar; flavone glycosides; resin; tannin; organic acids (Hoffman,
1996).
Oil of Juniper is given as a diuretic, stomachic and carmitive in indigestion, flatulence,

and diseases of the kidney and bladder (Grieve, 1984).
Juniperus communis: Young shoots of Juniper have a marked action in severe cases of
hepatic insufficiency. It is indicated for the very deficient liver in the phase of
degeneration; jaundice, various types of cirrhosis etc, Juniper also gives good results in
cases of "air swallowing" where it appears to have a regulatory effect on the digestive
neurovegetative system (Van Wyk, 1995).
For centuries, juniper has been a folk remedy for urinary-tract problems, including
urinary retention and gallstones. It has also been used successfully to treat gout, a
condition marked by painful inflammation of the joints caused by deposits of uric acid
and high uric acid content in the blood. The berry can also help the body rid itself of
toxins, therebyuseful inconditions ofexcess toxicity (Mindell, 2000).
Both these gemmothempeutic prepnrntions (Olea CIINJpaca and Junipous communlsv are
troditionnlly used together for the treatment ofhypercholesterolaemia (Ietau, 1998).
32
2.8.8 Conclusion
When handled responsively, according to the guidelines worked out in clinical

experimentation, gemmothempy offers excellent results. Clinical Gemmotherapy is a
valuable adjunct for health professionals. whatever their approach-homeopathic,
allopathic, generalist or specialist. Treating system by system, organ-by-organ, the
method increases tissue defences and re-establishes upset local metabolisms. Through
elective localised action on the different eliminatory organs of the human body,
gemmotherapy ensures deep and dumble detoxifying which promotes the general well
being ofthe patient. Effective but devoid ofany toxicity, gernmotherapy can be perfectly
integrated into the ideal therapy situation as described by Hippocmtes: If Nature alone
cannot heal, Art shall learn to excite gentle efforts, stimulating her to rid the surcharge at
no risk. Through Clinical Gemmothernpy the patient will be brought gently and rapidly
towards greaterwell being closer to a cure(Tetau, J998).
33
CHAPTERTIIREE-MATERIALSAND METHODOLOGY
3.1 Study Design
3.1.1 Research Leeation
The collection of deta for the trial took place at the Technikon Witwntesmnd Health
Clinic. Doomfontein campus.
3.1.2 Study Population
The study population consisted of human subjects. A total of thirty subjects were used for
the trial. consisting ofnineteen females and eleven males.
3.1.3 Treatment
Each subject took the medication for a period of'three months and came in for a fasting
lipid profile once a month.
3.2 The Research Methodology
3.2.1 Collection ofresearch subjects
After Ethics clearance was obtained for this trial study. the researcher proceeded to
advertise for the collection of volunteers for the study. An advert was placed in the
EdenvaleJDedfordview News. advertising free cholesterol testing and fn:e treatmeru, The
response from the edven was good but not sufficient to collect the entire sample. Funher
advertising was carried out using pamphlets. which the researcher handed out to difTen:nt
pharmacies and health shops in the Eastern and Northern suburbs.as well as on the TWR
premises.
After II period of approximately six weeks a complete countof thirty volunteers were
obtained for the trial. The group of volunteers were. at the time of the trial. not on any
medication for their high cholesterol. between the ages of twenty-five and seventy five
years and they had to have a base level reading for the Total Cholesterol of more than S.S
mmol/L.
The researcher recorded contact details and arrangements for their initial blood test were
made telephonically.
On meeting each volunteer for the study, the researcher handed out a consent form,
information sheet and questionnaire to each participant (see Appendix D).
The participants were required to read and answer the questions and sign the consent
form.
Dates and times for scheduling the four blood samples for each participant were co-
ordinated, spacing each test no longer than four weeks apart.
An independent person from the study divided the thirty participants in the trial study into
two groups on a random basis. Fifteen patients were placed ineach group A and group B
respectively. The researcher did not knowwhich group was the placebo group and which
was the medication group until the end of the trial period.
During the course of the trial period six participants withdrew from the study, three from
each group leaving a total of twelve patients in each of the respective placebo and
medication groups.
3.2.2 Collection orthe blood sample
Venous blood was drawn from each participant in the trial and was analysed for the total
cholesterol, low-density lipoprotein, high-density lipoprotein and triglyceride levels. A
35
starting level was included at the commencement of the trial for each subject after which
a further three blood samples were collected at the end of each month. In total four
readings were collected for each subject.
For each of the thirty participants an initial base line blood sample was done to confirm a
Total Cholesterol reading of more than 55 mmoVL. Prior to each blood test, the patients
were advised by the researcher to adhere to the fasting requirements of 12hours before
the test. A further three tests were carried out for each pnrticipant, every four weeks.
For each testing the researcher confirmed with each patient the night before, and
reminded him or her to fast for the twelve hours. The trial began in July and testing was
scheduled every Monday, Tuesday, and Friday. The researcher was present at each
testing to follow up onany questions the patients had.
The blood samples were obtained by venous extraction, by qualified phlebotomists. All
the blood samples were taken on the TWR premises, at the pathology laboratory. After
the blood sample was obtained it was sent tothe labomtory foranalysis.
3.2.3 Blood Sample Analysis
The blood samples were analysed by the TWR pathology laboratory under the
supervision of the laboratory pathologist, Mr De Villiers. The reagents used to test for
Total Cholesterol, LDL Cholesterol, HDL Cholesterol and Triglycerides are the
regulatory reagents required, and are obtained from TRACE, Dynamic Stabilization
Technology.
The methodology carried out for each testing is clearly explained and laid out in the
pamphlets that accompany the reagents used. It isa very lengthly explanation, and for the
purposes of this study, reference to the catalogue numbers for the methodology of
analysis is made: (Truce Catalogue No TR 13421, TR 13448).
36
purposes of this study, reference to the catalogue numbers for the methodology of
analysis is made: (Trace Catalogue NoTR 13421, TR 13448).
Aller analysis ofthe blood samples, a printed out copy of the results was made available
for the researcher to collect and file under each respective patient's details.
These values were tabulated and used for data analysis.
3.2.4 Medication
The medication used in the trial was glycerine macerates, which are liquid preparations.
They are prepared by dissolving primary materials of plant origin (buds, young shoots,
and more rarely rootlets, seeds or bark) in a mixture of equal masses of alcohol and
glycerol.
Extracts from Olea eueopaea and Juniperus communis plants, were used as the active
gcmmothcrapeutic medicines in the study. These two gemmotherapcutic substances were
both prepared in 0 I potencies and were prepared by Natura laboratories, according to the
regulations set by the French Pharmacopoeia (seeappendix A).
The medicine was packaged in 50ml bottles, labelled Group A forthe placebo or control
group. and Group B for the experimental group.
Arrangements for ordering the medication were co-ordinated by the researcher with
Natura Laboratories. An order for 90 bottles (45 for each placebo and medication group
for the course of three months) of medication was placed by fax, stating the required
labelling format as above. A report of confirmation ofanalysis WIlS obtained at the endof
the trial to confirm which group was theplacebo and which was the medicated group(see
appendix A).
37
3.2.5 Administration of the medicine
The instructions for administering the medication was both explained to the patients by
the researcher and was written for reference in the instruction sheets handed out at the
start of the trial.
Each subject was instructed to take twenty drops of the medicine twice daily every day
for three months. One boule lasted each subject one-month but the patients were assured
Ihat if they damaged or lost the medication it would be replaced at no cost. Six extra
bottles were required to replace the damaged or lost ones, this was again ordered and
received from Natura Laboratories as described previously.
3.2.6 The Trial Period
The trial began in the second week of July 2000 with the majority of the patients having
had their initial test performed in the last two weeks. The trial period was carried over a
three-month period, from July to August (month one), August to September (month two),
and September to October (monththree).
3.2.7 Data Collection
After the completion of the trial period, the data was consolidated into a table format by
the researcher and confirmation of which was the placebo and medicated group was
obtained from Nanna.
Raw data from the blood test results obtained for the initial. month one, month two and
month three, for the twenty-four patients who completed the trial was collected. The
Total Cholesterol, HOL-C, LDL-C, and Triglyceride readings were collected.
38
3.2.8 Statistical Analysis
A meeting with the TWR staff statitician was held and under his advice, values for
variance (difference) and averages were to be used for the statistical analysis of the
results.
These values were methodically worked out. By taking the readings from the third month
and subtracting them from the initial month's reading, to obtain the variance values for
each patient. The average values were calculated by adding all the readings for each
patient for the respective TC, HDL. LDL, and Triglycerides, for each month.
Under the supervision ofMr DeVilliers (the TWR laboratory Pathologist) the researcher
used the computer system at the TWR to statistically analyse the data, the programme
Sigma Plot was used. The secretary in room 2304 on the Doomfontein TWR campus co-
ordinated fur the use of the computer.
Using the variance values obtained the Unpaired Two-Sample T Test type of analysis
was used to obtain graphical representation ofthe data. For the average values no type of
analysis was required as the values were plotted ona graph.
39
CIIAllTER FOUR- RESULTS OF TilE STUDY
4.1 Results
The results were transformed into statistics and graphs using the Sigma Plot and Sigma
Stars computer programmes, Analysis of the statistics were done using the Unpaired 2
Sample T test method of'analysis for the variance values, and Sigma Plot for the average
values,
40
in
- month tri
11
10
8 I
•
1
7
... 6
3 . 1. _ _- . - -----r---,---- - - -l
o 2 3 4
Tim (months)
From th mph it cnn be n th t th re \ a light d re lu

for b th group from the tart o f th trial to th nd of the third m nth. h bigg t
d re currcd in th I t m nth of treatment. n m nths t\\ and th n th
ph.
It i int tin tnt th t th up nnd up m
th . Thi
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ClI
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~ ups, \\ ith the M·di ali n r lip h a v in v In lJl '
10
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month ire tment. I twe rn III mil tw
11I'r th' U I.
, 11111 h the S ill ' I' It III n
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, he m ph h w: the han , that

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rh iph h \ lin limo I id mti ,II in 'a' r I th r up .
II
Ihe lin" fth i mph h w an In 'a' in the Tri I , iride I 'vel , ' I ' i ll , du rin the
Ii 't III nth of treatm ' I1 t, with uddcn de re: C I1d III nrh II \\ bv ,
lev .llin lit in the third rn nth , 'I h ' P II '01 of' thc imil I' f r both II I '
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00
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Ihen: i 110 tati ti all , nific: nt d ifferen e in the esulu (1'- 0.. I).
Ihcre i. . Ii htly realer lev I v ru n c in the PI. roup re. ults.

CHAPTER FIVE - DISCUSSION OFTliE RESULTS
5.1 Evaluation of the Results
The results from this trial study did not show any statistical significance, however the
graphs for each of the Total Cholesterol, LOL-Cholesterol, HOL-Cholesterol and
Triglycerides did follow positive trends. The Total Cholesterol, LOL-Cholesterol and
Triglycerides showed a decrease in values and the HDL-eholesterol showed an increase
in values over the trial period. However it is interesting and unexpected to find that the
results for the placebo group followed the same trends as forthe Medication group.
5.2 Decreasing Values for Total Cholesterol, LDL - Cholesterol and

Triglycerides
The slight decrease in Total Cholesterol. Triglycerides and LDL'(holesterol in the

Medication group could be explained by the effect of Olea europaea and Juniperus
communis. The strong influence of the placebo effect on the Placebo group could have
influenced the positive trend seen in this group throughout the trial.
Persons who choose to participate in a health-oriented study may be more interested in

health issues overall and more likely to involve themselves in projects with potential
health benefits and may. therefore. be more likely to change behaviours on their 0\\11
(Wang. et al.• 1998).
The consequence of studying such n motivated group is that everyone is likely to change.
which may have influenced the research results.
The greatest change in both groups occurred towards the end of the trial, which indicates
that the trial period was not long enough to measure the overall effect, it needs to be
extended in order to assess the trend.
49
The trial took place over the seasonal period ofwinter moving into a warmer autumn and
ending at the start of summer, which could have also strongly influenced the cholesterol
levels.
Cholesterol levels are higher in winter thansummer (Oberman, etat, 1992).
The amount and composition of dietary fat affects plasma cholesterol, those fats
containing mainly saturated fats, such as animal fats and butter. tend to mise plasma
cholesterol (Smith. er at, 1998).
The influence of the participant's diets cannot be excluded as possibly affecting the
results. The participants agreed to not make any changes to their diets and exercise
regimes. but were not placed on a diet or monitored in this regard.
Values from this trial showed close similarity in both groups with little variance, the size
ofthe sample group must also be considered as a reason for this. The trial group was too
small limitingthevariance and average values.
5.3 HDL - Cholesterol
The slight increase in the trend of the HOL-Cholesterol values for both groups once again
could show the effect of the gemmothempeutic substances; Olea europaea and Juniperus
communis forthe Medication group and thestrong influential effect of the placebo effect
on the Placebo group.
Little is known about the effectiveness of these gemmothempeutic substances; Olea

europaea and Juniperus communis, on clinical trials so there is lillie evidence to support
orexplain the research results.
so
CHAPTER SIX· CONCLUSIONS AND RECOMMENDATIONS
6.1 Conclusions
This research trial did not prove the effectiveness of Olea europaea and Juniperus
communis statistically, for the treatment of hypercholesterolaemia over a brief period of
three months.
However the results did follow a pattern, which would be expected for positive treatment
results, this could therefore be considered for further research, using a larger study over a
longer period of time.
6.2 Recommendations
The results all showed the most significant changes in the last month oftreatment. With
this evidence it can be concluded that the trial period was not long enough to establish
statistically significant results, a larger and longitudinal study may have revealed
statistically significant benefits.
The small sample group was another limiting factor to this trial. As it is impossible to
ensure that the sample group adheres to the research study's requirements, some of the
sample group decided to withdmw from the study, leaving a smaller sample group than
was anticipated.
This limited the comparison of the results between the Placebo and Medication groups,
resulting in very small insignificant variancevalues.
It is recommended that a much larger sample group be included in any future studies of
this type.
The seasonal variation may have also influenced the results.
51
To limit the outside factors on the research trial results. it is recommended that the trial
be done over a year so that seasonal variation can be noted throughout the year, or even
two years to compare values from the previous seasons.
There are many factors to consider when treating human subjects. as the many outside
influences like diet. lifestyle. and even the mental influence ofthe placebo effect could all
influence the results.
The participants' diet and lifestyle regimes were not strictly controlled or monitored in
this trial, with the result that these factors could have influenced their decisions to change
their diets and increase their exercise levels. They were asked not to change their diets.
but this is a difficult factor to control. It is recommended that for future research a
method be implemented to monitor these factors moreeffectively and closely.
The research trial did not include an equal number of men to women, with unequal ages
too. It could be recommended that the ratio of men to women be kept equal in future
studies.
All these factors have limited the effectiveness of this trial study's results. The
researcher, in hind - sight has seen the many short- comings of the study, but still feels
that the positive trends that started to emerge from the results warrant further
investigation.
S2
nEFERENCES
Cataldo. C.B.• Rolfes, S.R. and Whitney, E.N. (1998) Understanding Clinical Nutrition
2'" Edition. United States of America: Wadsworth Publishing Company.
Council on Scientific Affairs. (1993) Dietary and Pharmacological Thempy for the Lipid
Risk Factors. Journal ofthe American Medical Association, vol. 250, no 14.
De Pasquale, R., Monforte, M.T.• Trozzi, A., Raccuia, A., Tommasini, S. and Ragusa, S.
(1991) Plantes mediclnales et phyotheraple, vol XXV, p.134-140.
Grieve. M. (1984) AModem Herbal. Great Britain: Watson and Vinnie.
Harper, C.R. and Jacobson, T.A. (1999) New perspectives on the management of low
levels of high-density lipoprotein cholesterol. Archives ofInternal Medicine, vol. 159, p.
1049-1057.
Hoffman, D. (1996). The Complete Illustrated Holistic Herbal. Great Britain: Element
Books Limited.
Lee, R.D. and Nieman, D.C. (1993) Nutritional Assessment. United States of America:
WM.C. BrownCommunications Inc.pp 216,217.
Lindbloom, EJ. (1999) Treating average cholesterol levels in patients with coronary
ancry disease. Journal o/Family Practice, vol, 48, p. 94-95.
Loughrey, M.C., Rimm E., Heiss G. & Rifni N. (1999) Race and gender differences in
coni blood lipoproteins. Elsevier Science, Atherosclerosis 148 (2000) 57·65.
MIMS, (August 1999) Medical Mim.... S"ecialitie.f, vol.3, no. 8, pp. 113-116.
53

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Drawing of blood was performed at the Technikon Pathology Laboratory following an

LISf OFGRAPIIS vii

DEFINITION OF TERMS viii

1.1 THE PROBLEM 2

CHAPTER TWO - LITERATURE REVIEW 5

2.1 ATHEROSCLEROSIS, CHOLESTEROL

3.1 STUDY DESIGN 34

CHAPTER FIVE - DISCUSSION 49

CHAPTER SIX-CONCLUSIONS AND RECOMMENDATIONS

CONFIRMATION REPORT FOR MEDICATION

Table one: Standards for CHO risk factors. 5

Table two: Selected lipid and lipoprotein measures (mg/dl.) 23

Table three: Effects ofOlea europaea leaves and shoots and 31

usr OF GRAPHS page

GraphOne: Represents the changes in TC (Total cholesterol)

GraphTwo: Represents the decrease in values for TC betweenthe

GraphThree: Represents the average values ofLDL-C for placebo

Graph Five: Represents the average values forHDL-e levels taken

Graph Six: Represents the increase in HDL-C levels,

Graph Seven: Represents the average triglyceride values for placebo 47

The first decimal dilution

1.1 The Problem

Primary prevention through behavioural modification has been designated as a first-line

1.2 The Aim

1.3 Justification for the study

1.4 The use of Gemmotherapy

Gemmothempy is a form ofPhytothempy (plant medicine), using fresh plant buds. It is

1.5.1 Delimitation One

1.5.2 Delimitation Two

People on alternate medication fur hypercholesteroaemia were not permitted to

participate in this trial.

1.5.3 Delimitation Three

Pregnant women were not permitted to participate inthis trial.

1.5.4 Delimitation Four

1.6.1 Assumption One

It is assumed that the patients took the medicationas prescribed.

1.6.2 Assumption Two

1.6.3 Assumption Three

1.6.4 Assumption Four

2.1 Atherosclerosis, Cholesterol and Coronary Heart Disease (CHD)

Increased concentration of cholesterol in plasma is associated with a higher risk of

TABLE 1: STANDARDS FOR CnD RISK FACTORS

2.2.1 Dtfinition and causes of Atherosclerosis

This study therefore raises the important question of whether lipoprotein-associated

Lipoprotein-associated phospholipase A2 may promote atherogenesis, perhaps by

In direct comparison of the usefulness of levels of various serum-based markers, Ridker

Low-density lipoprotein (LDL) is the mnjor cholesterol-carrying particle in plasma.

In addition to epidemiological evidence, rodent studies suggest raising HDL-C levels

2.4 Associated Risk Faetors for enD

2.4.1 Diet and Obesity

2.4.5 Alcohol and smoking

A strong relationship between consumption ofcoffee and bloodcholesterol concentrntion

2.4.7 Seasonal Variation

A strong relationship between consumption of coffee and bloodcholesterol concentration

2.4.7 Seasonal Variation

2.5 The Influence ofRace and Gender on Lipoproteins

LipidlApoprotein White Men White Women Black Men Black Women

Oestrogen plays a cardioprotective role in women in the prevention of coronary hean

Numerous studies have documented the value of lifestyle modification in improving

2.7 Drug Treatment

Gemfibrozil, 600mg twice a day, increases HDL-C levels by an average of II %. This