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Abana, a herbomineral
drug, was found useful in controlling hypercholesterolemia. In the
present series, the indigenous formulation, Abana, was given in
normal as well as in cases of essential hypertension and angina
pectoris. Abana reduces total cholesterol and triglycerides. A significant
increasing trend was noticed in high-density lipoprotein cholesterol
levels. It was found that Abana has the capacity to regulate hypercholesterolaemia
and hypertriglyceridemia by regulating abnormal lipoprotein metabolism.
Thus the use of, Abana may be advocated for the prevention and management
of coronary heart disease.
A
large number of reports are available to show the significant role
of lipoproteins in the incidence of coronary heart disease (CHD).
It is currently proved that high levels of low density lipoprotein
cholesterol (LDL-C) are deleterious. Similarly, a large number of
reports have indicated that high density lipoprotein cholesterol
level (HDL-C) is inversely related to the incidence of CHD8,7,4.
The role of very low density lipoprotein cholesterol (VLDL-C) as
a risk factor is less certain. LDLs are the major cholesterol, carrying
lipoproteins in the plasma. LDL receptors on liver cells are responsible
for the removal of LDLs9,13. The small amount of LDLs
can be cleared by extrahepatic tissues. Ultimately, HDL-C may accept
cholesterol from extrahepatic tissues and transfer it to VLDLs and
LDLs. Finally, cholesterol carried on these latter lipoproteins
is removed by the liver6.
In
recent years the significance of plasma cholesterol levels in the
occurrence of CHD has been repeatedly emphasised. The mechanisms
for the synthesis, transport and catabolism of cholesterol are understood
much better today than a mere decade ago . The significant contribution
of Goldstein and Brown1, which resulted in the discovery
of cell surface receptors for LDL, is fundamental to our understanding
of the need to control cholesterol levels1,6. The finding
of these workers provide a rational means for controlling cholesterol
concentrations. Based on the Framingham Study, Castelli, et al.2
demonstrated that the proportion of the total cholesterol (TC) carried
by HDL-C is a consistent and important indicator of coronary risk
in both sexes over the age of 49 years2. The Lipid Research
Clinics Coronary Primary Prevention Trial reported in 1984 that
reduction of plasma cholesterol levels in turn reduces the frequency
of CHD11. Several large field surveys confirm the positive
correlation between the concentration of plasma cholesterol and
risk of CHD. The authentic data from the Framingham Heart Study
and the Lipid Research Clinics Programme showed identical findings
regarding the levels of cholesterol concentration and incidence
of CHD2,5. Several drugs have been advocated for the
modification of different lipoprotein levels. Currently available
drugs for the treatment of hypercholesterolemia have many side effects.
Till now a positive benefit/risk ratio for the cholesterol-lowering
drugs has been difficult to prove.
Several
herbomineral drugs have been advocated for the prevention and management
of CHD. The significance of Terminalia arjuna has recently
been established in the management of ischaemic heart disease14.
The drug Abana is a herbomineral compound advocated for the prevention
and management of CHD. Abana contains Terminalia arjuna, Withania
somnifera, Tinospora cordifolia, Phyllanthus emblica, Terminalia
chebula, Glycyrrhiza glabra, Asparagus racemosus, Boerhaavia diffusa,
Centella asiatica, Convolvulus pluricaulis, Nardostachys jatamansi,
Cyperus rotundus, Acorus calamus, Piper longum, Makaradwaja, etc.,
in different quantities.
Abana
was given in apparently normal individuals and in diagnosed cases
of essential hypertension and angina pectoris.
In
order to study the clinical efficacy of Abana on lipoprotein metabolism,
a careful clinical trial was carried out in selected normal, as
well as essential hypertension and angina pectoris cases.
Seventy-four
diagnosed cases of essential hypertension and angina pectoris were
included in our trial. Thirty-nine cases were suffering from essential
hypertension and the remaining 35 from angina pectoris. To compare
the results 30 apparently normal individuals were also selected.
Only mild to moderate cases of essential hypertension were included.
Total lipid profiles were carried out in all cases. Different fractions
of lipoproteins were measured following the method developed by
Laurell10.
After
the initial investigations Abana was given to all three groups,
two tablets t.i.d., continuously for 12 weeks. Placebo was introduced
in the same manner to both normal and disease groups. All the investigations
were repeated after 4 weeks to compare the results.
Abana
showed a significant influence on TC levels (Table 1). In normal
cases TC level showed a significant decreasing trend (p<0.05).
TC also significantly reduced in essential hypertension and angina
pectoris cases. TG showed similar decreasing trends in the above
two conditions (Table 2). In normal cases Abana enhanced the HDL-C
level (Table 3). A low level of HDL-C was noticed in essential hypertension
and angina pectoris cases, but after 12 weeks of Abana therapy a
significant increasing trend in HDL-C was noticed in both the disease
groups. LDL-C showed a high level in both essential hypertension
and angina cases. After 12 weeks of Abana therapy LDL-C showed a
significant decrease in the normal as well as in the diseased group
(Table 4) VLDL-C also reduced in clinical conditions but in normal
cases Abana could not show any change in VLDL-C level (Table 5).
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Table
1: Changes in total cholesterol levels following oral administration
of Abana in different groups (mean ± SDmg/dl)
|
|
Group
|
Normal
|
Essential
hypertension
|
Angina
pectoris
|
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
|
Placebo
|
179.79
± 31.36
|
191.53
± 27.96
|
250.11
±38.76
|
247.24
± 34.55
|
269.52
± 28.68
|
265.23
± 35.12
|
| |
n=12
|
n=12
|
n=12
|
|
Treated
|
188.16*
± 27.89
|
170.19*
± 21.68
|
282.49l
± 45.42
|
240.72l
± 42.03
|
278.30n
± 48.78
|
233.78n
± 49.63
|
| |
n=18
|
n=27
|
n=23
|
| Placebo
p not significant Treated *p<0.05 lp<0.01
np<0.001 |
|
Table
2: Changes in triglyceride levels following Abana treatment
(mean ± SDmg/dl)
|
|
Group
|
Normal
|
Essential
hypertension
|
Angina
pectoris
|
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
|
Placebo
|
138.10
± 28.00
|
145.71
± 33.00
|
208.02
± 36.42
|
203.08
± 36.92
|
243.15
± 36.24
|
227.35
± 44.22
|
| |
n=12
|
N=12
|
n=12
|
|
Treated
|
143.49*
± 42.62
|
125.73*
± 35.43
|
235.59l
± 25.27
|
211.91l
± 33.41
|
236.00n
± 45.47
|
203.94n
± 32.77
|
| |
N=18
|
N=27
|
n=23
|
| Placebo
p not significant Treated *p<0.05 lp<0.01
np<0.02 |
|
Table
3: Changes in HDL-C following Abana therapy (mean ± SDmg/dl)
|
|
Group
|
Normal
|
Essential
hypertension
|
Angina
pectoris
|
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
|
Placebo
|
49.15
± 7.00
|
48.94
±7.64
|
36.34
± 8.61
|
37.42
± 7.59
|
38.05
± 8.15
|
40.25
± 9.21
|
| |
n=12
|
N=12
|
N=12
|
|
Treated
|
50.10*
± 7.55
|
54.11*
± 6.50
|
37.91l
± 11.49
|
49.69l
± 13.31
|
35.59n
± 8.68
|
43.38n
± 9.50
|
| |
n=18
|
N=27
|
N=23
|
| Placebo
p not significant Treated *p<0.05 lp<0.01
np<0.01 |
|
Table
4: Changes in LDL-C in different clinical groups (mean ± SD
mg/dl)
|
|
Group
|
Normal
|
Essential
hypertension
|
Angina
pectoris
|
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
|
Placebo
|
92.35
± 22.18
|
101.82
± 25.31
|
158.45
± 26.42
|
151.93
± 20.20
|
182.62
± 25.01
|
170.51
± 31.72
|
| |
n=12
|
N=12
|
N=12
|
|
Treated
|
98.89*
± 21.73
|
83.41*
± 18.78
|
170.96l
± 35.39
|
136.37l
± 36.32
|
180.75n
± 47.25
|
138.66n
± 46.45
|
| |
n=18
|
N=27
|
N=23
|
| Placebo
p not significant Treated *p<0.05 lp<0.01
np<0.01 |
|
Table
5: Changes in VLDL-C levels after oral administration of Abana
(mean ± SDmg/dl)Group
|
| |
Normal
|
Essential
hypertension
|
Angina
pectoris
|
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
Initial
|
12
weeks
|
|
Placebo
|
35.29
± 12.03
|
40.78
± 13.49
|
53.32
± 16.18
|
57.89
± 18.45
|
65.76
± 19.58
|
69.95
± 19.59
|
| |
n=12
|
N=12
|
n=12
|
|
Treated
|
40.23*
± 12.64
|
32.94*
± 11.56
|
73.60l
± 23.43
|
53.67l
± 27.80
|
63.17n
± 19.51
|
48.29n
± 16.08
|
| |
n=18
|
N=27
|
n=23
|
| Placebo
p not significant Treated *p<0.05 lp<0.02
np<0.01 |
Abnormal
plasma lipoprotein levels are closely related to atherosclerosis
and coronary artery disease. Significant elevations in the concentration
of any one of the lipoproteins may cause hypercholesterolemia. Therefore
a proper understanding of the mechanism of lipoprotein metabolism
is important in the prevention and management of CHD. Currently
available drugs for the management of abnormal lipoproteins do not
provide satisfactory results. From the present observation Abana
shows a profound influence on the regulation of lipoprotein metabolism.
Reduction in the serum cholesterol levels in essential hypertension
and angina pectoris cases indicate the significance of Abana in
the prevention of coronary heart disease. The currently available
drugs have shown adverse side-effects and hence such drugs cannot
be advocated for continuous use. On the contrary Abana did not demonstrate
any adverse side-effects even after continuous oral administration.
Dubey et al.3 found significant decreasing trends
in the levels of cholesterol and triglycerides (TG) following oral
administration of Abana in CHD cases. It is possible that this herbomineral
compound might regulate the abnormal elevations of TC and TG either
by decreasing the production or by increasing the clearance of lipoproteins.
Castelli
et al.2 reported the significance of HDL-C in
the prevention of atherogenesis. From the present study it is evident
that Abana has increased the HDL-C in hypertension and angina pectoris
cases. Hence, it can be concluded that Abana may prevent the future
occurrence of CHD in likely victims.
Some
of the ingredients of Abana like Terminalia arjuna, Nardostachys
jatamansi and Glycerrhiza glabra have been advocated
in the indigenous system of medicine for the prevention of cardiovascular
disorders. Singh et al.12 observed a hypotensive
and bradycardic effect of Terminalia arjuna in dogs. Phyllanthus
emblica has been reported to increase body resistance against
disease and decay. It might be possible that Phyllanthus emblica
may also increase HDL-C levels.
LDL-C
was also reduced in hypertension and angina pectoris cases. This
further indicates the significance of Abana in the prevention of
CHD. The relationship between high concentrations of LDL-C and the
incidence of CHD has been established. The role of the LDL receptor
in the liver is recognised as the crucial element in the regulation
of cholesterol levels. Abana has shown a significant influence on
LDL levels, though the changes are not consistent in normal cases.
At present it is difficult to infer the modes of action of Abana
in the reduction of LDL-C levels. It is possible that some of the
components of Abana reduce LDL-C by the action on LDL receptors
in the liver.
VLDL-C
showed a decreasing trend in essential hypertension as well as in
cases of angina pectoris after Abana therapy. The significance of
VLDL-C as a risk factor has not been proved so far. It requires
comprehensive study to establish a relationship between VLDL-C and
the incidence of CHD.
In
brief, an increasing trend of HDL levels indicates the antiatherogenic
property of Abana. Hence Abana can be advocated as a protective
measure against atherosclerosis, hypertension and coronary heart
disease.
-
Brown, M.S., Goldstein, J.I.: Lipoprotein receptors
in the liver. Control signals for plasma cholesterol traffic.
J. Clin. Invest. 72 (1986), 743-747.
-
Castelli, W.P., Rober, J., Garrison, P.W.F.,
Wilson, R.D., Abbot, S., Kalorisdian, W. and Kannel, B. Incidence
of coronary heart disease and lipoprotein cholesterol levels.
The Framingham Study. J. Am. med. Assoc. 256 (1986),
2835-2838.
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Dubey, G.P., Agarwal, A., Srivastava, V.K.,
Agarwal, U. and Udupa, K.N. Management of risk factors of coronary
heart disease with an indigenous compound Abana.
Probe XXV (1985), 46-55.
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Garden, T., Castelli, W.P., Hjortland, M.C.
et al. High density lipoprotein as a protective factor
against coronary heart disease. The Framingham Study. Ann.
J. Med. 62 (1977), 707-714.
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Gorden, D.J. Plasma high density lipoprotein
cholesterol and coronary heart disease in hypercholesterolaemic
men. Circulation 72 (1985), 111-185.
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Grundy, Scott, M. Cholesterol and coronary
heart disease. A New Era. J. Am. Med. Assoc. Vol. 256:
(1986), 2849-2858.
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Keys, A. Alpha lipoprotein (HDL) cholesterol
in the serum and risk of coronary heart disease and death. Lancet
ii (1980), 603-606.
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Keys, A., Karvonen, M.J. Punsar, S. et al.
HDL serum cholesterol and 24 years mortality of men in Finland.
Int. J. Epidemiol. 13 (1984), 428-435.
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Kovanen, P.T., Bilheimer, D.W., Goldstein,
J.I. et al. Regulatory role for hepatic low density lipoprotein
receptors in vivo in the dog. Proc. Natl. Acad. Sci.
U.S.A. 78 (1981), 1194-1198.
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Laurell, S., Scand . J. Lab. Clin. Invest.
18 (1966), 668.
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Lipid Research Clinical Programme. The Lipid
Research Clinics coronary primary prevention trial results.
Reduction in incidence of coronary heart disease. J. Am.
Med. Assoc. 251 (1984), 351-364.
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Singh, N., Kapoor, K.K., Singh, S.P., Shankar,
K., Sinha, J.N. and Kohli, R.P. Mechanism of cardiovascular
action of Terminalia arjuna. Planta Medica 45 (1982),
102.
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Spady, D.K., Bilheimer, D.W. and Dietschy,
J.M. Rates of receptor-dependent and independent low density
lipoprotein uptake in the hamster. Proc. Natl. Acad. Sci.
U.S.A. 80 (1983), 3499-3503.
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Udupa, K.N. Scope of use of T. arjuna
in ischaemic heart disease. Ann. Natl. Acad. Indian Med.
1 (1986), 54-58.
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