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Hyperlipidemia whether it is primary or secondary to take high lipid-content diets can cause coronary artery disease. This condition can be prevented and treated by allopathy related drugs like vitamin B3, and statins. As these drugs have potential to develop severe side effects, many cardiologists have approved utilization of medicinal herbs to control hyperlipidemia. We selected its hypolipidemic and weight lost effects in primary and secondary hyperlipidemic patients. Type of Research study: It was placebo-controlled study. Area of research: Research was conducted in Jinnah hospital, Lahore, Pakistan. Duration of study: It was three months, from January 2014 to June 2014.Materials, methods and results: Already well understood, clearly explained written consent was taken from sixty hyperlipidemic patients age range from 18 to 70 years. Both gender male and female patients were enrolled. Patients were randomly divided in two groups 30 patients were on drug ginger pasted-powder advised to take 5 grams in divided doses with their normal diet for the period of three months. Thirty patients were on placebo pastedwheat powder, with same color as of ginger powder, advised to take 5 grams in divided doses with their normal diet for the period of three months. Their base line lipid profile and body weight was recorded at start of treatment and were advised to come for check-up, fortnightly. When duration of study was over, their lipid profile and body weight was measured and compared statistically with pre-treatment values. Three months treatment with 5 grams of Ginger decreased LDL-cholesterol 17.41%, total-cholesterol 8.83% and body weight 2.11%. When compared with placebo group, all changes in mentioned parameters were significant bio-statistically.Conclusion: It was concluded from results of study that active ingredients of ginger lower plasma lipids and body weight significantly, eventually preventing development of coronary artery disease in primary and secondary hyperlipidemic patients.
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Effects of Ginger on LDL-C, Total Cholesterol and Body Weight
Shah Murad*, Khalid Niaz and Hina Aslam
Department of Pharmacology, Akbar Niazi Teaching Hospital, Islamabad, Pakistan
*Corresponding author: Shah Murad, Professor of Pharmacology, Akbar Niazi Teaching Hospital, Islamabad, Pakistan, Tel: +923142243415; E-mail:
Shahhmurad65@imdcollege.edu.pk
Rec date: February 08, 2018; Acc date: February 10, 2018; Pub date: February 18, 2018
Copyright: © 2018 Murad S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Hyperlipidemia whether it is primary or secondary to take high lipid-content diets can cause coronary artery
disease. This condition can be prevented and treated by allopathy related drugs like vitamin B3, and statins. As
these drugs have potential to develop severe side effects, many cardiologists have approved utilization of medicinal
herbs to control hyperlipidemia. We selected its hypolipidemic and weight lost effects in primary and secondary
hyperlipidemic patients. Type of Research study: It was placebo-controlled study. Area of research: Research was
conducted in Jinnah hospital, Lahore, Pakistan. Duration of study: It was three months, from January 2014 to June
2014.
Materials, methods and results: Already well understood, clearly explained written consent was taken from
sixty hyperlipidemic patients age range from 18 to 70 years. Both gender male and female patients were enrolled.
Patients were randomly divided in two groups 30 patients were on drug ginger pasted-powder advised to take 5
grams in divided doses with their normal diet for the period of three months. Thirty patients were on placebo pasted-
wheat powder, with same color as of ginger powder, advised to take 5 grams in divided doses with their normal diet
for the period of three months. Their base line lipid profile and body weight was recorded at start of treatment and
were advised to come for check-up, fortnightly. When duration of study was over, their lipid profile and body weight
was measured and compared statistically with pre-treatment values. Three months treatment with 5 grams of Ginger
decreased LDL-cholesterol 17.41%, total-cholesterol 8.83% and body weight 2.11%. When compared with placebo
group, all changes in mentioned parameters were significant bio-statistically.
Conclusion: It was concluded from results of study that active ingredients of ginger lower plasma lipids and body
weight significantly, eventually preventing development of coronary artery disease in primary and secondary
hyperlipidemic patients.
Keywords: Hyperlipidemia; Ginger; LDL-cholesterol
Introduction
To prevent coronary artery disease (CA), hypolipidemic medicines
play major role. Many hypolipidemic drugs have already been proved
to be useful in lowering serum lipid levels in patients [1]. However, its
side eects in long term treatment were more reported and its prices
were still expensive. us, eorts to develop eective and better
hypolipidemic drugs had led to the discovery of natural medicinal
herbs [2].
e benecial uses of medicinal plants in traditional system of
medicine of many cultures are extensively documented [3]. Several
plants have been used as dietary adjuvant and in treating the number
of diseases even without any knowledge on their proper functions and
constituents [4]. Over 80% of the world population uses natural
remedies as medicine and over 70% of doctors in Germany prescribe
plant-based medicines [5]. Ginger (
Zingiber ocinale
) is a natural
dietary component, which has hypolipidemic, antiplatelet aggregation,
antioxidant and anticarcinogenic properties [6].
Ginger is indigenous to southern China, spreading eventually to
the Spice Islands, other parts of Asia and subsequently to West
Africa and the Caribbean [7]. Ginger was exported
to Europe via India in the rst century AD as a result of the
lucrative spice trade. India remains the largest producer of ginger [8].
Hypolipidemic and antiplatelet therapy is an eective approach for
preventing coronary heart disease [9]. Ginger components are
suggested as a potential new class of platelet-activation inhibitors
without the potential side eects of aspirin, which is most commonly
used in this approach. In a comparison of gingerols and analogs with
aspirin, ginger compounds were found to be less potent compared to
aspirin in inhibiting arachidonic acid-induced platelet release and
aggregation and COX activity.
However, several analogs had a signicant inhibitory eect,
suggesting that further development of more potent gingerol analogs
might have value as an alternative to aspirin therapy in preventing
ischemic heart disease [10,11]. Mechanism by which ginger may lower
cholesterol is well understood by scientists and other researchers.
ey explain that ginger activates an enzyme that increases body's
use of cholesterol and lowers it. Several studies show that ginger can
lower experimentally induced high cholesterol in animals, but more
studies on ginger's eect on humans with high cholesterol are needed
before the substance can be touted as a treatment for high cholesterol
[12].
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ISSN: 2471-2663
Clinical & Medical Biochemistry
Murad et al., Clin Med Biochem 2018, 4:2
DOI: 10.4172/2471-2663.1000140
Research Article Open Access
Clin Med Biochem, an open access journal
ISSN: 2471-2663
Volume 4 • Issue 2 • 1000140
Materials and Methods
Research study was conducted at Jinnah hospital Lahore Pakistan,
from January 2014 to June 2014. Written consent was taken from sixty
hyperlipidemic patients age range from 18 to 70 years. Both gender
male and female patients were enrolled. Patients were randomly
divided in two groups 30 patients were on drug ginger pasted-powder
advised to take 5 grams in divided doses with their normal diet for the
period of three months. irty patients were on placebo pasted-wheat
powder, with same color as of ginger powder, advised to take 5 grams
in divided doses with their normal diet for the period of three months.
eir base line lipid prole (for total serum cholesterol, LDL-
cholesterol) and body weight was recorded at start of treatment and
were advised to come for check-up, fortnightly. When duration of
study was over, their lipid prole and body weight was measured and
compared statistically with pre-treatment values. Serum total
cholesterol was estimated by the enzymatic calorimatic method. Serum
LDL-cholesterol was calculated by Friedwald formula [5].
LDL Cholesterol=Total Cholesterol-(Triglycerides/5+HDL
Cholesterol)
Body weight was determined by conventional method of usual
weight machine data were expressed as the mean ± SD and paired ‘t’
test was applied to determine statistical signicance as the dierence.
A probability value of <0.05 was considered as non-signicance and
P<0.001 was considered as highly signicant change in the results.
Results
ree months treatment with 5 grams of Ginger reduced LDL-
cholesterol from 185.21 ± 2.01 to 157.72 ± 1.90 mg/dl, which is highly
signicant change in the parameter (p-value <0.001). Serum total
cholesterol at baseline was 251.11 ± 2.00 mg/dl, which reduced to
230.71 ± 1.77 mg/dl. is change is highly signicant statistically, with
p-value <0.001. Mean body weight decreased from 79.01 ± 2.91 kg to
77.32 ± 2.61 kg in three months therapy.
All changes are highly signicant statistically, having p-value
<0.001. In placebo group LDL-Cholesterol, serum total cholesterol and
body weight reduction was 0.18, 0.77, and 0.22% respectively. All these
changes are non-signicant (p-value >0.05). Detailed changes are
shown in following tables (Tables 1 and 2)
Parameter Pretreatment Post-treatment Change in % p-value
LDL-Cholesterol 185.21 ± 2.01 157.72 ± 1.90 17.41% <0.001
Total-Cholesterol 251.11 ± 2.00 230.71 ± 1.77 8.83% <0.001
Body weight 79.01 ± 3.01 77.32 ± 2.61 2.11% <0.05
Table 1: Showing pretreatment, post treatment values, change in percentage and their statistical signicance in DRUG GROUP (n=27).
Parameter Pretreatment Post-treatment Change in % p-value
LDL-Cholesterol 143.25 ± 1.99 142.98 ± 2.61 0.18% >0.05
Total-Cholesterol 190.47 ± 2.71 188.99 ± 2.50 0.77% >0.05
Body weight 76.73 ± 2.19 76.56 ± 2.71 0.22% >0.05
Table 2: Showing pretreatment, post treatment values, change in percentage and their statistical signicance in PLACEBO GROUP (n=30). Key: ±
indicates standard error of mean, p-value >0.05 indicates non-signicant and P<0.001 indicates highly signicant change in lipid prole. LDL-C
means low density lipoprotein cholesterol mg/dl, T-C means total serum cholesterol mg/dl, and body weight is measured in kg.
Discussion
In our research study ginger was used in thirty male and female
hyperlipidemic patients for three months, which reduced LDL-
cholesterol from baseline value of 185.21 ± 2.01 mg/dl to 157.72 ± 1.90
mg/dl. It is 17.4% change in this parameter, which is highly signicant
change statistically with p-value of <0.001. ese results match with
results of Bordia et al. [13] who mentioned that nearly same eects of
ginger may be achieved when the drug is used for three months.
He has mentioned detailed explanations regarding eects of ginger
in hyperlipidemic and hyperglycemic conditions. ese results are in
contrast with study results of omson et al. [14] who observed less
eect on LDL-cholesterol, i.e., from 179.57 ± 2.29 mg/dl to 176.92 ±
2.11 mg/dl when they used three grams of ginger for the period of 6
months in 82 hyperlipidemic subjects.
ese variations and too much contrast in these two comparable
studies may be sample size, long duration of administration of
chemical compound/drug. In our observation serum total cholesterol
reduced from 251.11 ± 2.00 mg/dl to 230.71 ± 1.77 mg/dl. Vaes and
Chyka [15] observed almost same changes in serum total cholesterol
when they used 2 grams ginger powder, twice daily for the period of
one month.
eir results augment and support results of our research work. Our
results in the parameter also match with results of study conducted by
Chrubasek et al. [16] who observed same changes in serum total
cholesterol. Five grams of ginger in our study reduced body weight of
30 male/female patients from 79.01 ± 2.91 kg to 77.32 ± 2.61 kg by 3
months therapy. Nurtjahja-Tjendraputra et al. [17] also observed same
changes by their research study. is proves and augments our research
results. Fuhrman et al. [18] described presence of various chemical
ingredients in ginger which are responsible to decrease high levels of
serum lipid levels and decreased blood pressure in hyperlipidemic
patients.
Citation: Murad S, Niaz K, Aslam H (2018) Effects of Ginger on LDL-C, Total Cholesterol and Body Weight. Clin Med Biochem 4: 140. doi:
10.4172/2471-2663.1000140
Page 2 of 3
Clin Med Biochem, an open access journal
ISSN: 2471-2663
Volume 4 • Issue 2 • 1000140
Our results are in contrast with study results of Guh et al. [19] who
proved that there is no signicant eect on body weight when 2 grams
of ginger powder daily was used for two months, in one hundred
volunteers having secondary hyperlipidemia. Possible and guessed,
scientic reason for this dierence may be type of hyperlipidemia, i.e.,
we included both primary and secondary hyperlipidemic patients, and
they only included secondary hyperlipidemic patients.
Active ingredients of ginger were studied by Rohta et al. [20] and
proved to be eective in lowering lipoproteins and Apo proteins.
Apoproteins are integral part of lipoproteins like VLDL, LDL, HDL,
and IDLs which are caring dierent lipids from plasma to tissues in
human body.
Conclusion
It was concluded from the study that use of raw ginger 5 grams daily
for three months reduced LDL-cholesterol highly signicantly, while
this dose of herb has moderate hypolipidemic eects on total
cholesterol and body weight in hyperlipidemic patients.
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Citation: Murad S, Niaz K, Aslam H (2018) Effects of Ginger on LDL-C, Total Cholesterol and Body Weight. Clin Med Biochem 4: 140. doi:
10.4172/2471-2663.1000140
Page 3 of 3
Clin Med Biochem, an open access journal
ISSN: 2471-2663
Volume 4 • Issue 2 • 1000140
... According to the similarities between the mentioned symptoms and hypothyroid symptoms, warm remedies such as ginger are recommended by traditional medicine practitioners for these patients [20]. Besides, several scientific investigations have confirmed the therapeutic effects of ginger on hyperlipidemia [21,22], insulin resistance [23,24], and obesity [22,25], which are all common comorbidities in hypothyroid patients. Recent studies also have shown the protective effect of ginger against thyroid damage in animals and humans [16,26,27]. ...
... Human studies also support these results. Murad et al. indicated that the daily consumption of 5 g of ginger powder for 12 weeks can reduce the TChol concentration in the healthy population [21]. Besides, Mushtaq et al. showed a significant decrease in the TChol concentration after 30 days of treatment with 3 g of ginger powder in patients with hyperlipidemia [44]. ...
... Similar to our study, Attari et al. illustrated that the administration of 2 g of ginger for 12 weeks in obese women significantly reduced the BMI and waist circumference compared with the baseline and the placebo group [17]. Also, Murad et al. demonstrated that the consumption of 5 g of ginger powder for 3 months significantly decreased the body weight in hyperlipidemic patients [21]. In a study conducted by Mozaffari et al. on 88 patients with type 2 diabetes, it was shown that the daily consumption of 3 g of ginger powder for 8 weeks did not affect the BMI [50]. ...
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Primary hypothyroidism is a common disease. Some patients have persistent symptoms despite normal serum thyroid-stimulating hormone (TSH) levels. Ginger is reported to be beneficial in relieving similar symptoms. Our aim was to evaluate the efficacy of ginger supplementation in relieving persistent symptoms in these patients. In this randomized, double-blind, placebo-controlled clinical trial, 60 hypothyroid patients aged 20–60 years with normal serum TSH concentrations were randomly allocated to two equal parallel study groups of ginger (500 mg twice a day) or placebo for 30 days. Hypothyroid symptoms were evaluated as the primary outcome using the Thyroid Symptom Rating Questionnaire (ThySRQ) before and after the intervention. Anthropometric measures and laboratory indices including TSH, triglyceride (TG), total cholesterol (TChol), and fasting blood sugar (FBS) were considered as secondary outcomes. A significant lower mean total ThySRQ score (8.63 ± 5.47 vs. 15.76 ± 6.09, P < 0.001 ) was observed in the ginger group compared to the control group. Ginger led to significant improvements in the mean scores of the weight gain, cold intolerance, constipation, dry skin, appetite, memory loss, concentration disturbance, and feeling giddy or dizzy domains ( P < 0.001 ). However, no significant improvements were observed in hair loss, nail fragility, hearing, hoarseness, speech, and depression or feeling down ( P > 0.05 ). Ginger supplementation also led to a significant decrease in body weight, body mass index, waist circumference, serum TSH, FBS, TG, and TChol levels compared to the placebo. In summary according to preliminary results of this study, ginger supplementation can help relieve persistent hypothyroid symptoms. Also, it may have beneficial effects in terms of weight reduction and regulation of the FBS and lipid profile in hypothyroid patients.
... Ginger is a strong antioxidant substance and may either mitigate or prevent generation of free radicals and protect the cells from lipid oxidation [22]. Hence, ginger is known to have many health benefits and applied to treat respiratory diseases [23], nausea [24], and a cholesterol-lowering herb [25]. Furthermore, it has reported that ginger possesses other several beneficial pharmacological effects including gastroprotective [26], antiviral [27], and antidiabetic [28]. ...
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Arogyavardhini vati, an Ayurvedic polyherbal formulation has been used for liver and skin disorders in the Ayurvedic system of medicine. However, toxicity due to the presence of heavy metals in this traditional medicine is a matter of concern. To evaluate the safety of Arogyavardhini vati on brain, liver and kidney in rats. Arogyavardhini vati at doses of 50, 250 and 500mg/kg (1, 5 and 10 times of human equivalent dose respectively), mercury chloride (1mg/kg) and normal saline were administered orally to male Wistar rats for 28 days. Behavioral parameters were assessed on day 1, 7th, 14th and 28th using Morris water maze, passive avoidance, elevated plus maze and rota rod. Biochemical parameters (acetyl-cholinesterase activity, malondialdehyde, reduced glutathione), histopathology and mercury level in brain, liver, kidney were assessed at the end of the experiment. There was no significant change in behavioral parameters, acetyl-cholinesterase activity, liver function (ALT, AST, ALP and bilirubin) and kidney (serum urea and creatinine) function tests at all doses of Arogyavardhini vati (50, 250 and 500mg/kg) as compared to normal control. However, significant change was observed in mercury chloride treated group. Mercury chloride treated group as well as Arogyavardhini vati treated groups (50, 250 and 500mg/kg) showed increased levels of mercury in brain, liver and kidney as compared to normal control. Histopathological results showed significant cytoarchitectural changes in brain, liver and kidney architecture in mercury chloride treated group. Whereas, normal cytoarchitecture was observed at all doses of Arogyavardhini vati. The finding of the present study suggests that Arogyavardhini vati in the doses equivalent up to 10 times of the human dose administered to rats for 28 days does not have appreciable toxicological effects on brain, liver and kidney.
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To assess the long-term efficacy and use of fenofibrate together with a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor ("statin") in the treatment of elevated levels of triglycerides and low-density lipoprotein (LDL) cholesterol, we conducted a study that compared a before- and after-case series. The study involved 80 patients with a diagnosis of combined hyperlipidemia and existing coronary artery disease (81% of patients) or outpatients with > or = 3 risk factors for coronary artery disease who had been receiving treatment at a tertiary care center. Fasting biochemical measures were obtained at baseline during monotherapy with a statin consisting of pravastatin 20 mg once daily or simvastatin 10 mg once daily (39 patients) or fenofibrate 300 mg once daily (41 patients), and during a 2-year period of combination therapy. This combination therapy comprised fenofibrate 300 mg once daily or micronized fenofibrate 200 mg once daily taken together with pravastatin 20 mg once daily (63 patients) or simvastatin 10 mg once daily (17 patients). The main outcome measures were: (1) absolute and percent change in total cholesterol, triglycerides, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol; (2) percentage of patients with alanine aminotransferase > or = 2x the upper limits of normal on any occasion; (3) percentage of patients with creatinine kinase > or = 3 times the upper limits of normal on any occasion; (4) absolute changes in alanine aminotransferase and creatinine phosphokinase; and (5) months on combination therapy. Patients receiving combination therapy had a mean total cholesterol (+/- standard error of the mean [SEM]) that was significantly decreased by 26+/-1%, triglycerides by 41+/-3%, and LDL cholesterol by 28+/-2%, and mean HDL cholesterol that was significantly increased by 22+/-6%. These changes correspond to mean absolute changes of total cholesterol: -75+/-5 mg/dL; triglycerides: -94+/-13 mg/dL; LDL cholesterol: -52+/-5 mg/dL; and HDL cholesterol: 5+/-1 mg/dL. During combination treatment, alanine aminotransferase increased by 2+/-2 U/liter (not significant) and creatinine phosphokinase decreased by 4+/-13 U/liter (not significant). During treatment, 8 patients (10%) had transitory isolated elevations in alanine aminotransferase levels > or = 2 times the upper limits of normal and 2 patients (2.5%) had an isolated and transitory elevation of creatinine kinase (> or = 3x but < 6x upper limits of normal) without associated muscle symptoms. Patient-years on combination therapy equaled 220.6 (average 2.06 years per patient). The results demonstrated that combination treatment with fenofibrate and low-dose simvastatin or pravastatin is generally safe and effective for the treatment of combined hyperlipidemia in patients with normal hepatic and renal function.
Article
The in vitro binding of bile acids by okra (Abelmoschus esculentus), beets (Beta vulgaris), asparagus (Asparagus officinalis), eggplant (Solanum melongena), turnips (Brassica rapa rapifera), green beans (Phaseolus vulgaris), carrots (Daucus carota), and cauliflower (Brassica oleracea botrytis) was determined using a mixture of bile acids secreted in human bile at a duodenal physiological pH of 6.3. Six treatments and two blank incubations were conducted, testing various fresh raw vegetables on an equal dry matter basis. Considering cholestyramine (bile acid-binding, cholesterol-lowering drug) as 100% bound, the relative in vitro bile acid binding on dry matter (DM) and total dietary fibre (TDF) basis was 1-16% and 2-54%, respectively. Bile acid binding for okra was significantly higher than for all the other vegetables tested. For beets, binding values were significantly higher than for asparagus. Binding values for asparagus were significantly higher than for eggplant, turnips, beans green, carrots and cauliflower. These results point to the health promoting potential of okra > beets > asparagus > eggplant = turnips = green beans = carrots = cauliflower, as indicated by their bile acid binding, on a dry matter basis.
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We describe a screening test for hypolipidemic agents in which compounds are administered orally to fasted rats after a single intravenous injection of 225 mg Triton WR-1339/kg and serum cholesterol and triglycerides are measured 43 hr post-Triton. Conditions for the screen were established by studying interrelationships between serum cholesterol, triglycerides and Triton levels during the post-Triton period and the effects of Triton dose, route of administration and fasting on serum lipid levels and drug hypocholesterolemic activity. The test detects compounds which inhibit lipid biosynthesis or stimulate lipid catabolism. Several drugs with different mechanisms of action which are hypolipidemic in man, including nicotinic acid,D-thyroxine, triparanol, nafoxidine HCl and clofibrate are active in this system. Results with standard hypolipidemic agents are reproducible and conform well to performance levels of the screen predicted from statistical analysis.
Article
The purpose of this investigation was to determine the antiplatelet mechanism of gingerol. Gingerol concentration-dependently (0·5–20 μm) inhibited the aggregation and release reaction of rabbit washed platelets induced by arachidonic acid and collagen, but not those induced by platelet-activating factor (PAF), U46619 (9,11-dideoxy-9α,11 α-methano-epoxy-PGF2α) and thrombin. Gingerol also concentration-dependently (0·5–10μ m) inhibited thromboxane B2 and prostaglandin D2 formation caused by arachidonic acid, and completely abolished phosphoinositide breakdown induced by arachidonic acid but had no effect on that of collagen, PAF or thrombin even at concentrations as high as 300 μ m. In human platelet-rich plasma, gingerol and indomethacin prevented the secondary aggregation and blocked ATP release from platelets induced by adenosine 5′-diphosphate (ADP, 5 μ m) and adrenaline (5 ä m) but had no influence on the primary aggregation. The maximal antiplatelet effect was obtained when platelets were incubated with gingerol for 30 min and this inhibition was reversible. It is concluded that the antiplatelet action of gingerol is mainly due to the inhibition of thromboxane formation.
Article
In a placebo-controlled study the effect of ginger and fenugreek was examined on blood lipids, blood sugar, platelet aggregation, fibrinogen and fibrinolytic activity. The subjects included in this study were healthy individuals, patients with coronary artery disease (CAD), and patients with non-insulin-dependent diabetes mellitus (NIDDM) who either had CAD or were without CAD. In patients with CAD powdered ginger administered in a dose of 4 g daily for 3 months did not affect ADP- and epinephrine-induced platelet aggregation. Also, no change in the fibrinolytic activity and fibrinogen level was observed. However, a single dose of 10 g powdered ginger administered to CAD patients produced a significant reduction in platelet aggregation induced by the two agonists. Ginger did not affect the blood lipids and blood sugar. Fenugreek given in a dose of 2.5 g twice daily for 3 months to healthy individuals did not affect the blood lipids and blood sugar (fasting and post prandial). However, administered in the same daily dose for the same duration to CAD patients also with NIDDM, fenugreek decreased significantly the blood lipids (total cholesterol and triglycerides) without affecting the HDL-c. When administered in the same daily dose to NIDDM (non-CAD) patients (mild cases), fenugreek reduced significantly the blood sugar (fasting and post prandial). In severe NIDDM cases, blood sugar (both fasting and post prandial) was only slightly reduced. The changes were not significant. Fenugreek administration did not affect platelet aggregation, fibrinolytic activity and fibrinogen.
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Circulating levels of C-reactive protein (CRP) may constitute an independent risk factor for cardiovascular disease. How CRP as a risk factor is involved in cardiovascular disease is still unclear. By reviewing available studies, we discuss explanations for the associations between CRP and cardiovascular disease. CRP levels within the upper quartile/quintile of the normal range constitute an increased risk for cardiovascular events, both in apparently healthy persons and in persons with preexisting angina pectoris. High CRP responses after acute myocardial infarction indicate an unfavorable outcome, even after correction for other risk factors. This link between CRP and cardiovascular disease has been considered to reflect the response of the body to the inflammatory reactions in the atherosclerotic (coronary) vessels and adjacent myocardium. However, because CRP localizes in infarcted myocardium (with colocalization of activated complement), we hypothesize that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis. CRP constitutes an independent cardiovascular risk factor. Unraveling the molecular background of this association may provide new directions for prevention of cardiovascular events.
Article
The availability of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has revolutionised the treatment of lipid abnormalities in patients at risk for the development of coronary atherosclerosis. The relatively widespread experience with HMG-CoA therapy has allowed a clear picture to emerge concerning the relative tolerability of these agents. While HMG-CoA reductase inhibitors have been shown to decrease complications from atherosclerosis and to improve total mortality, concern has been raised as to the long term safety of these agents. They came under close scrutiny in early trials because ocular complications had been seen with older inhibitors of cholesterol synthesis. However, extensive evaluation demonstrated no significant adverse alteration of ophthalmological function by the HMG-CoA reductase inhibitors. Extensive experience with the potential adverse effect of the HMG-CoA reductase inhibitors on hepatic function has accumulated. The effect on hepatic function for the various HMG-CoA reductase inhibitors is roughly dose-related and 1 to 3% of patients experience an increase in hepatic enzyme levels. The majority of liver abnormalities occur within the first 3 months of therapy and require monitoring. Rhabdomyolysis is an uncommon syndrome and occurs in approximately 0.1% of patients who receive HMG-CoA reductase inhibitor monotherapy. However, the incidence is increased when HMG-CoA reductase inhibitors are used in combination with agents that share a common metabolic path. The role of the cytochrome P450 (CYP) enzyme system in drug-drug interactions involving HMG-CoA reductase inhibitors has been extensively studied. Atorvastatin, cerivastatin, lovastatin and simvastatin are predominantly metabolised by the CYP3A4 isozyme. Fluvastatin has several metabolic pathways which involve the CYP enzyme system. Pravastatin is not significantly metabolised by this enzyme and thus has theoretical advantage in combination therapy. The major interactions with HMG-CoA reductase inhibitors in combination therapy involving rhabdomyolysis include fibric acid derivatives, erythromycin, cyclosporin and fluconazole. Additional concern has been raised relative to overzealous lowering of cholesterol which could occur due to the potency of therapy with these agents. Currently, there is no evidence from clinical trials of an increase in cardiovascular or total mortality associated with potent low density lipoprotein reduction. However, a threshold effect had been inferred by retrospective analysis of the Cholesterol and Recurrent Events study utilising pravastatin and the role of aggressive lipid therapy is currently being addressed in several large scale trials.