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Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy
Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy
Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy
Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy
Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmaceutiche, Università degli Studi di Milano, Milano, Italy
Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy
Centro Dislipidemie, A. O. Ospedale Niguarda Cà Granda, Milano, ItalyDipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy
Nutraceutical effectiveness on total and LDL-cholesterol reduction is similar to pravastatin.
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Nutraceutical treatment is useful and safe in subjects with moderate cardiovascular risk.
Background
Primary cardiovascular prevention may be achieved by lifestyle/nutrition improvements and specific drugs, although a relevant role is now emerging for specific functional foods and nutraceuticals.
Objectives
The aim of this study was to evaluate the usefulness of a nutraceutical multitarget approach in subjects with moderate cardiovascular risk and to compare it with pravastatin treatment.
Subjects
Thirty patients with moderate dyslipidemia and metabolic syndrome (according to the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults) were included in an 8-week randomized, double-blind crossover study and took either placebo or a nutraceutical combination that contained red yeast rice extract, berberine, policosanol, astaxanthin, coenzyme Q10, and folic acid (Armolipid Plus). Subsequently, they were subjected to another 8-week treatment with pravastatin 10 mg/d. This dosage was selected on the basis of its expected −20% efficacy in reducing low-density lipoprotein-cholesterol.
Results
Treatment with Armolipid Plus led to a significant reduction of total cholesterol (−12.8%) and low-density lipoprotein-cholesterol (−21.1%), similar to pravastatin (−16% and −22.6%, respectively), and an increase of high-density lipoprotein-cholesterol (4.8%). Armolipid Plus improved the leptin-to-adiponectin ratio, whereas adiponectin levels were unchanged.
Conclusions
These results indicate that this nutraceutical approach shows a lipid-lowering activity comparable to pravastatin treatment. Hence, it may be a safe and useful option, especially in conditions of moderate cardiovascular risk, in which a pharmacologic intervention may not be appropriate.
The approach to lipid disorders has recently developed a keen interest in the metabolic syndrome (MetS), a clinical condition characterized by a series of cardiovascular (CV) risk factors, that is, dyslipidemia, arterial hypertension, hyperglycemia, and central adiposity, which involves >25% adults in Europe.
Despite the still ongoing debate about the factors that lead to the MetS and on the appropriateness of the diagnosis, correction of the associated risk factors by lifestyle changes and eventually medications appears to be of potential value in reducing the rates of morbidity and mortality in affected subjects.
Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.
The interest for a nutraceutical approach to metabolic disorders is growing either because few new drugs in this area are currently reaching the market
or because patients with metabolic conditions suitable for a nutraceutical approach seem to appreciate a therapeutic management that does not involve drug treatment.
Combined extractives of red yeast rice, bitter gourd, chlorella, soy protein, and licorice improve total cholesterol, low-density lipoprotein cholesterol, and triglyceride in subjects with metabolic syndrome.
This is particularly the case of hyperlipidemias, largely treated with drugs (eg, statins) of proven efficacy but plagued, in fact, by a relatively high incidence of clinical side effects, such as myalgia and myopathy.
Extracts of red yeast rice (RYR), Monascus purpureus, have been widely used for therapy of patients with CV disorders in China for centuries, because they contain a family of naturally occurring statins (monacolins), one of which is monacolin K/lovastatin, a well-known inhibitor of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase. The use of RYR extracts in the treatment of hypercholesterolemia is currently well established worldwide.
Berberine is a natural compound from the Chinese folk medicine, generally indicated for intestinal conditions, but recently shown to exert a cholesterol-lowering activity.
Effects of a nutraceutical combination (berberine, red yeast rice and policosanols) on lipid levels and endothelial function randomized, double-blind, placebo-controlled study.
It is an isoquinoline alkaloid extracted from many herbal plants (Coptidis rhizoma, Hydrastis canadensis, Berberis vulgaris) which exerts its lipid-lowering effect by increasing the hepatic expression of the low-density lipoprotein (LDL) receptor (LDLR) gene at the posttranscriptional level by stabilizing its mRNA,
Moreover, berberine is able to reduce hepatic total cholesterol (TC) and triglyceride (TG) synthesis through the activation of adenosine monophosphate–activated protein kinase that leads to the inactivation of HMG-CoA and acetyl-CoA carboxylase enzymes.
They are a mix of aliphatic alcohols derived from sugar cane (Saccharum officinarum L). The clinical pharmacology of policosanols is not fully understood, but findings suggest suppression of HMG-CoA reductase and increased LDL cholesterol (LDL-C) degradation via enhanced hepatic binding and internalization.
Another nutraceutical compound proposed in this area is astaxanthin, which is a xanthophyll carotenoid pigment found in marine animals. It inhibits lipid peroxidation and LDL-C oxidation.
The main objective of the present study was the evaluation of the effect of treatment with Armolipid Plus (Rottapharm S.p.A., Monza, Italy), a nutraceutical combination that contains RYR extract (with 3 mg of monacolin K), berberine, policosanols, folic acid, coenzyme Q10, and astaxanthin on a set of biomarkers associated with the cardiometabolic risk in patients with moderate MetS and the comparison of its efficacy with pravastatin 10 mg/d, a standard low-dose statin treatment. Studied biomarkers include both lipid and glucometabolic profiles, as well as circulating adipokines and proinflammatory molecules.
Methods
Study design and population
The study was performed at the Centro Dislipidemie (A. O. Ospedale Niguarda Ca'Granda, Milan, Italy) in the period from September 2011 to May 2012 and was designed for a randomized, double-blind, placebo-controlled, crossover trial. The study was conducted in accordance with the guidelines of the Declaration of Helsinki, and the study protocol was approved by the ethics committee of A. O. Ospedale Niguarda Ca'Granda. Written informed consent was obtained from each subject. After a run-in period of 2 weeks, patients were randomly assigned to receive either Armolipid Plus (1 pill/d, containing 200 mg of RYR [equivalent to 3 mg of monacolin k], 500 mg of berberine, 10 mg of policosanols, 0.2 mg of folic acid, 2.0 mg of coenzyme Q10, and 0.5 mg of astaxanthin; RYR contained in Armolipid Plus was citrinine and aflatoxins free; the amount of heavy metals [nickel, arsenic, lead, mercury, selenium] was below the total amount of 10 ppm) or placebo (1 pill/d, identical in taste and appearance to the Armolipid Plus pill and containing microcrystalline cellulose, iron oxide brown 70, Compritol E ATO (Gattefossé, Saint-Priest, Lyon, France), magnesium stearate) for 8 weeks. After a 4-week break, the second phase was initiated. After a further 4-week washout period, all patients received pravastatin 10 mg/d for 8 weeks. This dosage was selected according to its expected −20% efficacy in reducing LDL-C.
Thirty patients, 23 men and 7 women with 3 (n = 20) or 4 (n = 10) of the 5 MetS criteria as listed by the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults,
Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.
were selected and completed the study. Nobody met all 5 of the MetS criteria. The inclusion criteria were patients of both sexes, age > 18 years, diagnosis of MetS, and LDL-C within the range of 130 to 170 mg/dL. The exclusion criteria were pregnancy; presence of chronic liver disease, renal disease, or severe renal impairment treated with antidiabetic medications or insulin; untreated arterial hypertension; obesity (body mass index; calculated as weight divided by height squared; kg/m2] ≥ 30); pharmacologic treatments known to interfere with the study treatment; and patients who were enrolled in another research study in the past 90 days. All patients were in primary prevention and free from liver/kidney disorders potentially affecting the response to treatment and were not on any drug that affected lipid/lipoproteins or glycemic profile, including thiazolidinediones or corticosteroids. At the time of the study entry, 16 of 30 patients were on standard antihypertensive treatment, which was maintained for the entire duration of the study, including washout and pravastatin periods (Table 1). At the screening visit, subjects were instructed to follow a normocaloric/low-lipid diet (approximately 2000 kcal, consisting of 55% carbohydrates, 20% proteins, and 25% lipids). Clinical and biochemical evaluations were performed at the beginning and at the end of each treatment period. At all visits, patients underwent a fasting blood sampling and a full clinical examination, including the evaluation of height, body weight, abdominal and hip circumferences, heart rate, and arterial blood pressure. Plasma samples were immediately separated by centrifugation, and aliquots were immediately stored at −20°C for subsequent assays. Primary end point of the study was the reduction of LDL-C in the Armolipid Plus arm. Secondary end points were the reduction of total cholesterol and the changes of other cardiometabolic and inflammatory biomarkers related to cardiometabolic risk. Data retrieval, analysis, and manuscript preparation were solely the responsibility of the authors.
Table 1Concomitant medications (unchanged over the entire study duration)
TC, TGs, HDL-C, glucose, aspartate aminotransferase (AST), alanine aminotransferase, gamma-glutamyltranspeptidase, and creatine phosphokinase isoenzymes were measured by standard enzymatic techniques. LDL-C was calculated according to the Friedewald formula. Commercial enzyme-linked immunosorbent assay kits were used according to manufacturer's specifications to quantify plasma leptin, adiponectin, resistin, high-sensitivity interleukin-6, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1, C-reactive protein (all from R&D System, Minneapolis, MN), and insulin (Millipore, Billerica, MA). The homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated as follows: HOMA-IR = [fasting glucose (mmol/L) × insulin/22.5].
Statistical analysis
Assuming a drop-out rate of up to 20%, a sample size of 30 patients will provide a 90% power to deem as significant, with an α level of 0.05 and a within-subject reduction in LDL-C of 12% ± 20% (mean ± SD), which is one-half of the estimated effect of pravastatin 10 mg/d.
For TGs, AST, and alanine aminotransferase, log-transformations were used to achieve normality. The effect of either placebo or Armolipid Plus on the different biomarkers was calculated as follows: mean of intermediate (after 4 weeks) and final (after 8 weeks) measures minus the baseline measure [ie, mean (LDL4weeks, LDL8weeks) − LDLbaseline], and the differences (expressed as Δ) were then compared. The effect of pravastatin on the different variables was evaluated as the absolute variation from baseline and compared with the effect of Armolipid Plus. Continuous variables are indicated as mean ± SD, if normally distributed, or as median (interquartile range), if not. All differences were assessed by paired Student's t test, whereas comparisons between arms were evaluated by 2-sample t test. All tests are 2-sided, and P values < .05 are considered as statistically significant. Statistical analysis was performed by using the SAS Software version 9.2 (SAS Inc, Cary, NC).
Results
Study population
The main baseline clinical and biochemical data, including adipokines and inflammatory molecules (Table 2), indicate that the study subjects showed moderate dyslipidemia and mild MetS (3/5 or 4/5 MetS criteria), no relevant insulin resistance, and no relevant systemic low-grade inflammation. Armolipid Plus and pravastatin treatments were well tolerated by all patients, who did not report any significant side effects, including gastrointestinal tract or neuromuscular symptoms. Treatment with Armolipid Plus resulted in an overall reduction of MetS criteria in 21 of 30 subjects (70%), which resulted in <3 criteria after intervention in 10 subjects, who thus did not fall within the MetS definition anymore (data not shown).
Table 2Main baseline clinical and biochemical characteristics of the study population
Characteristics
Value
No. of participants (men/women)
30 (23/7)
Age, years
55.4 ± 9.7
Smokers, n (%)
11 (36.7)
Weight, kg
77.5 ± 9.2
BMI
26.8 ± 2.4
Waist circumference, cm (men; n = 23)
96.3 ± 7.9
Waist circumference, cm (women; n = 7)
91.7 ± 5.1
Systolic blood pressure, mm Hg
123.0 ± 12.3
Diastolic blood pressure, mm Hg
80.7 ± 5.7
Heart rate, bpm
68.4 ± 6.9
Total cholesterol, mmol/L
6.11 ± 0.76
LDL-C, mmol/L
3.83 ± 0.57
HDL-C, mmol/L
1.04 ± 0.18
TGs, mmol/L
2.46 (1.76, 3.39)
Fasting glucose, mmol/L
4.57 ± 1.06
Insulin, mU/L
6.1 ± 4.1
HOMA-IR
1.2 ± 0.8
Uric acid, mg/dL
5.3 ± 1.1
CRP, mg/dL
0.21 ± 0.23
AST, U/L
21.0 (20.0, 23.3)
ALT, U/L
23.5 (18.8, 32.3)
GGT, U/L
32.7 ± 23.4
CPK, U/L
106.4 ± 36.5
Leptin, ng/mL
16.5 ± 13.1
Adiponectin, μg/mL
6.3 ± 4.2
Resistin, ng/mL
8.8 ± 3.7
IL-6, pg/mL
1.4 ± 1.2
sICAM-1, ng/mL
256.6 ± 66.5
sVCAM-1, ng/mL
969.1 ± 276.9
ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index (calculated as weight divided by height squared; kg/m2); CPK, creatine phosphokinase; CRP, high-sensitivity C-reactive protein; GGT, gamma glutamyl transpeptidase; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment of insulin resistance; IL-6, interleukin 6; IQR, interquartile range; LDL-C, low-density lipoprotein cholesterol; sICAM-1, soluble intercellular adhesion molecule-1; SVCAM-1, soluble vascular cell adhesion molecule-1; TG, triglyceride.
Values are mean ± SD or median (interquartile range).
Effect of Armolipid Plus treatment on lipid, metabolic, and inflammatory biomarkers
Primary and secondary end points at baseline did not differ between the placebo and Armolipid Plus groups (Table 3) or between the Armolipid Plus and pravastatin groups (Table 4), except for HDL-C, which was slightly lower at baseline in the Armolipid Plus group, and uric acid, which was higher at baseline in the pravastatin group. Clinical parameters (body weight, waist circumference, systolic blood pressure, diastolic blood pressure, heart rate) were not affected collectively by treatment with either placebo or Armolipid Plus (not shown). In the placebo arm, no significant variation in the biochemical parameters was observed. Armolipid Plus treatment resulted in a highly significant decrease of TC (–12.8%; P = .0001) and LDL-C (−21.1%; P = .0001) (Fig. 1) and a significant increase of HDL-C (4.8%; P < .05), whereas TG levels were unchanged (Table 3). A small, but significant average increase of AST (5.2%; P < .05) was observed with Armolipid Plus treatment, although it did not exceed the reference values in any patient. Armolipid Plus treatment reduced plasma leptin (−8.5%; P < .05) and did not affect plasma adiponectin, producing a trend toward reduction of the leptin-to-adiponectin ratio (−17.8%; P = .158). No changes were found in plasma concentrations of insulin, resistin, interleukin-6, soluble vascular cell adhesion molecule-1, and sICAM-1 (Table 3). No significant difference in the principal end point was observed between the crossover arms (Fig. 1), thus ruling out a carry-over effect.
Table 3Summary of primary and secondary end points (Armolipid Plus and placebo)
Armolipid Plus
Placebo
P value for Comparison of Δ Armolipid Plus vs Δ placebo
Figure 1Time course of LDL-C in the 2 crossover arms (group A [n = 14] and B [n = 16]). Armolipid Plus treatment period is indicated by the dotted (group B) and the solid (group A) lines. Data are expressed as mean ± SD. LDL-C, low-density lipoprotein cholesterol.
Effects of pravastatin treatment and comparison with Armolipid Plus treatment
Treatment with pravastatin reduced TC (−16%; P = .0001), LDL-C (−22.6%; P = .0001), and uric acid (−5.2%; P = .013) (Table 4). A TG reduction (−13.4%) was also observed, although it was not statistically significant (P = .08). Pravastatin treatment was also associated with a significant reduction of plasma adiponectin levels (−11.1%; P = .008), increased the leptin-to-adiponectin ratio (12.1%; P = .036), and reduced sICAM-1 concentration (−5.2%; P < .015) (Table 4). Armolipid Plus and pravastatin effects were similar on all biochemical parameters, including a significant reduction of TC and LDL-C, except for uric acid and AST (both reduced by pravastatin; P < .05) and the leptin-to-adiponectin ratio (increased by pravastatin; P < .05).
Discussion
This randomized, placebo-controlled, crossover study in patients with moderate dyslipidemia and mild MetS features attempted to explore the potential of Armolipid Plus, a nutraceutical combination that contains RYR, berberine, and other components, on TC, LDL-C, and inflammatory/metabolic markers associated with CV risk. The treatment was quite effective in reducing TC and LDL-C levels, with an efficacy comparable to that of 10 mg of pravastatin, a standard statin therapy used in our study as a reference treatment. In addition, Armolipid Plus treatment had the advantage to reduce leptin concentrations, leaving adiponectin unchanged, whereas pravastatin treatment produced a reduction of both adiponectin and the leptin-to-adiponectin ratio. Treatment with Armolipid Plus also resulted in an overall reduction of MetS criteria in 21 of 30 subjects.
Armolipid Plus, containing a daily dose of RYR extract equivalent to approximately 3 mg of monacolin K (lovastatin), in the present report showed comparable or better results than a series of Chinese randomized controlled studies,
based on RYR administration corresponding to daily intakes of approximately 5 to 10 mg of monacolin K. In addition, in 2 secondary prevention studies in the Chinese population, the investigators used either 2 capsules of Xuezhikang, containing approximately 2.5 to 3.2 mg of monacolin K, in the case of a randomized study in middle-aged patients with coronary disease
or 2 capsules of Xuezhikang, each containing 2.5 to 3.2 mg of monacolin K and a small quantity of lovastatin hydroxy acid, in another study of elderly patients with coronary disease.
Beneficial impact of Xuezhikang on cardiovascular events and mortality in elderly hypertensive patients with previous myocardial infarction from the China Coronary Secondary Prevention Study (CCSPS).
In both studies, LDL-C reduction was comparable, and remarkable reductions of coronary heart disease incidence and deaths were observed. The relative decrease of the primary CV end point in the former study was 45% with a reduction of CV and total mortality of 30% and 32%, respectively.
Beneficial impact of Xuezhikang on cardiovascular events and mortality in elderly hypertensive patients with previous myocardial infarction from the China Coronary Secondary Prevention Study (CCSPS).
In the United States, RYR daily doses equivalent to up to 18 mg of monacolin K are allowed by the Food and Drug Administration as a “drug” treatment, and reports from the United States indicate daily doses up to 10 mg of lovastatin are equivalent.
In addition to this well-known lipid-lowering activity of RYR, mainly related to HMG-CoA reductase inhibition, the concomitant presence of other nutraceutical ingredients contributes to the lipid-lowering activity of Armolipid Plus. In particular, berberine is known to increase the expression of LDLR and to act as an insulin sensitizer.
LDLR up-regulation possibly gives a major contribution to the remarkable cholesterol-lowering activity of Armolipid Plus, which are equivalent to that of pravastatin 10 mg/d. A recent meta-analysis has evaluated the clinical trials published on berberine.
Although the methodologic quality of those studies was generally low, the final analysis showed that administration of berberine produced a significant reduction in TC, TGs, and LDL-C, with a remarkable increase in HDL-C. Thus, the observed 4.8% increase of HDL-C by Armolipid Plus treatment might possibly depend on the presence of berberine as well as on that of astaxanthin. The latter was reported to raise HDL-C and adiponectin concentrations in subjects with mild hyperlipidemia,
with a 12% HDL-C increase at the lower dosage tested (6 mg/d).
In addition to the lipid profile, adipose-derived molecules are known to affect CV risk assessment. Armolipid Plus treatment reduced plasma leptin and did not affect plasma adiponectin, with an improved (−17.8%) leptin-to-adiponectin ratio, whereas pravastatin reduced adiponectin and increased the leptin-to-adiponectin ratio. Interestingly, reduced adiponectin levels
and increased leptin-to-adiponectin ratios are considered potentially major risk factors for CV disease. More in detail, the leptin-to-adiponectin ratio was found directly correlated with the intima-media thickness,
Metabolic syndrome, adipokines and hormonal factors in pharmacologically untreated adult elderly subjects from the Brisighella Heart Study historical cohort.
Among Armolipid Plus components, it is relevant to observe that RYR negatively affects adipocyte differentiation through the down-regulated expression of several adipocyte-specific genes, including leptin.
Study of the effects of monacolin k and other constituents of red yeast rice on obesity, insulin-resistance, hyperlipidemia, and nonalcoholic steatohepatitis using a mouse model of metabolic syndrome.
Evid Based Complement Alternat Med.2012; 2012: 892697
In patients with MetS, berberine (300 mg three times daily) was found to reduce plasma leptin and the leptin-to-adiponectin ratio, with a moderate and nonsignificant increase of adiponectin levels.
Berberine improves insulin sensitivity by inhibiting fat store and adjusting adipokines profile in human preadipocytes and metabolic syndrome patients.
Evid Based Complement Alternat Med.2012; 2012: 363845
Berberine has indeed been shown to inhibit adipogenesis in vitro and to promote the assembly of high molecular weight adiponectin, thus increasing the high molecular weight-to-total adiponectin ratio, which results in greater insulin sensitivity.
Armolipid Plus and nutraceuticals with similar composition, in addition as a treatment alternative to specific drugs (ie, statins, ezetimibe), might also be useful as add-on therapy to achieve a greater LDL-C–lowering response as well as an HDL-C–raising response. Some data with the use of single components of Armolipid Plus in addition to statins are already present in the literature. Berberine improved the lipid-lowering efficacy of simvastatin
; the effect of policosanols on the lipoprotein profile remains controversial because recent trials with policosanols in combination with statins failed in replicating the beneficial findings observed in the early trials.
The combination of RYR/berberine/policosanols and ezetimibe was found more effective than each treatment alone in reducing LDL-C in subjects with heterozygous familial hypercholesterolemia.
Nutraceutical pill containing berberine versus ezetimibe on plasma lipid pattern in hypercholesterolemic subjects and its additive effect in patients with familial hypercholesterolemia on stable cholesterol-lowering treatment.
For the concern about the potential advantages of such combination on the adipokine profile, it should be noted that statins have been reported to inconsistently affect plasma adiponectin levels, possibly because of the specific compound tested and the different study populations,
making complex the otherwise interesting evaluation of such combined therapy. To our knowledge, no data are available on this combination therapy; hence, this issue needs to be further addressed.
Conclusion
In conclusion, the present report shows that a small dose of RYR associated with berberine and other nutraceutical compounds (Armolipid Plus) improves the lipid profile in an equivalent way to a low dose of a standard statin. In addition, Armolipid Plus, possibly because of the presence of astaxanthin, also increases HDL-C levels and improves the leptin-to-adiponectin ratio. In view of the high interest of physicians and patients for innovative well-tolerated treatments for moderate dyslipidemia/MetS, Armolipid Plus is potentially of significant clinical value in the management of cardiometabolic risk.
Acknowledgments
The study was supported by an unrestricted grant to Centro Dislipidemie (A. O. Ospedale Niguarda Cà Granda, Milano, Italy) from Rottapharm S.p.A. (Monza, Italy). The expert statistical contribution of Dr. Fabrizio Veglia is gratefully acknowledged. All authors have seen and have approved the present study. No authors have any conflict of interest.
Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.
Combined extractives of red yeast rice, bitter gourd, chlorella, soy protein, and licorice improve total cholesterol, low-density lipoprotein cholesterol, and triglyceride in subjects with metabolic syndrome.
Effects of a nutraceutical combination (berberine, red yeast rice and policosanols) on lipid levels and endothelial function randomized, double-blind, placebo-controlled study.
Beneficial impact of Xuezhikang on cardiovascular events and mortality in elderly hypertensive patients with previous myocardial infarction from the China Coronary Secondary Prevention Study (CCSPS).
Metabolic syndrome, adipokines and hormonal factors in pharmacologically untreated adult elderly subjects from the Brisighella Heart Study historical cohort.
Study of the effects of monacolin k and other constituents of red yeast rice on obesity, insulin-resistance, hyperlipidemia, and nonalcoholic steatohepatitis using a mouse model of metabolic syndrome.
Evid Based Complement Alternat Med.2012; 2012: 892697
Berberine improves insulin sensitivity by inhibiting fat store and adjusting adipokines profile in human preadipocytes and metabolic syndrome patients.
Evid Based Complement Alternat Med.2012; 2012: 363845
Nutraceutical pill containing berberine versus ezetimibe on plasma lipid pattern in hypercholesterolemic subjects and its additive effect in patients with familial hypercholesterolemia on stable cholesterol-lowering treatment.
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