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Phyto Nova Lipinat^TM Selected Abstracts

1. Diagnosis, management and prevention of the common dyslipidaemias in South Africa.
2. Mechanism of Action of Niacin.
3. Significant reduction in free fatty acids during the entire night is achieved with inositol hexanicotinate.
4. Plant sterols and dietary cholesterol exert independent effects on plasma cholesterol. Plant sterol efficacy is not affected by varying levels of cholesterol intake.
5. The addition of niacin to phytosterols synergistically increases HDL-cholesterol levels.
6. The cholesterol-lowering action of phytosterols occurs through competition with dietary and biliary cholesterol for intestinal absorption in mixed micelles. However, recent evidence suggests that phytosterols may regulate proteins implicated in cholesterol metabolism both in enterocytes and hepatocytes.
7. Inositol hexaniacinate (IHN) is effective in the treatment of hyperlipidemia, Raynaud’s disease and intermittent claudication.
8. Niacin alters lipoprotein metabolism in novel ways, and mediates other beneficial nonlipid changes that may be atheroprotective.
9. Niacin significantly reduces low-density lipoprotein cholesterol, triglyceride and lipoprotein(a) levels, while increasing high-density lipoprotein cholesterol levels.
10. Niacin therapy is appropriate for many types of lipid abnormalities, including complex dyslipidemias.

1. Diagnosis, management and prevention of the common dyslipidaemias in South Africaclinical guideline, 2000. South African Medical Association and Lipid and Atherosclerosis Society of Southern Africa Working Group.
S Afr Med J. 2000 Feb;90(2 Pt 2):164-74, 176-8.
The optimum management of dyslipidaemia requires a comprehensive, diagnostic work-up. This, minimally, includes: Characterisation of any hyperlipidaemic disorder present. Identification of additional risk factors so as to assess overall (global) risk of future coronary heart disease (CHD). The global risk is best assessed by a calculation combining the risk factors in the individual. In severe monogenic dyslipidaemias and in patients with confirmed pre-existing CHD the risk is usually high; in most such cases the use of lipid-modifying drugs (LMDs) is indicated. Assessment of psychosocial, economic and educational factors relevant to management. Prevention and cost-effective management of even moderately dyslipidaemic patients require appropriate modification of lifestyle: avoidance of tobacco smoking, participation in regular exercise, and a health-promoting diet. Depending on individual circumstance, vigorous, personalised intervention and expert assistance from dieticians, biokineticists and other health care personnel may determine success. The correct choice of patient for drug treatment is a key therapeutic decision and is best done after full lifestyle modification. Recent evidence confirms that appropriately prescribed LMD therapy can lower morbidity and mortality from CHD as well as all-cause mortality. Patients with the following features are candidates for LMD therapy: have clinical CHD and a low-density lipoprotein cholesterol (LDLC) level > 3.0 mmol/l despite optimum non-pharmacological intervention, or suffer from familial hypercholesterolaemia (FH) or equivalent severe, monogenic disorder, or have a 10-year risk of an acute clinical coronary event of > 20% (or > 30% risk if extrapolated to the age of 60 years) owing to the presence of the hyperlipidaemia alone or in combination with contributory risk factors. The ideal target LDLC concentration is < or = 3 mmol/l, but a reduction of at least 45% should be regarded as a minimum target in severe cases who do not reach this goal. Successful therapy requires on-going attention to compliance, therapeutic response and side-effects, and may necessitate adjustment or reinforcement. Concurrent or contributory conditions, such as smoking, hypertension and diabetes mellitus, must also be treated along with the clinically manifest CHD. Severely hyperlipidaemic, complicated or unresponsive high-risk cases should be referred to an appropriate specialist or lipid clinic. Prevention of CHD in the community should be encouraged through public and professional education, the provision of community facilities for exercise and recreation, and legislation directed at reducing the use of tobacco products and ensuring the appropriate labelling of food products.

2. Mechanism of Action of Niacin.
Vaijinath S. Kamanna, and Moti L. Kashyap. Am J Cardiol 2008;101[suppl]:20B 26B.
Nicotinic acid (niacin) has long been used for the treatment of lipid disorders and cardiovascular disease. Niacin favorably affects apolipoprotein (apo) B containing lipoproteins (eg, very-low-density lipoprotein [VLDL], low-density lipoprotein [LDL], lipoprotein[a]) and increases apo A-I containing lipoproteins (high-density lipoprotein [HDL]). Recently, new discoveries have enlarged our understanding of the mechanism of action of niacin and challenged older concepts. There are new data on (1) how niacin affects triglycerides (TGs) and apo B containing lipoprotein metabolism in the liver, (2) how it affects apo A-I and HDL metabolism, (3) how it affects vascular anti-inflammatory events, (4) a specific niacin receptor in adipocytes and immune cells, (5) how niacin causes flushing, and (6) the characterization of a niacin transport system in liver and intestinal cells. New findings indicate that niacin directly and noncompetitively inhibits hepatocyte diacylglycerol acyltransferase 2, a key enzyme for TG synthesis. The inhibition of TG synthesis by niacin results in accelerated intracellular hepatic apo B degradation and the decreased secretion of VLDL and LDL particles. Previous kinetic studies in humans and recent in vitro cell culture findings indicate that niacin retards mainly the hepatic catabolism of apo A-I (vs apo A-II) but not scavenger receptor BI mediated cholesterol esters. Decreased HDL apo A-I catabolism by niacin explains the increases in HDL half-life and concentrations of lipoprotein A-I HDL subfractions, which augment reverse cholesterol transport. Initial data suggest that niacin, by inhibiting the hepatocyte surface expression of _-chain adenosine triphosphate synthase (a recently reported HDL apo A-I holoparticle receptor), inhibits the removal of HDL apo A-I. Recent studies indicate that niacin increases vascular endothelial cell redox state, resulting in the inhibition of oxidative stress and vascular inflammatory genes, key cytokines involved in atherosclerosis. The niacin flush results from the stimulation of prostaglandins D2 and E2 by subcutaneous Langerhans cells via the G protein coupled receptor 109A niacin receptor. Although decreased free fatty acid mobilization from adipose tissue via the G protein coupled receptor 109A niacin receptor has been a widely suggested mechanism of niacin to decrease TGs, physiologically and clinically, this pathway may be only a minor factor in explaining the lipid effects of niacin.

3. Nocturnal inhibition of lipolysis in man by nicotinic acid and derivatives.
Kruse W, Kruse W, Raetzer H, Heuck CC, Oster P, Schellenberg B, Schlierf G. Eur J Clin Pharmacol. 1979 Aug;16(1):11-5.
The effect of nicotinic acid and several derivatives on the nocturnal level of free fatty acids was studied in 12 healthy young women and men. Free fatty acids are an important precursor of plasma triglycerides and their concentration is highest at night. The drugs used were nictinic acid, beta-pyridyl-carbinol, mesoinositol hexanicotinate and xantinol nicotinate. The highest plasma nicotinic acid level was observed with beta-pyridyl-carbinol, but significant reduction in free fatty acids during the entire night was only achieved with inositolhexanicotinate and xantinol nicotinate. There was no correlation between the plasma levels of free fatty acids and nicotinic acid at any sampling time. If prolonged reduction in free fatty acid concentration is desired in the therapy of hyperlipidemias, the inositol and xantinol esters of nicotinic acid appear to be superior to the other preparations.

4. Efficacy of plant sterols is not influenced by dietary cholesterol intake in
hypercholesterolemic individuals.
Amira N. Kassis, Catherine A. Vanstone, Suhad S. AbuMweis, Peter J.H. Jones. Metabolism Clinical and Experimental 57 (2008) 339 346.
Plant sterols (PSs) reduce plasma total and low-density lipoprotein cholesterol (LDL-C) levels by reducing cholesterol absorption; however, it is not known whether the level of dietary cholesterol intake has an impact on the efficacy of PSs on blood lipids. The purpose of this study was to determine the effect of high vs low dietary cholesterol levels on the lipid-lowering efficacy of free PSs.
The study was a semirandomized, double-blind, crossover trial consisting of four 28-day feeding phases each separated by a 4-week washout period. Otherwise healthy hypercholesterolemic subjects (n = 22) consumed each of (a) low-cholesterol control (C"S"), (b) high-cholesterol control (C+S"), (c) 22 mg PSs per kilogram of body weight with a low-cholesterol diet (C"S+), and (d) 22 mg PSs per kilogram of body weight with a high-cholesterol diet (C+S+). Blood was drawn on the first and last 2 days of each phase to measure plasma total cholesterol, LDL-C, highdensity lipoprotein cholesterol, and triacylglycerols as well as plasma campesterol and ≤-sitosterol concentrations. Dietary cholesterol had no effect on PS efficacy as a cholesterol-lowering agent because no interaction was found between the 2 factors. However, dietary cholesterol and PS intake had significant independent effects on plasma total cholesterol, LDL-C, and high-density lipoprotein cholesterol levels. ≤-Sitosterol levels in plasma increased (P b .0001) as a result of PS supplementation. Data from the present study indicate that, although PSs and dietary cholesterol exert independent effects on plasma cholesterol, PS efficacy is not affected by varying levels of cholesterol intake.

5. Combination of dietary phytosterols plus niacin or fenofibrate: effects on lipid profile and atherosclerosis in apo E-KO mice.
Behzad Yeganeha, Ghollam-Reza Moshtaghi-Kashanianb, Vanessa DeClercqa, Mohammed H. Moghadasianc. Journal of Nutritional Biochemistry 16 (2005) 222 228.
Patients with mixed dyslipidemias (increased LDL cholesterol and triglyceride as well as low HDL cholesterol levels) benefit from a combination of lipid-modifying drugs such as statins, niacin, fibrates and ezetemibe. However, safety, tolerability and cost are a concern in drug combination therapy. Dietary phytosterols reduce LDL cholesterol, and niacin or fenofibrate primarily reduces triglyceride and increases HDL-cholesterol levels. Thus, we hypothesized that a combination of phytosterols with niacin or fenofibrate will synergistically impact lipoprotein profile and atherogenesis in apo E-KO mice. Phytosterols alone significantly reduced plasma total cholesterol levels (14.1 vs. 16.9 mmol/L, P b.05) and the extent of atherosclerosis (0.42 vs. 0.15 mm2, P b.05). The addition of fenofibrate to phytosterols increased plasma total cholesterol levels by N50% (14.1 vs. 21.6 mmol/L, P b.05) and decreased HDLcholesterol concentrations by 50% (0.8 vs. 0.4 mmol/L). These changes were accompanied by slight reductions in the extent of atherosclerosis (0.42 vs. 0.34 mm2, P N.05) as compared to controls, suggesting other potential anti-atherogenic effects of fenofibrate. Unlike fenofibrate, niacin caused an increase of 150% ( P b.05) in HDL-cholesterol concentrations and a decrease of 22% ( P b.05) in total cholesterol levels which were associated with significant reductions (65%, P b.05) in atherosclerotic lesion size as compared to controls. Neither the addition of niacin nor of fenofibrate reduced plasma triglyceride levels. In conclusion, the addition of niacin to phytosterols synergistically increases HDL-cholesterol levels, while a combination of phytosterols and fenofibrate results in no synergistic effects in apo E-KO mice. Further studies in other animal models are needed to establish synergetic effects between these lipid-modifying dietary and pharmacological agents.

6. New insights into the molecular actions of plant sterols and stanols in cholesterol metabolism.
Calpe-Berdiel L, Escol‡-Gil JC, Blanco-Vaca F. Atherosclerosis. 2008 Jul 6.†
Plant sterols and stanols (phytosterols/phytostanols) are known to reduce serum low-density lipoprotein (LDL)-cholesterol level, and food products containing these plant compounds are widely used as a therapeutic dietary option to reduce plasma cholesterol and atherosclerotic risk. The cholesterol-lowering action of phytosterols/phytostanols is thought to occur, at least in part, through competition with dietary and biliary cholesterol for intestinal absorption in mixed micelles. However, recent evidence suggests that phytosterols/phytostanols may regulate proteins implicated in cholesterol metabolism both in enterocytes and hepatocytes. Important advances in the understanding of intestinal sterol absorption have provided potential molecular targets of phytosterols. An increased activity of ATP-binding cassette transporter A1 (ABCA1) and ABCG5/G8 heterodimer has been proposed as a mechanism underlying the hypocholesterolaemic effect of phytosterols. Conclusive studies using ABCA1 and ABCG5/G8-deficient mice have demonstrated that the phytosterol-mediated inhibition of intestinal cholesterol absorption is independent of these ATP-binding cassette (ABC) transporters. Other reports have proposed a phytosterol/phytostanol action on cholesterol esterification and lipoprotein assembly, cholesterol synthesis and apolipoprotein (apo) B100-containing lipoprotein removal. The accumulation of phytosterols in ABCG5/G8- deficient mice, which develop features of human sitosterolaemia, disrupts cholesterol homeostasis by affecting sterol regulatory element-binding protein (SREBP)-2 processing and liver X receptor (LXR) regulatory pathways. This article reviews the progress to date in studying these effects of phytosterols/phytostanols and the molecular mechanisms involved.

7. Inositol Hexaniacinate: A Safer Alternative to Niacin.
Kathleen A. Head, N.D. Alternative Medicine Review 1996;1(3):176-184.
Niacin has long been prescribed for the treatment of various cardiovascular conditions, particularly the hyperlipidemias. It has been proven effective at lowering VLDL, LDL, total cholesterol and triglyceride levels while raising HDL levels. The side effects of niacin which may occur at the dosages often required for therapeutic efficacy, ranging from flushing and pruritus to hepatoxicity and impaired glucose tolerance, often prove troubling for both patient and practitioner. The need for a safer approach to niacin supplementation has resulted in the investigation of niacin esters. One of the most widely studied of these is inositol hexaniacinate (IHN). In numerous trials it has been found to be virtually free of the side effects associated with conventional niacin therapy. Extensive research has found IHN to be effective in the treatment of hyperlipidemia, Raynaud’s disease and intermittent claudication. A number of other conditions which respond favorably to niacin therapy such as hypertension, diabetes, dysmennorhea and alcoholism bear further investigation.

8. Niacin therapy in atherosclerosis.
Meyers CD, Kamanna VS, Kashyap ML. Curr Opin Lipidol. 2004 Dec;15(6):659-65.
PURPOSE OF REVIEW: Well designed, randomized, placebo-controlled studies show that niacin prevents cardiovascular disease and death. Unfortunately, early studies and anecdotal evidence have limited its use by promoting the opinion that niacin is intolerable and contraindicated in diabetes. As evidence mounts that treating multiple lipid risk factors decreases cardiovascular risk, the use of niacin in the treatment of atherosclerosis is experiencing somewhat of a renaissance. RECENT FINDINGS: Emerging clinical evidence shows that niacin is both safe and effective in diabetes. Niacin beneficially alters lipoprotein subclass distribution and when used in combination with statins, has additional effects on lipoproteins. Niacin selectively and directly inhibits hepatic diacylglycerol acyltransferase 2, but not diacylglycerol acyltransferase 1, thus inhibiting hepatic triglyceride synthesis and very low density lipoprotein secretion. The recent discovery and characterization of a membrane-bound nicotinic acid receptor (HM74) explains niacin's acute inhibition of adipocyte lipolysis, but the role of HM74 in lowering triglycerides is unclear. Niacin possesses antioxidant, antiinflammatory, and other beneficial effects on atherosclerosis unrelated to lipid lowering. Finally, niacin appears to activate nuclear transcription factors such peroxisome proliferator activator receptor gamma, possibly via prostaglandin metabolism. SUMMARY: New data indicate that niacin alters lipoprotein metabolism in novel ways, and mediates other beneficial nonlipid changes that may be atheroprotective. This information forms the rationale for the use of niacin in combination with agents possessing complementary
mechanisms of action (e.g. statins) for cardiovascular risk reduction beyond that observed with monotherapy. Further research into the specific mechanisms of niacin may identify additional targets for future drug development.

9. New perspectives on the use of niacin in the treatment of lipid disorders.
McKenney J. Arch Intern Med. 2004 Apr 12;164(7):697-705.
Therapy with niacin (nicotinic acid) is unique in that it improves all lipoprotein abnormalities. It significantly reduces low-density lipoprotein cholesterol, triglyceride, and lipoprotein(a) levels, while increasing high-density lipoprotein cholesterol levels. This makes niacin ideal for treating a wide variety of lipid disorders, including the metabolic syndrome, diabetes mellitus, isolated low highdensity lipoprotein cholesterol, and hypertriglyceridemia. Niacin-induced changes in serum lipid levels produce significant improvements in both coronary artery disease and clinical outcomes. Niacin is currently available in 3 formulations (immediate release, extended release, and long acting), which differ significantly with respect to their safety and efficacy profiles. Immediate-release niacin is generally taken 3 times a day and is associated with adverse flushing, gastrointestinal symptoms, and elevations in blood glucose levels. Long-acting niacin can be taken once daily and is associated with significantly reduced flushing, but its metabolism increases the risk of hepatotoxic effects. Extended-release niacin, also given once daily, has an absorption rate intermediate between the other formulations and is associated with fewer flushing and gastrointestinal symptoms without increasing hepatotoxic risk.

Clinical update on the use of niacin for the treatment of dyslipidemia.
Berra K. J Am Acad Nurse Pract. 2004 Dec;16(12):526-34. PURPOSE: To provide nurse practitioners (NPs) with clinical and practical information about the use of niacin in the treatment of dyslipidemia. DATA SOURCES: Research-based and review articles in the medical literature and National Cholesterol Education Program guidelines. CONCLUSIONS: Niacin provides beneficial effects on all major lipid fractions, particularly high-density lipoprotein cholesterol and triglycerides. Niacin also reduces low-density lipoprotein (LDL) cholesterol; lipoprotein (a); and the number of highly atherogenic small, dense LDL particles. Niacin promotes angiographic regression when used in combination with other drugs that lower LDL cholesterol and can reduce cardiovascular risk in patients with coronary heart disease. Several niacin formulations are available, but the safety (i.e., from hepatotoxicity) and tolerability (i.e., severity of flushing) of these niacin formulations may differ. IMPLICATIONS FOR PRACTICE: Niacin therapy is appropriate for many types of lipid abnormalities, including complex dyslipidemias. NPs can take several steps to minimize potential side effects of niacin therapy and to ensure that patients adhere to this important intervention.

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