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I imagine most readers of this blog would expect a group of subjects to do better on a Paleolithic diet as compared to a standard American diet, but there are few studies actually making the comparison. One was posted yesterday in the Advance-0nline-Publication section of the European Journal of Clinical Nutrition that shows subjects following a Paleolithic diet made major metabolic changes, and made them rapidly

Spiller GA, Jenkins DJ, Cragen LN, Gates JE, Bosello O, Berra K, Rudd C, Stevenson M, Superko R.Effect of a diet high in monounsaturated fat from almonds on plasma cholesterol and lipoproteins.J Am Coll Nutr. 1992 Apr;11(2):126-30.PMID: 1315812 [Pub

Ballesteros MN, Cabrera RM, Saucedo Mdel S, Fernandez ML.Dietary cholesterol does not increase biomarkers for chronic disease in a pediatric population from northern Mexico.Am J Clin Nutr. 2004 Oct;80(4):855-61.PMID: 15447890 [PubMed - indexed for M

Modulation of inflammatory cytokines by omega-3 fatty acids. Kang JX, Weylandt KH. Subcell Biochem. 2008;49:133-43. Review. PMID: 18751910

Improvement of the recurrence-free interval using biological adjuvant therapy in uveal melanoma. Tallberg T, Uusitalo R, Sarna S, Seregard S, Werschnik C. Anticancer Res. 2000 May-Jun;20(3B):1969-75. PMID: 10928136

Resolvin D1, protectin D1, and related docosahexaenoic acid-derived products: Analysis via electrospray/low energy tandem mass spectrometry based on spectra and fragmentation mechanisms. Hong S, Lu Y, Yang R, Gotlinger KH, Petasis NA, Serhan CN. J Am Soc Mass Spectrom. 2007 Jan;18(1):128-44. Epub 2006 Oct 19. PMID: 17055291 doi:10.1016/j.jasms.2006.09.002    

Essential fatty acids and their metabolites could function as endogenous HMG-CoA reductase and ACE enzyme inhibitors, anti-arrhythmic, anti-hypertensive, anti-atherosclerotic, anti-inflammatory, cytoprotective, and cardioprotective molecules.\nDas UN.\nLipids Health Dis. 2008 Oct 15;7:37. Review.\nPMID: 18922179 \ndoi:10.1186/1476-511X-7-37

Dietary cis-monounsaturated fatty acids and metabolic control in type 2 diabetes. Ros E. Am J Clin Nutr. 2003 Sep;78(3 Suppl):617S-625S. Review. PMID: 12936956

Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) study: a randomized trial of the effect of vitamins E and C on 3-year progression of carotid atherosclerosis. Salonen JT, Nyyssönen K, Salonen R, Lakka HM, Kaikkonen J, Porkkala-Sarataho E, Voutilainen S, Lakka TA, Rissanen T, Leskinen L, Tuomainen TP, Valkonen VP, Ristonmaa U, Poulsen HE. J Intern Med. 2000 Nov;248(5):377-86. PMID: 11123502 DOI: 10.1046/j.1365-2796.2000.00752.x Conclusions. Our study shows that a combined supplementation with reasonable doses of both vitamin E and slow-release vitamin C can retard the progression of common carotid atherosclerosis in men. This may imply benefits with regard to other atherosclerosis-based events.

Six-year effect of combined vitamin C and E supplementation on atherosclerotic progression: the Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study. Salonen RM, Nyyssönen K, Kaikkonen J, Porkkala-Sarataho E, Voutilainen S, Rissanen TH, Tuomainen TP, Valkonen VP, Ristonmaa U, Lakka HM, Vanharanta M, Salonen JT, Poulsen HE; Antioxidant Supplementation in Atherosclerosis Prevention Study. Circulation. 2003 Feb 25;107(7):947-53. PMID: 12600905 doi: 10.1161/01.CIR.0000050626.25057.51 Conclusions- These data replicate our 3-year findings confirming that the supplementation with combination of vitamin E and slow-release vitamin C slows down atherosclerotic progression in hypercholesterolemic persons.

"Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell."

Extended-release niacin or ezetimibe and carotid intima-media thickness. Taylor AJ, Villines TC, Stanek EJ, Devine PJ, Griffen L, Miller M, Weissman NJ, Turco M. N Engl J Med. 2009 Nov 26;361(22):2113-22. Epub 2009 Nov 15. PMID: 19915217 Conclusions This comparative-effectiveness trial shows that the use of extended-release niacin causes a significant regression of carotid intima-media thickness when combined with a statin and that niacin is superior to ezetimibe. (ClinicalTrials.gov number, NCT00397657 [ClinicalTrials.gov] .

Endothelial-Vasoprotective Effects of High-Density Lipoprotein Are Impaired in Patients With Type 2 Diabetes Mellitus but Are Improved After Extended-Release Niacin Therapy. Sorrentino SA, Besler C, Rohrer L, Meyer M, Heinrich K, Bahlmann FH, Mueller M, Horváth T, Doerries C, Heinemann M, Flemmer S, Markowski A, Manes C, Bahr MJ, Haller H, von Eckardstein A, Drexler H, Landmesser U. Circulation. 2009 Dec 21. [Epub ahead of print] PMID: 20026785 doi: 10.1161/CIRCULATIONAHA.108.836346 Conclusions-HDL from patients with type 2 diabetes mellitus and metabolic syndrome has substantially impaired endothelial-protective effects compared with HDL from healthy subjects. ER niacin therapy not only increases HDL plasma levels but markedly improves endothelial-protective functions of HDL in these patients, which is potentially more important.

Clinical Implications of JUPITER (Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) in a U.S. Population Insights From the ARIC (Atherosclerosis Risk in Communities) Study Yang EY et al. J Am Coll Cardiol, 2009; 54:2388-2395, doi:10.1016/j.jacc.2009.10.006 Conclusions: ARIC participants with elevated hs-CRP and low LDL-C had a CVD event rate of 1.57% per year over 6.9 years, similar to the CVD event rate noted in the JUPITER study placebo group (1.36% per year over 1.9 years). The association of hs-CRP ≥2.0 mg/l with increased CVD risk and mortality regardless of LDL-C provides us a simple method of using age and hs-CRP level for identifying higher risk individuals. (Atherosclerosis Risk in Communities study; NCT00005131)

Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. Kong W, Wei J, Abidi P, Lin M, Inaba S, Li C, Wang Y, Wang Z, Si S, Pan H, Wang S, Wu J, Wang Y, Li Z, Liu J, Jiang JD. Nat Med. 2004 Dec;10(12):1344-51. Epub 2004 Nov 7. PMID: 15531889 doi:10.1038/nm1135 We identify berberine (BBR), a compound isolated from a Chinese herb, as a new cholesterol-lowering drug. Oral administration of BBR in 32 hypercholesterolemic patients for 3 months reduced serum cholesterol by 29%, triglycerides by 35% and LDL-cholesterol by 25%. Treatment of hyperlipidemic hamsters with BBR reduced serum cholesterol by 40% and LDL-cholesterol by 42%, with a 3.5-fold increase in hepatic LDLR mRNA and a 2.6-fold increase in hepatic LDLR protein. Using human hepatoma cells, we show that BBR upregulates LDLR expression independent of sterol regulatory element binding proteins, but dependent on ERK activation. BBR elevates LDLR expression through a post-transcriptional mechanism that stabilizes the mRNA. Using a heterologous system with luciferase as a reporter, we further identify the 5' proximal section of the LDLR mRNA 3' untranslated region responsible for the regulatory effect of BBR. These findings show BBR as a new hypolipidemic drug with a mechanism of action different from that of statin drugs.

Long-term consumption of a carbohydrate-restricted diet does not induce deleterious metabolic effects. Grieb P, K?apcin'ska B, Smol E, Pilis T, Pilis W, Sadowska-Krepa E, Sobczak A, Bartoszewicz Z, Nauman J, Stan'czak K, Langfort J. Nutr Res. 2008 Dec;28(12):825-33. PMID: 19083495 doi:10.1016/j.nutres.2008.09.011 These results indicate that long-term (>1 year) compliance with a low-CHO high-fat "optimal diet" does not induce deleterious metabolic effects and does not increase the risk for cardiovascular disease, as evidenced by maintenance of adequate glycemic control and relatively low values for conventional cardiovascular risk factors.

"18 645 patients with a total cholesterol of 6·5 mmol/L or greater were recruited from local physicians throughout Japan between 1996 and 1999. Patients were randomly assigned to receive either 1800 mg of EPA daily with statin (EPA group; n=9326) or statin only (controls; n=9319) with a 5-year follow-up. The primary endpoint was any major coronary event, including sudden cardiac death, fatal and non-fatal myocardial infarction, and other non-fatal events including unstable angina pectoris, angioplasty, stenting, or coronary artery bypass grafting. Analysis was by intention-to-treat. Findings At mean follow-up of 4·6 years, we detected the primary endpoint in 262 (2·8%) patients in the EPA group and 324 (3·5%) in controls-a 19% relative reduction in major coronary events (p=0·011). Post-treatment LDL cholesterol concentrations decreased 25%, from 4·7 mmol/L in both groups. Serum LDL cholesterol was not a significant factor in a reduction of risk for major coronary events. Unstable angina and non-fatal coronary events were also significantly reduced in the EPA group. Sudden cardiac death and coronary death did not differ between groups. In patients with a history of coronary artery disease who were given EPA treatment, major coronary events were reduced by 19% (secondary prevention subgroup: 158 [8·7%] in the EPA group vs 197 [10·7%] in the control group; p=0·048). In patients with no history of coronary artery disease, EPA treatment reduced major coronary events by 18%, but this finding was not significant (104 [1·4%] in the EPA group vs 127 [1·7%] in the control group; p=0·132)."