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Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia -- Krauss et al. 83 (5): 1025 -- American Journal of Clinical Nutrition Changes in peak LDL diameter (Table 2) and mass concentrations of LDL subfractions (Table 3) induced by each of the diets were reflected by changes in the proportions of subjects exhibiting LDL subclass pattern B (Figure 2). There were linear reductions in the prevalence of pattern B as a function of reduced carbohydrate intake after both the stable-weight and weight-loss periods. However, the slopes of these relations differed (P = 0.04) such that the magnitude of the reduction in expression of pattern B induced by weight loss increased in association with the percentage of carbohydrate intake. Conclusions: Moderate carbohydrate restriction and weight loss provide equivalent but nonadditive approaches to improving atherogenic dyslipidemia. Moreover, beneficial lipid changes resulting from a reduced carbohydrate intake were not significant after weight loss. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT. Am J Clin Nutr. 2006 May;83(5):1025-31; quiz 1205. Erratum in: Am J Clin Nutr. 2006 Sep;84(3):668. PMID: 16685042

Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. Zhang Y, Li X, Zou D, Liu W, Yang J, Zhu N, Huo L, Wang M, Hong J, Wu P, Ren G, Ning G. J Clin Endocrinol Metab. 2008 Jul;93(7):2559-65. Epub 2008 Apr 8. PMID: 18397984 doi:10.1210/jc.2007-2404 Conclusions: Berberine is effective and safe in the treatment of type 2 diabetes and dyslipidemia.

Low carbohydrate diets improve atherogenic dyslipidemia even in the absence of weight loss. Feinman RD, Volek JS. Nutr Metab (Lond). 2006 Jun 21;3:24. PMID: 16790045 doi:10.1186/1743-7075-3-24

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May;119(5):1322-34. Epub 2009 Apr 20. PMID: 19381015 doi: 10.1172/JCI37385. Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

Traditional chinese medicine in treatment of metabolic syndrome. Yin J, Zhang H, Ye J. Endocr Metab Immune Disord Drug Targets. 2008 Jun;8(2):99-111. Review. PMID: 18537696 Berberine from rhizoma coptidis is an oral hypoglycemic agent. It also has anti-obesity and anti-dyslipidemia activities. The action mechanism is related to inhibition of mitochondrial function, stimulation of glycolysis, activation of AMPK pathway, suppression of adipogenesis and induction of low-density lipoprotein (LDL) receptor expression.

The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gómez AL, Scheett TP, Volek JS. J Nutr. 2002 Jul;132(7):1879-85. PMID: 12097663

The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels. Mooradian AD, Haas MJ, Wong NC. Endocr Rev. 2006 Feb;27(1):2-16. Epub 2005 Oct 21. Review. PMID: 16243964 One of the factors contributing to the increased risk of developing premature atherosclerosis is low plasma concentrations of high-density lipoprotein (HDL) cholesterol (HDLc). Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). The low plasma concentrations of HDL could be the result of increased fractional clearance and reduced expression of apo A-I. To this end, nutrients play an important role in modulating the fractional clearance rate, as well as the rate of apo A-I gene expression. Because medical nutrition therapy constitutes the cornerstone of management of dyslipidemias, it is essential to understand the mechanisms underlying the changes in HDL level in response to alterations in dietary intake. In this review, we will discuss the effect of select nutrients on serum HDLc and apo A-I levels. Specifically, we will review the literature on the effect of carbohydrates, fatty acids, and ketones, as well as some of the nutrient-related metabolites, such as glucosamine and the prostanoids, on apo A-I gene expression. Because there are multiple mechanisms involved in the regulation of serum HDLc levels, changes in gene transcription do not necessarily correlate with clinical observations on serum levels of HDLc.

Eggs modulate the inflammatory response to carbohydrate restricted diets in overweight men. Ratliff JC, Mutungi G, Puglisi MJ, Volek JS, Fernandez ML. Nutr Metab (Lond). 2008 Feb 20;5:6. PMID: 18289377 Carbohydrate restricted diets (CRD) consistently lower glucose and insulin levels and improve atherogenic dyslipidemia [decreasing triglycerides and increasing HDL cholesterol (HDL-C)]. We have previously shown that male subjects following a CRD experienced significant increases in HDL-C only if they were consuming a higher intake of cholesterol provided by eggs compared to those individuals who were taking lower concentrations of dietary cholesterol. Here, as a follow up of our previous study, we examined the effects of eggs (a source of both dietary cholesterol and lutein) on adiponectin, a marker of insulin sensitivity, and on inflammatory markers in the context of a CRD. Conclusion A CRD with daily intake of eggs decreased plasma CRP and increased plasma adiponectin compared to a CRD without eggs. These findings indicate that eggs make a significant contribution to the anti-inflammatory effects of CRD, possibly due to the presence of cholesterol, which increases HDL-C and to the antioxidant lutein which modulates certain inflammatory responses.

Lipoic acid improves hypertriglyceridemia by stimulating triacylglycerol clearance and downregulating liver triacylglycerol secretion. Butler JA, Hagen TM, Moreau R. Arch Biochem Biophys. 2009 Feb 20. [Epub ahead of print] PMID: 19232511 doi:10.1016/j.abb.2009.01.024