Separate effects of reduced carbohydrate intake an...[Am J Clin Nutr. 2006] - PubMed Result
"BACKGROUND: Low-carbohydrate diets have been used to manage obesity and its metabolic consequences. OBJECTIVE: The objective was to study the effects of moderate carbohydrate restriction on atherogenic dyslipidemia before and after weight loss and in conjunction with a low or high dietary saturated fat intake. DESIGN: After 1 wk of consuming a basal diet, 178 men with a mean body mass index (in kg/m(2)) of 29.2 +/- 2.0 were randomly assigned to consume diets with carbohydrate contents of 54% (basal diet), 39%, or 26% of energy and with a low saturated fat content (7-9% of energy); a fourth group consumed a diet with 26% of energy as carbohydrate and 15% as saturated fat. After 3 wk, the mean weight loss (5.12 +/- 1.83 kg) was induced in all diet groups by a reduction of approximately 1000 kcal/d for 5 wk followed by 4 wk of weight stabilization. RESULTS: The 26%-carbohydrate, low-saturated-fat diet reduced triacylglycerol, apolipoprotein B, small LDL mass, and total:HDL cholesterol and increased LDL peak diameter. These changes were significantly different from those with the 54%-carbohydrate diet. After subsequent weight loss, the changes in all these variables were significantly greater and the reduction in LDL cholesterol was significantly greater with the 54%-carbohydrate diet than with the 26%-carbohydrate diet. With the 26%-carbohydrate diet, lipoprotein changes with the higher saturated fat intakes were not significantly different from those with the lower saturated fat intakes, except for LDL cholesterol, which decreased less with the higher saturated fat intake because of an increase in mass of large LDL. 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."

Last sentence seems misleading. If you look at the data in the study, subjects improved while weight loss accrued. Once weight loss was acheived, those same subjects did not show further improvement in markers. This is very different from saying that low carb diet won't help those who begin the diet in an already lean state won't benefit. Rebuttal to the study was given by doctors who noticed the same error. See Westman et al. reply below.
Carbohydrate restriction is effective in improving atherogenic dyslipidemia even in the absence of weight loss -- Westman et al. 84 (6): 1549 -- American Journal of Clinical Nutrition
"Krauss et al (1) are to be congratulated on the data presented in their recent article in the Journal, one of the strongest cases for dietary carbohydrate restriction to date. At the same time, we have concerns about the misleading and confusing way in which the data were presented and interpreted and about the scarcity of citations of other publications that are supportive of these findings (2-4). Because of the significance of these data for health, careful and appropriate conclusions are extremely important."
Increased plasma concentrations of lipoprotein(a) ...[Am J Clin Nutr. 2007] - PubMed Result
"BACKGROUND: Low-fat, high-carbohydrate (LFHC) diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)] and of triacylglycerol- rich lipoproteins (TRLs). OBJECTIVE: We tested whether increases in plasma Lp(a) induced by an LFHC diet are related to changes in TRLs. DESIGN: Healthy men (study 1; n = 140) consumed for 4 wk each a high-fat, low-carbohydrate diet (HFLC; 40% fat, 45% carbohydrate) and an LFHC diet (20% fat, 65% carbohydrate). Plasma lipids; lipoproteins; apolipoprotein (apo) B, A-I, and C-III; and Lp(a) were measured at the end of each diet. In a second group of men following a similar dietary protocol (study 2; n = 33), we isolated apo(a)-containing particles by immunoaffinity chromatography and determined the concentrations of apo C-III in ultracentrifugally isolated subfractions of apo B-containing lipoproteins. RESULTS: In study 1, plasma concentrations of Lp(a) (P < 0.001), triacylglycerol (P < 0.001), apo B (P < 0.005), apo C-III (P < 0.005), and apo C-III in apo B-containing lipoproteins (non-HDL apo C-III) (P < 0.001) were significantly higher with the LFHC diet than with the HFLC diet. Stepwise multiple linear regression analysis showed that the association of changes in Lp(a) with changes in non-HDL apo C-III was independent of changes in body mass index, apo B, LDL cholesterol, and HDL cholesterol. Plasma lipid and lipoprotein changes were similar in study 2, and we found that both total apo C-III and the apo C-III content of apo(a)-containing particles were increased in a TRL fraction consisting predominantly of large VLDL particles [TRL-apo(a)]. CONCLUSIONS: The increase in plasma Lp(a) with an LFHC diet is significantly associated with an increase in non-HDL apo C-III. Enrichment of TRL-apo(a) with apo C-III may contribute to this dietary effect on Lp(a) concentrations."
Obesity and lipids. [Curr Cardiol Rep. 2005] - PubMed Result
"Obesity increases cardiovascular risk through multiple mechanisms. Abdominal (visceral) adiposity is metabolically active and is largely responsible for the atherogenic dyslipidemia, hyperinsulinemia, hypertension, chronic inflammatory state, and prothrombotic state that constitute the metabolic syndrome, and the subsequent increased risk for cardiovascular disease and acute coronary events. Cholesterol guidelines for assessing cardiovascular risk have traditionally focused on low-density lipoprotein (LDL) levels, and reduction of plasma LDL has been shown to reduce cardiovascular events and total mortality. However, the cardiovascular risks associated with the dyslipidemia of obesity--characterized by low levels of high-density lipoprotein; increased triglycerides; increased subfractions of small, dense LDL; and increased levels of apolipoprotein B-100--are also now well recognized."
Consumption of fructose-sweetened beverages for 10...[Br J Nutr. 2008] - PubMed Result
"Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19 % (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD."
Protein in optimal health: heart disease and type ...[Am J Clin Nutr. 2008] - PubMed Result
"Diets with increased protein and reduced carbohydrates have been shown to improve body composition, lipid and lipoprotein profiles, and glycemic regulations associated with treatment of obesity and weight loss. Derived from these outcomes, high-protein, low-carbohydrate diets are also being examined for treatment of heart disease, metabolic syndrome, and type 2 diabetes. High-protein, low-carbohydrate diets have been found to have positive effects on reducing risk factors for heart disease, including reducing serum triacylglycerol, increasing HDL cholesterol, increasing LDL particle size, and reducing blood pressure. These diets appear particularly attractive for use with individuals exhibiting the atherogenic dyslipidemia of metabolic syndrome. High-protein, low-carbohydrate diets have also been investigated for treatment of type 2 diabetes with positive effects on glycemic regulation, including reducing fasting blood glucose, postprandial glucose and insulin responses, and the percentage of glycated hemoglobin. Specific effects of increasing protein compared with reducing carbohydrates have not been extensively investigated. Additional research is needed to determine specific levels of protein, carbohydrate, and fat for optimum health of individuals who differ in age, physical activity, and metabolic phenotypes."

Good Calories, Bad Calories
by Gary Taubes
The Fat Resistance Diet
Unlock the Secret of the Hormone Leptin to: Eliminate Cravings, Supercharge Your Metabolism, Fight Inflammation, Lose Weight & Reprogram Your Body to Stay Thin
by Leo Galland

Related Posts