Significant heterogeneity was not observed by nut type or other factors .
Tree nut intake  lowers total cholesterol , LDL cholesterol , ApoB , and triglycerides .
The major determinant of cholesterol lowering appears to be nut dose rather than nut type .
BACKGROUND The effects of nuts on major cardiovascular disease ( CVD ) risk factors , including dose-responses and potential heterogeneity by nut type or phytosterol content , are not well established .
OBJECTIVES We examined the effects of tree nuts ( walnuts , pistachios , macadamia nuts , pecans , cashews , almonds , hazelnuts , and Brazil nuts ) on blood lipids [ total cholesterol , low-density lipoprotein ( LDL ) cholesterol , high-density lipoprotein , and triglycerides ] , lipoproteins [ apolipoprotein A1 , apolipoprotein B ( ApoB ) , and apolipoprotein B100 ] , blood pressure , and inflammation ( C-reactive protein ) in adults aged ≥18 y without prevalent CVD .
Effects of almond dietary supplementation on coronary heart disease lipid risk factors and serum lipid oxidation parameters in men with mild hyperlipidemia.
OBJECTIVES Oxidation and level of plasma lipids are closely implicated in the development of coronary heart disease ( CHD ) . Dietary almond supplementation may participate in beneficial effects on CHD lipid risk factor levels and their susceptibility to oxidative modification . The aim of this study was to evaluate the effects of dietary supplementation with almond on serum lipid levels and their relation to lipid oxidation parameters in men with mild hyperlipidemia . DESIGN Thirty ( 30 ) healthy volunteer men ( age 45.57 ± 7.14 years and body-mass index 24.29 ± 2.15 kg/m(2 ) ) with mild hyperlipidemia received 60 g almond daily  for 4 weeks . OUTCOME MEASURES Overnight fasting blood sample s were obtained before and after supplementation . Serum levels of lipids , lipoproteins , and apolipoproteins and copper-induced serum lipid oxidation were determined . Lipid oxidation was followed by monitoring of the change of conjugated dienes in diluted serum after addition of Cu(2 + ) . A number of quantitative parameters including lag-time , maximal rate of oxidation ( V-max ) , and maximal amount of lipid peroxide products ( OD-max ) were evaluated . RESULTS After 4 weeks , almond supplementation significantly decreased low-density lipoprotein cholesterol , total cholesterol ( TC ) , and apolipoprotein B100 ( apo-B100 ) . At baseline , there was little correlation between lipid risk factors and lipid oxidation parameters , but a positive correlation was observed between TC and lag-time ( r = 0.6 , p = 0.001 ) , negative correlation between TC with V-max and OD-max ( r = -0.65 , p < 0.001 and r = -0.61 , p = 0.001 ) , and also positive correlation between apo-B100 with V-max and OD-max ( r = 0.48 , p = 0.01 and r = 0.54 , p = 0.003 ) after almond supplementation . CONCLUSIONS These results demonstrated that almond supplementation , in addition to lowering effects on serum levels of CHD lipid risk factors , may contribute to a dramatic change in the relation of lipid risk factors and susceptibility of serum lipids to oxidative modification . This may be due to the distribution of different almond phenolic antioxidants in different components of serum including nonlipoprotein molecules such as serum albumin
Significant heterogeneity was not observed by nut type or other factors .
Tree nut intake  lowers total cholesterol , LDL cholesterol , ApoB , and triglycerides .
The major determinant of cholesterol lowering appears to be nut dose rather than nut type .
BACKGROUND The effects of nuts on major cardiovascular disease ( CVD ) risk factors , including dose-responses and potential heterogeneity by nut type or phytosterol content , are not well established .
OBJECTIVES We examined the effects of tree nuts ( walnuts , pistachios , macadamia nuts , pecans , cashews , almonds , hazelnuts , and Brazil nuts ) on blood lipids [ total cholesterol , low-density lipoprotein ( LDL ) cholesterol , high-density lipoprotein , and triglycerides ] , lipoproteins [ apolipoprotein A1 , apolipoprotein B ( ApoB ) , and apolipoprotein B100 ] , blood pressure , and inflammation ( C-reactive protein ) in adults aged ≥18 y without prevalent CVD .