TY - JOUR
T1 - Oxidation, lipoproteins, and atherosclerosis
T2 - Which is wrong, the antioxidants or the theory?
AU - Williams, Kevin Jon
AU - Fisher, Edward A.
PY - 2005/3
Y1 - 2005/3
N2 - Purpose of review: Paradoxically, many well-established components of the heart-healthy lifestyle are pro-oxidant, including polyunsaturated fat and moderate alcohol consumption. Moreover, antioxidant supplements have failed to decrease cardiovascular risk in extensive human clinical trials to date. Recent progress in understanding the roles of oxidants in regulating VLDL secretion and as essential signaling molecules supports the concept that oxidation may be beneficial in certain circumstances but damaging in others. We summarize recent data on the roles played by oxidative metabolism in different tissues and pathways, and address whether it is currently advisable to use antioxidant supplements to reduce cardiovascular risk. Recent findings: Our recent study reported that in liver cells, polyunsaturated fatty acids increased reactive oxygen species, which in turn lowered the secretion of the atherogenic lipoprotein, VLDL, in vitro and in vivo. Antioxidant treatments prevented VLDL-lowering effects of polyunsaturated fatty acids in vitro, suggesting that supplemental antioxidants could either raise apolipoprotein-B-lipoprotein plasma levels in vivo, or impair the response to lipid-lowering therapies. The failure of antioxidants to decrease cardiovascular disease risk in many trials is also discussed in the context of current models for atherosclerosis progression and regression. Summary: Oxidation includes distinct biochemical reactions, and it is overly simplistic to lump them into a unitary process that affects all cell types and metabolic pathways adversely. Guidelines for diet should adhere closely to what has been clinically proved, and by this standard there is no basis to recommend antioxidant use, beyond what is inherent to the 'heart healthy' diet in order to benefit cardiovascular health.
AB - Purpose of review: Paradoxically, many well-established components of the heart-healthy lifestyle are pro-oxidant, including polyunsaturated fat and moderate alcohol consumption. Moreover, antioxidant supplements have failed to decrease cardiovascular risk in extensive human clinical trials to date. Recent progress in understanding the roles of oxidants in regulating VLDL secretion and as essential signaling molecules supports the concept that oxidation may be beneficial in certain circumstances but damaging in others. We summarize recent data on the roles played by oxidative metabolism in different tissues and pathways, and address whether it is currently advisable to use antioxidant supplements to reduce cardiovascular risk. Recent findings: Our recent study reported that in liver cells, polyunsaturated fatty acids increased reactive oxygen species, which in turn lowered the secretion of the atherogenic lipoprotein, VLDL, in vitro and in vivo. Antioxidant treatments prevented VLDL-lowering effects of polyunsaturated fatty acids in vitro, suggesting that supplemental antioxidants could either raise apolipoprotein-B-lipoprotein plasma levels in vivo, or impair the response to lipid-lowering therapies. The failure of antioxidants to decrease cardiovascular disease risk in many trials is also discussed in the context of current models for atherosclerosis progression and regression. Summary: Oxidation includes distinct biochemical reactions, and it is overly simplistic to lump them into a unitary process that affects all cell types and metabolic pathways adversely. Guidelines for diet should adhere closely to what has been clinically proved, and by this standard there is no basis to recommend antioxidant use, beyond what is inherent to the 'heart healthy' diet in order to benefit cardiovascular health.
KW - Atherosclerosis
KW - Dietary supplements
KW - Fatty acids
KW - Oxidation
KW - VLDL
UR - http://www.scopus.com/inward/record.url?scp=14244251463&partnerID=8YFLogxK
U2 - 10.1097/00075197-200503000-00006
DO - 10.1097/00075197-200503000-00006
M3 - Review article
C2 - 15716791
AN - SCOPUS:14244251463
SN - 1363-1950
VL - 8
SP - 139
EP - 146
JO - Current Opinion in Clinical Nutrition and Metabolic Care
JF - Current Opinion in Clinical Nutrition and Metabolic Care
IS - 2
ER -