INTRODUCTION TO THE SCIENCE OF HUMAN AGING Mitochondrial Hypothesis of Aging Is Undergoing Revision Oxidative Stress Defined as a Deadly Free Radical-Mediated Chain Reaction: Case History of Paraquat Membranes of Deep-Sea Bacteria as Surrogates for Mitochondrial Membranes of Humans DARWINIAN SELECTION OF MEMBRANES ENABLING LONGEVITY Protective Mechanisms for EPA Membranes in C. elegans and Their Relationship to Life Span Remarkable Longevity of Queens of Social Insects Likely Involves Dietary Manipulation to Minimize Levels of Polyunsaturates and Decrease Membrane Peroxidation Membrane Peroxidation Hypothesis Helps Explain Longevity in Birds, Rodents, and Whales Did Longevity Help Humans Become Super Humans? REVISED MITOCHONDRIAL MEMBRANE HYPOTHESIS OF AGING Mitochondrial Diseases and Aging Have Much in Common Revised Mitochondrial Hypothesis of Aging Highlights Energy Deficiency Caused by Errors of Replication (Mutations) of mtDNA Benefits of Polyunsaturated Mitochondrial Membranes Mitochondrial Membranes as a Source of Reactive Oxygen Species (ROS) Mitochondrial Membranes as Major Targets of Oxidation MANY MECHANISMS HAVE EVOLVED TO PROTECT HUMAN MITOCHONDRIAL MEMBRANES, ENABLING LONGEVITY Apoptosis Caused by Oxidatively Truncated Phospholipids Can Be Reversed by Several Mechanisms, Especially Enzymatic Detoxification Selective Targeting of HUFAs Away from Cardiolipin and Beta-Oxidation Combine to Protect Mitochondrial Membranes Against Oxidative Damage Oxygen Limitation Protects Mitochondrial Phospholipids, Especially Cardiolipin Uncoupling Proteins (UCPs) of Mitochondria Purposely Waste Energy to Prevent Membrane Damage Mitochondrial Fission Protects against Oxidative Stress by Minting a Continuous Supply of Cardiolipin and Other Polyunsaturated Phospholipids Mitophagy Eliminates Toxic Mitochondria Longevity Genes Likely Protect Membranes Aging as a Cardiolipin Disease That Can Be Treated Index MEMBRANE HYPOTHESIS OF AGING Mitochondrial Diseases and Aging Have Much in Common Revised Mitochondrial Hypothesis of Aging Highlights Energy Deficiency Caused by Errors of Replication (Mutations) of mtDNA Benefits of Polyunsaturated Mitochondrial Membranes Mitochondrial Membranes as a Source of Reactive Oxygen Species (ROS) Mitochondrial Membranes as Major Targets of Oxidation MANY MECHANISMS HAVE EVOLVED TO PROTECT HUMAN MITOCHONDRIAL MEMBRANES, ENABLING LONGEVITY Apoptosis Caused by Oxidatively Truncated Phospholipids Can Be Reversed by Several Mechanisms, Especially Enzymatic Detoxification Selective Targeting of HUFAs Away from Cardiolipin and Beta-Oxidation Combine to Protect Mitochondrial Membranes Against Oxidative Damage Oxygen Limitation Protects Mitochondrial Phospholipids, Especially Cardiolipin Uncoupling Proteins (UCPs) of Mitochondria Purposely Waste Energy to Prevent Membrane Damage Mitochondrial Fission Protects against Oxidative Stress by Minting a Continuous Supply of Cardiolipin and Other Polyunsaturated Phospholipids Mitophagy Eliminates Toxic Mitochondria Longevity Genes Likely Protect Membranes Aging as a Cardiolipin Disease That Can Be Treated Index BR>Uncoupling Proteins (UCPs) of Mitochondria Purposely Waste Energy to Prevent Membrane Damage Mitochondrial Fission Protects against Oxidative Stress by Minting a Continuous Supply of Cardiolipin and Other Polyunsaturated Phospholipids Mitophagy Eliminates Toxic Mitochondria Longevity Genes Likely Protect Membranes Aging as a Cardiolipin Disease That Can Be Treated Index.