More than 7 billion people inhabit the earth and all of them are subject to aging. This book is aimed at persons interested in a molecular explanation of how our cells age. Human Longevity: Omega-3 Fatty Acids, Bioenergetics, Molecular Biology, and Evolution is built on the proposition that we age as our mitochondria age. It suggests a revised version of Harman’s famous hypothesis featuring mitochondrial oxidative and energy stresses as the root causes of aging.
Human cells are protected from the ravages of aging by a battery of defensive systems including some novel mechanisms against membrane oxidation introduced in this book. This concept is consistent with recent discoveries showing that mitochondria-targeted antioxidants prevent Huntington’s disease, Parkinson’s disease, and traumatic brain disease in animal models of neurodegeneration.
This book explores a unified theory of aging based on bioenergetics. It covers a variety of topics including an introduction to the science of human aging, the Darwinian selection of membranes enabling longevity, a revised mitochondrial membrane hypothesis of aging, and various mechanisms that protect human mitochondrial membranes, thereby enabling longevity.
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
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,
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
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