Evidence-Based Proactive Nutrition to Slow Cellular Aging

Robert Fried, Lynn Nezin

• Publisher: CRC Press
• Year: 2017
• ISBN:
  9781351700214
• Edition: 1
• Topic: Medicina
• Subtopic: Nutrizione, dietetica e bariatria

Recent research findings on the impact of nutrition on telomere length is unlocking the potential to combat premature aging at the cellular level. We have learned that while aging is a natural cellular process, premature aging is not and it can be positively impacted by an Evidence-Based Proactive Nutrition to Slow Cellular Aging diet plan.

This book examines key elements of the biology of cell aging and focuses on enhancing mitochondrial function and preventing abnormal cell turnover thus preserving telomere length. It details the cellular damage caused by free radicals and ROS, explains the salutary effects of antioxidants, and the body's need for adequate nitrates and other nutrient substrates from which the body derives nitric oxide (NO) to support cardiovascular health. This book is the first to feature a simple do-it-yourself test of the effects of the diet on the availability of NO for - heart health.

The book guides the reader through the rationale for a modified Mediterranean style diet that supplies the body with an adequate daily intake of essential nutrients, simple high antioxidants, and other functional foods. It includes simple, easy to prepare appealing recipes promoting a seamless transition to a healthy, age-defying lifestyle.

1 The Science of Longevity

1.1 INTRODUCTION

Our youth-obsessed culture is terrified of aging. This fear has spawned a growing literature claiming that the proper choice of foods, supplements, and caloric restriction can actually stop aging. As seductive as these claims may be, they lack the support of real scientific proof.

In contrast, this book, Evidence-Based Proactive Nutrition, describes a new science-based diet program designed to help avert premature body cell aging. This program is not an overpromise but a sensible approach to nutrition that is not only easy to implement but is also backed by reputable, scientific peer-reviewed research.

Aging is a natural cellular process, but premature aging is not a natural process. To understand how nutrition might avert premature aging, here is a brief preview of the process of normal aging. Virtually all cells in the human body will eventually cycle and be replaced by daughter cells by a process of cell division called mitosis. When the cells divide, the nucleus they contain divides as well and each daughter cell gets its share of the nucleus. There is actually a limit to the number of such cycles for any given cell before it cannot cycle anymore and then it dies. This limit, the “Hayflick limit,” (Hayflick 1965) is detailed later in this book. It is estimated that each cell may divide between 50 and 70 times over its lifespan and that were one to add up all such new generations, in ideal circumstances, that would come to about 120 years.

1.2 THE LENGTH OF TELOMERES DETERMINES THE LENGTH OF THE CELL LIFESPAN

The cell nucleus that a daughter cell “inherits” holds the chromosomes, thread-like strands of nucleic acids and protein carrying complex genetic information in the form of genes. Genes determine much about body shape, appearance, skills and talents, how we function, and even what disease we may suffer from or avoid.

The chromosomes are capped at each end with small structures, called telomeres, said to resemble the caps at the ends of shoelaces. It is thought that these prevent the chromosomes from spilling DNA each time a cell cycles. But, each time a cell cycles, the telomeres shorten perceptibly, and when they reach a given length, they are no longer viable and the cell dies.

1.3 FREE RADICALS ACCELERATE AGING

It is current dogma that aging is the aggregate of free-radical damage to body cells and to DNA. This explanation was proposed by Dr. Denham Harman, Emeritus Professor, University of Nebraska, Omaha (Harman 1992). Free radicals are toxic, ubiquitous chemically unstable forms of oxygen that can seriously damage and even destroy cells.

1.4 FREE RADICALS RESULT IN SHORTER TELOMERES

Free radicals typically combine in the body with hydrogen, lipids, or proteins, forming different reactive oxygen species (ROS) that attack cells and damage them, especially the cell membrane that encloses and protects each cell. Under ROS assault, cells cycle more rapidly, thus shortening the telomeres more rapidly with each cycle. The net effect is premature aging. Chapter 2 describes oxygen free radicals in detail, their major sources inside cells and outside, and their impact on telomeres.

1.5 A PROACTIVE NUTRITION PROGRAM CAN PREVENT FREE RADICAL CELL DAMAGE AND PROTECT TELOMERES

The damage to cells caused by free radicals and ROS can be considerably reduced by a diet program that supplies adequate antioxidants. In brief, antioxidants “neutralize” free radicals and reduce the formation of ROS. As will be shown in Chapter 3 on antioxidants, cells make all the antioxidants they need for protecting from the free radicals and ROS that they generate. But first, they need adequate nutrition support in the form of vitamins, minerals, enzymes, and other substances needed to make those antioxidants.

The protection afforded by antioxidants against toxic assaults on cells prevents premature cycling and so preserves telomere length for as long as possible, thereby averting premature aging.

This book will briefly describe elements of the biology of cell aging; detail the nature of free radicals, ROS, and antioxidant functions and interactions; detail the science that supports a nutrition approach to averting premature aging; and provide a list of simple high antioxidant foods, “functional foods,” and recipes as means to implement the diet program.

1.6 LIFESPAN CANNOT BE LENGTHENED BUT IT CAN BE SHORTENED

After a number of divisions, and before the chromosomes in a given cell run out of telomeres, the cell can opt to self-repair any damage or even to self-destruct. Otherwise, it will die when it runs out of telomeres. Whichever course it chooses when damaged, but while it still has telomeres, may depend to a large degree on nutrition. Curiously, the scientific evidence points to an unexplained “choice” and nutrition can influence that choice.

It is now known that maximum lifespan cannot be lengthened, nor can aging be stopped. However, the lifespan of cells can be significantly shortened by setting the stage for them to make that choice. Lifespan shortens when damage to cells—damage that could have been be avoided—causes them to divide more rapidly, thus abbreviating the telomeres more rapidly, and forcing them to choose division or self-destruction. The more rapidly cells divide, the more rapidly they will run out of telomeres and die, or else they may be so damaged that they will choose to die. This self-destruction is called apoptosis.

1.7 SOURCES OF FREE RADICALS

There are two main types of free radicals: exogenous and endogenous. Exogenous free radicals are those that come from the environment. They play an important role but can actually be avoided much of the time. However, the most common free radicals are endogenous, that is, they come from within the cells, and they result, as Dr. Harman pointed out, from oxidative metabolism in the mitochondria (Harman 1972).

Mitochondria are small structures in the cell that make it possible for it to use oxygen to fuel metabolism. The way that cells use oxygen to create and use energy, however, causes free radicals to form. This source of free radicals and the resulting ROS cannot be avoided, but their impact can be lessened to slow down cell cycling.

1.8 PROACTIVE NUTRITION

The basic purpose and aim of the Proactive Nutrition Program is to slow telomere shortening:

• We can slow telomere abbreviation by slowing the rate of cell division.
• We can slow the rate of cell division by protecting them from free radical and ROS damage.
• We can protect cells from free radical and ROS damage by supporting their antioxidant defense.

There are three components to the Proactive Nutrition Program:

• It is basically a Mediterranean type-food plan that is rich in plant-based sources of antioxidants, vitamins, amino acids, etc.
• It is inherently a modestly restricted calories diet. Restricted calories activate longevity-promoting genes in the sirtuin family involved in energy management and storage (as fat) in the body.
• It is supplemented with so-called “sirtfoods” that activate the SIRT1-related longevity-promoting gene.

1.9 DOCUMENTATION

In most cases, popular diets aim at weight loss. This diet is aimed at longevity regardless of one’s weight: a later section of this chapter will report that a study recently published in the Journal of the American Medical Association (JAMA) shows that baring extremes, overweight is not an obstacle to long life.

Much of what is in this book is quite new science. For that reason, the scientific sources supporting assertions or findings about the information presented here are thoroughly documented by citations of highly regarded conventional clinical/medical and other biological science sources. The information presented is based on conventional medical laboratory research methods, with the results published in prestigious, conventional medical journals, and accepted by the scientific community. Those rare cases where there is controversy will be indicated.

1.10 THE PLAN OF THE BOOK

Chapter 1 explains that one cannot prolong life but that it can be shortened. It describes how metabolism is the prime source of the oxygen free radicals that can cause accelerated cell division, telomere abbreviation, and therefore, premature aging. It also explains that normal, ordinary aging is not a disease, but that one can expect a natural age-related decline in function that is unavoidable. However, it is also pointed out that one can accelerate that decline by adverse lifestyle and diet choices causing premature aging.

Chapter 2 explains how metabolism results in the formation of toxic radical oxygen molecules, especially in mitochondria, and how these affect cell function and telomere length. The chapter also details how faced with oxygen radical attacks and the ensuing damage, cells may opt out by self-destruction.

Chapter 3 explains the nature of antioxidants and their action in combating toxic radicals that lead to telomere abbreviation. The chapter differentiates the antioxidants made by the body (endogenous) from those obtained through nutrition and the environment (exogenous), and it also provides information on United States Department of Agriculture (USDA) sources that list the antioxidant capacity of common foods.

Chapter 4 focuses on organelles in the cell in addition to mitochondria and shows how these are subject to radical attack that leads to cell damage and telomere abbreviation.

Chapter 5 discusses the gas nitric oxide (NO). The winners of the 1998 Nobel Prize in Medicine identified NO as a powerful antioxidant and as the “miracle molecule” that keeps the heart and blood vessels free of atherosclerotic sludge and keeps them “humming.” While the primary aim of this book is to describe how telomeres can be protected, it also focuses on nutritional factors known to help avert aging of the cardiovascular system and the heart by drawing on the experience of the authors with nutr...

Table of contents

• Title Page
• Copyright Page
• Dedication
• Table of Contents
• Preface
• Acknowledgments
• Authors
• Chapter 1 The Science of Longevity
• Chapter 2 Free Radicals Damage Cells
• Chapter 3 Antioxidants Neutralize Free Radicals
• Chapter 4 Preventing Premature Cell Cycling
• Chapter 5 Nitric Oxide Is Said to Be the “Miracle Molecule” That “Reverses Aging”
• Chapter 6 Three Common Diets Compared for Their Effects on Cell Aging
• Chapter 7 Proactive Nutrition: Enhancing the Mediterranean Diet
• Chapter 8 Selected Functional Foods That Combat Inflammation
• Index