Five to Thrive: Your Cutting-Edge Cancer Prevention Plan

Five to Thrive: Your Cutting-Edge Cancer Prevention Plan


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The inspirational concept of "thriving" is promoted in this groundbreaking plan, which pinpoints five specific pathways that are essential to preventing cancer: immunity, inflammation, hormones, insulin resistance, and detoxification/digestion. The strategy goes beyond basic advice on the immune system and dieting, describing in detail how the human body is designed to anticipate this sickness in the first place. Penned by actual cancer survivors, featuring accounts of current fighters, and including commentary from those who have lost loved ones to the disease, this guide weaves personal stories with a game plan for avoiding an all-too-common ailment.

Product Details

ISBN-13: 9781935297406
Publisher: Active Interest Media, Inc.
Publication date: 10/01/2011
Pages: 240
Product dimensions: 5.90(w) x 8.90(h) x 0.70(d)

About the Author

Lise Alschuler, ND, FABNO, is a board-certified naturopathic oncologist and the vice president of quality and education at Emerson Ecologics, a distributor of natural products to healthcare professionals. She practices naturopathic oncology with Naturopathic Specialists, LLC, and is the author of Mushrooms: Ancient Healing Wisdom. She lives in Lenox, Massachusetts. Karolyn A. Gazella is the publisher of the Natural Medicine Journal and the creator of the Healthy Living Guide series. She is the author of Osteoporosis: Strengthen Bones Naturally, Plant Oils, and Probiotics and the coauthor of Boost Your Health with Bacteria. She lives in Boulder, Colorado. They are the coauthors of The Definitive Guide to Cancer and cofounders of the multimedia educational initiative Cancer Thrivers.

Read an Excerpt

Five To Thrive

Your Cutting-Edge Cancer Prevention Plan

By Lise N. Alschuler, Karolyn A. Gazella

Active Interest Media, Inc.

Copyright © 2011 Lise N. Alschuler, ND, FABNO, and Karolyn A. Gazella
All rights reserved.
ISBN: 978-1-935297-40-6



This chapter and the next will take you on a journey into some fascinating and life-changing science. At times it may seem a bit daunting but hang in there! We promise that the understanding and insight you will gain has the power to transform your life into a powerful expression of your greatest potential. Let's begin by explaining epigenetics.

Epi what? What exactly is epigenetics? Simply put, epigenetics examines the idea that environmental factors influence the expression of our genes. Let's think about it this way: Our genes contain the instructions for who and what we are, but they do not function in a static manner. The various traits that characterize each of us as humans, such as having eyes in the front of our head and skin covering our bodies, are the result of instructions derived from genes that we inherited from our birth parents. These instructions are carried by certain genes found within every cell in the body. Yet not every organ in the body has eyes or skin. Why do these genes give instructions to make eyes only in the place where our eyes are located and not, say, on our knees? Because when we were in the womb and developing into a human body, the genes that code for eyes were blocked from being read in every cell except those destined to become our eyes. This example of the selective expression of our genes is perhaps the most elegant and sophisticated display of epigenetics. You — and all other unique beings — are the result of this beautifully orchestrated genetic expression.

Before we delve too much deeper and discover how epigenetics is at the core of cancer prevention, let's review the basics. This may seem a bit technical, but with these basic tools of understanding cancer development, or carcinogenesis, you will have the ability to understand how and why the Five to Thrive cancer prevention program works.

The foundation of epigenetics is the genome. Within each of our cells is a nucleus, which is home to our DNA. DNA is a coiled double helix that contains an individual's genome. The genome is estimated to contain 25,000 to 30,000 genes. Genes are made up of functional sequences of four different nucleotides. The order of the DNA nucleotides determines the message carried by that gene. This message is delivered in a process called transcription.

Transcription, which occurs when the genes are read by an enzyme called RNA polymerase, is the process that cells use to translate the messages contained in DNA into its essential structures and activities. Specific nucleotide sequences tell RNA polymerase where to begin reading and where to end. During genetic transcription, a portion of the DNA helix unwinds, and RNA polymerase sweeps along that strand of DNA reading the nucleotides as it cruises down the strand. As RNA polymerase reads the DNA, it copies what is read and builds its own mirror image of the gene sequence, called messenger RNA (mRNA). mRNA is identical to DNA, with the exception of one type of matched nucleotide. Once the mRNA strand has been completed, it is modified to clip out nonfunctional components of the genetic sequence and is then prepared for the next phase of genetic expression.

That next phase is called translation. The ribbon of nucleotides, mRNA, is fed through another cellular organelle called a ribosome. The ribosome is often referred to as a factory because it decodes the nucleotide message of the mRNA and matches each nucleotide with an amino acid. These amino acids are assembled in the specific order dictated by the mRNA. The formed chain of amino acids folds over itself into unique three-dimensional shapes known as proteins. Cellular proteins form the basis of all of the functioning molecules within cells (e.g., repair enzymes, messenger molecules, growth factors, hormones). Without these proteins, our cells would not function. The types and rate of protein synthesis have a lot to do with the health and function of our body.

Only the parts of the DNA that are unwound and exposed can be read. In fact, most of the DNA in any given cell is not being read at any given moment. The parts of the DNA held in tight coils or with molecules known as methyl groups stuck to their surface cannot be transcribed. Since these genes will not be read, the proteins that are ultimately coded from them will not be made, or expressed. From a functional perspective, this means that only certain portions of our DNA are expressed at any given time in any given cell. And here is where it gets interesting. The environment to which we expose ourselves through nutrition, environmental toxins, molecules of emotion, and other factors can dictate which parts of our DNA will be read. This dynamic silencing and activation of our genes is at the heart of epigenetics.

DNA is a coiled helix wrapped around big proteins called histones. Certain molecules can stimulate an enzyme to cause portions of the DNA to tightly wrap around the histones. As mentioned previously, these regions of tightly bound DNA cannot be transcribed. Other molecules will stimulate a different enzyme that causes the DNA to relax and uncoil itself so it can be transcribed. Like a light switch, gene expression is flipped on when it's relaxed and off when it's tightly coiled. Another way that the DNA can be influenced is when a big bulky methyl group sticks itself to a portion of the DNA. Just like bubble gum between two pages of a book, this methyl group prevents that portion of the DNA from being read. Another point of influence are microRNAs. These are small molecules that are key regulators of gene expression and primarily prevent genes from being read, often by adding the histones or methyl groups to DNA. Under deleterious influences, key microRNAs are themselves silenced or suppressed, and DNA transcription will be unleashed. This can ultimately lead to uncontrolled growth and cellular proliferation (i.e., cancer). Histone coiling, DNA methylation and microRNA activity are a reversible and dynamic regulatory circuit that controls the expression of our DNA. These processes are under the influence of molecules formed from our diet, environmental exposures, hormonal milieu, and even our psychological state. These external forces have the potential to support or disrupt this regulation. The outcome of these influences on our genetic expression is collectively referred to as our epigenome.

To understand the impact of the epigenome, think about identical twins. Identical twins share the exact same DNA, and when they are born, they are very difficult to tell apart. Even young identical twin children are typically more similar than dissimilar. However, as twins age, differences become apparent. This is most dramatic when one twin develops a disease such as cancer or diabetes, while the other remains healthy. Although the healthy twin may be at increased risk for developing the disease of his twin, it is not guaranteed. That is because the disease is the result of epigenetics.

If, for instance, one twin smoked cigarettes, which contain compounds that switch some genes on and others off, that twin's genome would be epigenetically altered. In fact, cigarette smoke alters the behavior of dozens of genes (e.g., it turns off certain repair and suppressor genes). Under the influence of cigarette smoke, cells that are damaged by things such as infection, radiation, or oxidation will not repair their damage, nor will they self- destruct. These damaged cells persist, and yet they don't function properly. Cigarette smoke also switches on some growth promoter genes. When switched on, these genes stimulate many functions of the cell, including cell division. In this scenario, damaged cells, unable to undergo repair, will replicate themselves at an increased rate. This, in essence, is cancer formation. The DNA in the twin who smokes is the same as the DNA in the twin who doesn't, but the DNA's behavior is markedly different.

DNA is under heavy epigenetic influence during times of rapid growth, such as fetal development and puberty. Epigenetic mechanisms are necessary for proper growth to occur. These epigenetic influences tend to be quite stable over our lifetime, which is why our eye color, for example, remains the same throughout our lives. While the expression of the genes that code for eye color may not change over time, the expression of other parts of the DNA is altered via epigenetic influences as a result of lifestyle, nutrition, and other factors. Let's look a little closer at how this connects to cancer development and prevention.


In a simplistic sense, cancer is either the result of normal expression of mutated genes or mutated expression of normal genes. In both scenarios, factors external to the DNA change the ultimate expression of the DNA. Let's start with genetic mutations. Some mutations occur spontaneously from exposure to genotoxic agents (things that are toxic or damaging to our DNA). These agents can be environmental pollutants such as cigarette smoke, industrial chemicals, and air pollution. We also sustain genetic damage from our own bodily processes. The normal process of detoxification of chemicals, medications, and hormones generates free radicals, which are highly reactive molecules that will damage DNA unless neutralized by antioxidants.

Even our own hormones, such as estrogen, can damage DNA. Estrogen is metabolized, or broken down, into different substances depending upon which metabolic enzymes are active. Some enzymes, such as cytochrome 1B1, metabolize estrogen into highly active DNA-damaging estrogen breakdown products. Environmental factors like cigarette smoke and certain air pollutants activate cytochrome 1B1. When cytochrome 1B1 is stimulated chronically, estrogen is preferentially broken down into a highly active, genotoxic metabolite. In this situation, our own estrogen is damaging to genes and is generally carcinogenic. Genetic mutations that occur over our lifetime are largely the result of an environmental factor that damages a susceptible area of our DNA. If these mutations are not repaired, and if they occur in a gene that influences cell growth, cancer can develop.

Some mutations are not accumulated, they are inherited. These mutated genes are passed from one generation to the next. Keep in mind that a genetic mutation is different than predisposition. For example, we may be predisposed to a certain illness because of dietary or lifestyle factors that we learned from our parents, but that does not mean that we inherited an actual mutated gene.

Every one of us has some inherited mutations. Fortunately, most of these mutations occur in genes that don't affect our well-being or life expectancy in a significant way. For this reason, we may never become aware of the mutations that we carry and will, in turn, pass along to our offspring. The nature of the mutation varies too. Genes can be composed of thousands of nucleotides. If we inherit a single mutation in a large gene, the change that this mutation creates in the gene may not significantly alter the code for the protein that is ultimately expressed from the gene. These types of mutations, referred to as single-nucleotide polymorphisms (SNPs) are numerous, and we are just beginning to understand their significance. Some SNPs are considered irrelevant to our health and well-being. Other SNPs carry grave significance.

Some of the more well-known SNPs with significant health implications are the inherited genetic mutations to the BRCA1 or BRCA2 genes (see sidebar on page 25). These mutations are examples of SNPs that impair the expression of the BRCA1 or BRCA2 genes. This can have very important health consequences, because BRCA1 and BRCA2 control transcription, regulate cell division, and stimulate cell repair — especially in breast and ovarian cells. Breast and ovarian cells that lack fully functional BRCA1 or BRCA2 are unable to detect DNA damage properly, utilize error-prone repair processes that lead to genomic instability, and divide more frequently. This can result in the development of cancer. While not a guarantee of developing cancer, BRCA1 and BRCA2 mutations can increase the possibility of developing breast cancer to 40 to 85 percent over one's lifetime, depending upon the type and number of SNPs to these genes. Even though these genetic mutations are clear risk factors for cancer, they do not inevitably lead to cancer. Epigenetic factors intervene.

Epigenetic factors can alter the risk of developing cancer, even in the face of genetic mutations. For instance, BRCA1 and BRCA2 mutation carriers who consume the greatest amount and diversity of fruits and vegetables have a lower risk of developing cancer than carriers who consume a narrow selection of fruits and vegetables and consume these foods infrequently. Furthermore, BRCA mutation carriers who prevent significant weight gain during adulthood through overall caloric restriction have lower risk of developing breast cancer. These findings suggest that epigenetic dietary factors can modify the significance of BRCA genetic mutations.

Another critical link between DNA mutation and cancer development is genomic instability. Genomic instability results from SNPs, from epigenetic silencing of genes that maintain stability, or from significant changes to larger sections of DNA. The resulting instability leaves the DNA prone to mutations. However, epigenetics can influence genetic stability as well. One example of this is a pilot study conducted in 2008 by Dean Ornish, MD, and colleagues, which assessed the impact of lifestyle on telomeres.

Telomeres are protective caps on the ends of chromosomes that lend stability to the chromosome. A chromosome is the linear strand of DNA and the histone and other associated proteins around which the strand is wrapped. Shortened telomeres on the ends of chromosomes cause the DNA to be unstable and are predictive of increased risk of bladder, head and neck, lung, and renal-cell cancers; worse progression and prognosis of patients with breast cancer and colorectal cancer; and increased risk of prostate cancer recurrence. Ornish and colleagues found that after three months of significant dietary changes, meditation, exercise, and supplement use, telomeres lengthened, conferring more stability to the chromosomes. The implication of this is that lifestyle can stabilize DNA, making it less vulnerable to damaging mutations.

The picture that emerges from these understandings is that the interplay between genetic mutations and genetic expression lies at the heart of cancer development. We cannot change inherited genetic mutations. We can, however, utilize our lifestyle to minimize exposure to further mutations and, importantly, to alter how our genes behave. Thus, to understand how to alter our epigenome is to understand how to best prevent cancer.

The picture that emerges from these understandings is that the interplay between genetic mutations and genetic expression lies at the heart of cancer development. We cannot change inherited genetic mutations. We can, however, utilize our lifestyle to minimize exposure to further mutations and, importantly, to alter how our genes behave. Thus, to understand how to alter our epigenome is to understand how to best prevent cancer.


Epigenetics depends upon the consistency and nature of the epigenetic influences to which our genes are exposed. Let's start with consistency. Epigenetic influences on our genes can be momentary blips — walking through a cloud of car exhaust, for example. The chemicals that you inhale from the exhaust will certainly influence the behavior of your genes, but the influence will be short-lived and ultimately not likely to be impactful in a long-term way. What happens though if you live near a busy intersection, walk to work along major roads every day, and work in a busy city? Now your exposure to the chemicals in car exhaust is daily and long-term. This is when the epigenetic influences exerted by these chemicals begin to make an impactful difference in how your genes behave.

Aside from the time we spent in the womb, epigenetic changes tend to accumulate over our lifetime. This means that epigenetics is the result of daily habits and exposures over months and years that create sustained changes in how our genes behave.

Our genes' behavior will only change if external influences are translated into molecular events around our DNA. This translation occurs via key bodily pathways. In fact, there are five key bodily pathways that are responsible for the vast majority of this translation. Understanding the link between the health of these pathways and our epigenome is at the heart of understanding our effective cancer prevention program.

Our genes exist within a dynamic molecular soup. The molecules floating in and around the DNA can influence the DNA "switches" and turn on or off certain genes. Thus, epigenetics is the result of the molecules to which the DNA is exposed. Just as the flavor of soup changes depending on which ingredients are added to the broth, the nature of epigenetic changes is dependent upon the molecules that consistently interact with our DNA.


Excerpted from Five To Thrive by Lise N. Alschuler, Karolyn A. Gazella. Copyright © 2011 Lise N. Alschuler, ND, FABNO, and Karolyn A. Gazella. Excerpted by permission of Active Interest Media, Inc..
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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