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Minimizing Nutrition through Genetics PDF Print E-mail
Written by T. Colin Campbell, Ph.D.   
Wednesday, 21 April 2004 08:50

Minimizing Nutrition through Genetics

ImageNearly everyone knows something about genes, the blueprint for our lives. Genes, embedded in our chromosomes, are the agents that biologically connect us to our parents and their parents and ancestors before them. Genes connect these generations mainly by using its DNA (deoxyribonucleic acid) and the extraordinary code that is buried therein.

We have about 30,000-35,000 genes. Collectively, they are refer-red to as the genome. Each gene provides the blueprint for making a uniquely different protein. The blueprint is a DNA code comprised of four chemicals, or nucleotide bases. The bases are strong together as a chain and their sequence is the code. DNA codes are like words made of letters, except only four “letters” and far longer sequences of letters are used, compared with words. (These “chains” actually are comprised of two mirror image chains wrapped around each other in the form of a double helix, somewhat like the fibers in a rope.)

T. Colin CampbellExcept for red blood cells, every cell in our body has the same family of genes that we get from our parents. Genes are located in the nucleus of every cell, including both the cells that provide for the everyday needs of our bodies and the cells that we use to reproduce our progeny. Each cell selects from the library of 30,000 to 35,000 genes those that serve their particular purposes. These selected genes provide the blueprints for the synthesis of unique proteins that are used as enzymes. Enzymes metabolize chemicals; that is, they convert substrate chemicals into products. The oxidation of sugar (glucose) to carbon dioxide and water, for example, involves a sequence of reactions, each of which requires a unique enzyme. The enzyme activity itself is influenced by a variety of factors, including the effect of its original structure that arises from the DNA template (or code), the amount of enzyme being made, and the cell’s requirement for the reaction products. This is an extraordinary process of making unique enzymes, beginning with the DNA code. Each cell is choosing those genes (from the 30,000-35,000) that suits its own purpose, then turning them on (or expressing them) when they are needed. Controlling this process is one of the wonders of Nature and its dynamic is almost beyond human comprehension.

When the cells of our bodies divide into two daughter cells to make new tissue, one of the DNA chains in the double helix goes to one daughter cell, the other to the second cell. Then, in each daughter cell, the complimentary (missing) chain is then synthesized to restore the original double helix. The DNA code therefore is identical to the parent cell and is faithfully passed on to successive generations of cells as they reproduce themselves and grow new tissue. In effect, the code is maintained throughout these successive generations of cells.

In a first step of the cell replication process, DNA directs the formation of a closely related nucleic acid, RNA. Then, the RNA, using the “hand-me-down” code of the DNA, directs the synthesis of the unique proteins, most of which act as enzymes that control the countless cellular reactions that sustain our lives. Unlike the 4 nucleotide bases used by DNA and RNA to create their own codes, RNA uses 10-15 different amino acids to make proteins, again in the image of its own code. Like DNA and RNA, proteins also exist as long chains but, instead, they use amino acids rather than nucleotide bases to create their own identities.

The code, first present in the DNA, is passed up the line from DNA to RNA to protein to enzymes and it is these latter that ultimately control biochemical reactions throughout our bodies. It is, therefore, little wonder that the genetic code initially embedded in the DNA of the genes is so highly regarded. The DNA code is a golden thread that gives biological stability and integrity before, during and after our lives.

Many people, both within and without the scientific community, have an unusually abiding faith in their genes. According to these folks, genes determine so much of who we are and how we respond, biologically speaking. This reverence for genes also includes our fate in getting serious diseases. You’ve heard it before: cancer and heart disease and obesity “run in the family” and there’s not a lot that we can do to keep them under control. For decades, even centuries, we have endlessly debated whether our genes (or “heredity”) directly cause these diseases or whether these genes act only when given resources and “permission” to do so. The question is: Do we blame the genes of our parents and their ancestors for our disease risks or can we take some responsibility for those diseases, all of which begin in our genes?

We have spent billions of dollars of your money during the past 10-15 years studying gene structures, functions and locations. This research is often justified in the hope that it will improve our ability to prevent and treat diseases. Many scientists have argued that by precisely knowing the structural identities of genes and their corresponding protein (enzyme) products, we could better develop custom-made drugs. For example, if we knew the structure of the enzyme arising from the gene, then we could develop a drug to specifically target this particular enzyme — and only this enzyme. By using this targeted approach, we could minimize the side effects usually encountered with drugs. This strategy is sometimes called molecular or personalized medicine, which many believe is the great medical promise of the future.

The field of molecular genetics has produced some extraordinary discoveries during the last half-century. The chemical structure of DNA was discovered almost 50 years ago and this paved the way to our understanding of its embedded code. There also were dramatic technical inventions that permitted investigation and manipulation of the tiniest amounts of DNA and its products. One of the most striking of these technical advances led to an ability to insert new genes into an organism’s genome, making the new organism (microorganism, animal, plant) transgenic. A version of this is also called gene therapy. Mapping the location of specific genes on our chromosomes likewise became possible. This led to the now famous Human Genome Project (http://www.ornl.gov/sci/techresources/Human_Genome/toc_expand.shtml), which led to the recent publication of the entire genome of the 30,000-35,000 genes. A race is now on to identify which genes play which roles in disease formation. This project is truly one of the great accomplishments of modern science.

Genetic research has been exceptionally exciting in recent years and in many cases, quite promising. We can identify individual people with far more certainty than ever before, while using the tiniest bit of biological tissue, as in criminal investigations. We can trace our ancestry, and the migration pathways that our forbearers followed. We can modify genes in plants and animals, so as to make new strains that do extraordinary things, like having bananas make human insulin.

The vast majority of our genes provide the blueprint for developing the health that Nature intended. A few genes, however, have strayed from the norm and have done the opposite, such as laying the groundwork for diseases like cancer, heart disease and other disease conditions. Genes go astray mostly because the nucleotide bases in the DNA chains have been altered. As a result, a different code emerges that leads to malformed enzymes and faulty reactions. Even slight chemical changes of single nucleotide bases (among thousands) can have huge life-threatening effects. These changes are often referred to as polymorphisms if originating in generations thousands or even millions of years ago or mutations if occurring during the present generation. Polymorphisms of past generations and mutations of the present generation can be caused in various ways, but many undoubtedly result from attacks by toxic chemicals.

Genetic polymorphisms generally represent only a tiny fraction of the genes — the proverbial needle in the haystack. But we now have technologies that can be used to detect them. This allows study of their potential associations with diseases or other distinctly different outcomes. However, the mere existence of a polymorphism does not mean that a serious disease or other outcome will always occur. They may occur only in the DNA chain obtained from one parent and remain unexpressed (i.e., it does not lead to the synthesis of an aberrant protein); they may involve a part of the DNA chain that has no obvious biological function; and they may act only when other DNA polymorphisms also are simultaneously present. Nonetheless, some of these genetic polymorphisms are known to associate with disease and, if so, they are generally known as disease-producing genes.

Some of these disease-producing genes (or polymorphisms) have the capability to cause disease almost by themselves. Merely being present in an individual seems to be enough. These diseases, however, are quite rare. In contrast, most diseases have a far more complex genetic blueprint. Nonetheless, the genetic basis for these diseases often gets overemphasized. A relatively small number of breast cancer cases, for example, are associated with the BRCA 1 and BRCA2 genes but the attention given to this genetic characteristic is way out of proportion to the number of women in the general population who will get the disease. Only 1 in 500 women in the general population carry these genes and only about half of these will get breast cancer, although some will be at higher risk for ovarian cancer. This is far from the general impression that I sometimes hear that breast cancer is a genetic disease. It certainly is interesting to remind ourselves that, regardless how much BRCA1 and BRCA2 are related to breast cancer, still only about half of the women with these genes will get the disease. This also means that half won’t. If only we knew what they are doing to keep them free of disease...?

Colon cancer is a similar story. Only about 1-3 percent of colon cancer cases are associated with known genes that are inherited; another 2-4 percent with no known gene associations nonetheless seem to be inherited from parents. Then another 15-20 percent of the cases tend to occur in families where colon cancer is more common. It should be remembered, however, that a tendency for cancer, of any kind, to be more common in some families than in others is not necessarily related to genes. Family members also tend to consume a similar diet and to live in similar environments.

There is a commonly held view that, because all biological events start from genes, we can therefore conclude that genes cause disease. If this were true, then it would be logical to identify the responsible gene (or genes), and modify it or its protein products before the disease starts. As stated above, this is the underlying premise of molecular medicine, a concept that I find to be naive and superficial, for two reasons. First, it implies that genes lead directly to disease and, second, it tends to simply that one or only a few genes, at most, are involved. Except for a few rare diseases, both assumptions are terribly misleading and wrong.

Genes don’t lead directly to disease. At a minimum they begin with DNA being transcribed into RNA, then the RNA is translated into protein, which may act as an enzyme. Each of these steps is influenced by a variety of factors. And finally, once the enzymes are made and activated, their corresponding reactions are exceptionally dynamic, inferring that they can be influenced by a variety of dietary and environmental factors.

Genes also don’t act alone in causing disease. Many people believed this a few short years ago but now we know that multiple genes are involved in almost all diseases. For example, earlier it was announced that the obesity gene had been discovered but now we know that there are at least a couple dozen genes affecting obesity. It gets even more complex than this. Regulation of body weight in a tiny worm species involves 417 genes from more than 16,000 genes examined! I wonder how many genes affect weight in humans who have 30,000-35,000 genes? And which one of these genes are the molecular medicine enthusiasts going to select for drug treatment? Maybe some kind of snake oil extract might work.

My main concern with genetic research is that the exceptionally dynamic processes that lie between the DNA code and the final disease outcome is far too often glossed over or even ignored. It is this highly dynamic system where nutrition plays a major role and the effect that it has is most impressive. When nutrition gets ignored, genes and drugs get emphasized — overemphasized.

I have been interested in this hypothesis for many years and, with my students and colleagues, have investigated it in my laboratory from several perspectives. For me, it has been the age-old question of Nature (genetic code) versus Nurture (nutrition and other environmental factors). In research on laboratory rats, we compared in many ways the relative effects of chemical carcinogens versus nutrition on cancer development. The chemical carcinogen that we most studied was aflatoxin, a mold toxin that causes liver cancer in rats. In fact, it is the most potent chemical carcinogen known, capable of causing cancer in virtually 100 percent of the rats that are exposed. Based on my observations of liver cancer in children in the Philippines, and on experimental animal research in India, we eventually learned, after about 15 years of research, that the consumption of animal-based protein, not the carcinogen, was the primary factor determining how fast tumors would grow. Decreasing consumption of animal protein (i.e., casein, the main protein of cow’s milk) or replacing it with plant protein (i.e., wheat gluten or soy protein) dramatically decreased the growth of tumors initiated with aflatoxin. The aflatoxin acted by modifying the gene (or genes) starting the cancer, but then this gene (or genes) became expressed only when animals were fed animal-based protein. Nutrition (i.e., protein) was overriding the genes (mutated by aflatoxin), even when using relatively modest levels of cow’s milk protein but very high doses of aflatoxin.

We also did much the same thing with experimental mice after mutating their cancer-causing gene by the hepatitis B virus. Again, animal protein consumption controlled the expression of the gene causing the cancer, turning it on when fed and turning it off when not fed. And so it went with other chemical carcinogens, other cancers, and other nutrients. The nutritional effect was far more significant than the gene effect — even when the gene effect was biased in favor of causing cancer.

Nutritional effects on experimental cancer in laboratory animals, however, needed to be confirmed in human studies. Our large comprehensive study of human diets and disease in China was therefore undertaken and was entirely consistent with our experimental animal results. Many other kinds of studies also confirm that nutrition overrides genes during the development of disease. One type of human study (now 100 or so) shows that people who migrate from a country with high disease risk to a country with low disease risk get the risk of the country to which they move. Most importantly in these studies, their genes remain the same and only their diets and lifestyles change. Therefore, the diet (and other lifestyle factors) is causing the altered disease risk, not the genes.

Another kind of experimental study design, for which there are several examples, involved comparison of disease occurrence for identical twins (with the same genes) versus non-identical twins (with individual sets of genes like other siblings). Identical twins should get the same cancers, etc., if genes were primarily responsible. However, there is little if any evidence that this is the case. And even where there is evidence of some concordance among identical twins (i.e., same disease consistency), it could be due to the dietary and environmental factors being more similar among identical twins than among non-identical twins.

These and many other findings have persuaded me that even though every disease (and other biological events) begins with genes, especially polymorphisms, this does not mean that genes are the primary cause. This idea is widely accepted by people who are serious readers of the evidence. On the basis of the migrant studies published 25-30 years ago (mentioned above), it was concluded that genes cause only 2-3 percent of cancers. Yet, reading the popular press, one would hardly get this impression.

See if you can figure this out: (a) virtually all Western diseases (cancers, heart disease, etc.) are caused by genes and (b) virtually no Western diseases are caused by genes. Both of these statements are correct; it depends on what is meant by the word cause. If one is talking about the first step in the chain of events that lead to disease, then (a) is correct. But if one is talking about causes that control gene expression —and therefore disease occurrence, then (b) is correct. Practically speaking, it is (b) that we live by. We can do virtually nothing about our own genes and I believe that there is little use in trying because it is scientifically illogical and naive. In contrast, we can control gene expression by the food that we eat. The evidence is now becoming so persuasive. And here is the main point: the nutritional components of plant-based foods — when consumed as food — are overwhelmingly capable of silencing disease-producing genes. This is a major reason why consuming plant-based foods is associated with lower rates of cancer, heart disease and other chronic degenerative diseases common to industrialized societies.

One final thought occurs to me. It concerns the U.S. National Cancer Institute (NCI, of the U.S. National Institutes of Health, NIH), who provides most of the cancer research money. Even though it is generally and conservatively acknowledged by NCI that diet and nutrition account for 10 times more cancers than do genes, why, then, is 10 times more funding — at a minimum — given to genetic research? I suspect you know why. Genetic research serves the drug industry; dietary research only serves the public. To add insult to injury: the taxpaying public pays the bill twice — taxes to do the research and drug costs to fix their diseases. What are we pretending not to know?


©Copyright 2004. All Rights Reserved. Health Science is the publication of the National Health Association. This article reprinted from the Spring 2004 issue.
























 

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