If you consider the vast number of divisions necessary to maintain 75 trillion living cells, the chances are that sometime, somewhere, something will go wrong. And it does. Sometimes the DNA contained in each cell, which must replicate itself completely before each cell division, becomes damaged. Sometimes it doesn't copy correctly. When the cell divides, the new daughter cells can contain this error, a mutation.

Luckily, most of these mutations do not matter. They do not occur in sections of the DNA in which there are active genes or do not disturb the action of a gene. The body doesn't even notice them. In contrast, lethal mutations are so significant that they kill the cell right away, at which point the mutation disappears and is not passed on. Probably 99.9 percent of all the mutations you undergo belong to one of these two classes.

Between the harmless and the lethal mutations is a third class of mutations, a tumor-causing mutation. These are the rare cancer-causing mutations that tell the cell to begin growing and dividing uncontrollably. Your body has a regulatory system that keeps the number of cells in your body at a more or less constant level. The genes that regulate this process are known as cell-cycle genes because they tell the cell when to divide, to grow, and to divide again. Some of these cell-cycle genes are known as 'proofreader' genes: they scan the DNA when it replicates, ensuring that no mutations have been acquired. If a mutation has occurred, the proofreaders either fix it or kill the cell. A few of these cell-cycle and proofreader genes are also known as oncogenes (cancer genes) because mutations in these genes are tied to the development of cancers. If a gene that is supposed to tell a cell to stop growing stops working— that is, mutates—then the cell grows uncontrollably, dividing faster than it should. Moreover, its daughter cells also inherit the mutation and grow out of control themselves. The effect multiplies, and soon there is a mass of rapidly dividing, quickly growing cells, a tumor, 'the Big C.'

Generally, your body is able to recognize abnormal cells and destroy them before they cause harm. By means of the proofreader genes and other anticancer genes, most abnormal cells are rooted out and excised. The general immune system also destroys many precancerous and early cancer cells. The exact mechanisms of this response are poorly understood: the immune system is not always able to recognize the differences between cancer cells and normal cells. However, it has long been known that people with healthier immune systems are less likely to develop cancers and that precancerous cells are often rooted out by the body. Research is increasingly showing the role that the general immune system plays in cancer prevention. Hence, your body prevents cancer by a double mechanism—one genetic, one immunologic. Cancers— the life-threatening kind—occur when a mutation develops, coupled with a failure of both protective systems, when each has 'aged' too much to stop the cell from taking over as a cancer.

The longer you live—that is, the more divisions your cells undergo—the more likely it is that you will undergo a mutation in a cell-cycle gene. It's the law of averages. A mutation assaults your first line of defense—the line of defense within the cell that protects the body. By exposing your body to harmful chemicals, radiation, or the buildup of free radicals, you increase your rate of mutation exponentially. The odds that you will undergo a mutation in the wrong place increase dramatically.

As you age, your second line of defense, your immune system, tends to be less vigilant and does not as readily detect and destroy these abnormalities. The weaker your immune system, the more likely that it will not provide the necessary backup. The longer you live, the more likely that you will get improper cell divisions, the more likely that the DNA in a specific cell will contain a mutation, and the more likely that your immune system won't be there to catch a mistake. The most important thing to remember is this: You can slow, and even reverse, the rate of ageing of the immune system.

The RealAge strategy for keeping your immune system young and avoiding cancer is twofold: (1) decrease your exposure to factors that increase DNA damage in your cells and (2) adopt behaviors that strengthen your immune response. You keep your RealAge young by avoiding exposure to factors that cause mutations and by boosting your immune system so it scavenges those mutations as well as possible. Doing all the things you can do to keep your immune system youthful can make your RealAge over twenty years younger.

Cancer Genes: What Do They Mean to You?

Although the vast majority of cancers are thought to stem from environmental causes, it is worth considering those people who have an inherited genetic predisposition to the disease. Almost every week a major news story reports the discovery of a new cancer gene. 'Researchers have identified the breast cancer gene.' 'Scientists announce the discovery of the colon cancer gene.' Most of these genes—or, more precisely, genetic mutations—run in families, isolated populations, or ethnic enclaves. They are mutations that lie in the germ line cells—that is, in the egg and sperm—and that get passed down from parent to child. They are often identified in populations that are endogamous, that is, in which people marry within the same group. The propensity for these specific genetic mutations occurs in such populations because the more closely related people are, the less their genetic variation. Since many of these mutations are recessive, appearing only when both parents are carriers, the trait is more likely to show up when both parents have a similar genetic background. Also, it is easier for researchers to trace genetic predisposition to a disease when they can trace a cultural and historical context, linking family histories with biologic events.

If you belong to a population that is at risk of a genetically linked cancer, the discovery of a gene can have an immediate impact. You can be tested for the gene to learn whether you have inherited it. Although this sounds ominous, and getting such tests can be frightening, there is a more positive way of thinking about it. By getting tested, you will know whether you have the gene. If you don't have it, you can quit worrying. If you do have it, you can minimize the risks and the ageing it can cause.

If you do not belong to the group at risk, the news about cancer genes is less immediate but no less important. By identifying mutated forms of a gene, researchers are better able to understand what a gene does when it functions normally and they are better able to target specific gene pathways that are implicated in specific forms of cancer. By understanding the biochemical processes by which a cancer grows, scientists get closer to understanding how we might prevent such cancers. Because all cancers are genetic—whether they are caused by an inherited mutation or an acquired one—the more we learn about the genetics involved in the development of cancers, the better prepared we will be to treat all cancers—and to prevent them.

Another thing: Inheriting a cancer gene does not mean that you will get cancer—it means that you have an increased risk of getting that particular type of cancer. People who inherit a form of a gene that causes cancer in 100 percent of the cases rarely survive childhood. When scientists say that they have 'found' a cancer gene, they mean that they have found a gene that, when mutated, increases a person's risk. For example, even though scientists refer to the recendy discovered BRCA-1 gene as the breast cancer gene, they are not being accurate. No woman really has a breast cancer gene—a gene whose function is to cause cancer. Instead, she may have inherited a copy of a gene that contains a specific mutation affecting the ability of that gene to function properly. The side effect is to increase her predisposition toward breast cancer.

Many of the so-called cancer genes are two-hit genes. Because we inherit chromosomes (DNA) from each parent, in many instances we have two working copies of a particular gene. If one doesn't work, the other covers for it. In many genetically linked cancers, a person inherits a working copy of the gene from one parent and a nonworking copy from the other. The odds of that person getting an acquired mutation in the one working copy in a particular cell of the body are much higher than the odds for people who have two working copies of the gene. People with two working copies would need to get two acquired mutations—a mutation in each copy of the gene in the same cell—to develop the same cancer. Other cancers require two mutations in two different genes, or the same copy of a gene. One mutation usually won't cause the cancer, but two will. This is true, for example, with certain eye cancers called retinoblastomas. Because there are millions of cells in the eye, the chances of an acquired mutation occurring in any one cell is relatively high. The chances of two acquired mutations occurring in exactly the right places is relatively low. However, we know that certain people are born with one of the mutations already. Hence, the odds of their developing another mutation over their lifetimes are extremely high, making them genetically predisposed to developing this type of cancer.

Recently, inherited links have been discovered for certain types of breast and colon cancers, allowing us to identify people who are predisposed to developing each of these diseases. Such mutations account for a minority of all such cancers. For example, in breast cancer, genetic predisposition is thought to account for less than 4 percent of all cases. However, genetic predisposition is implicated in nearly a third of all breast cancers that develop in women under age forty, showing just how much having one of these genes can affect one's risk.

Testing positive for a cancer gene can make your RealAge dramatically older, as you would then have the same likelihood of developing cancer as a much older person. For example, a thirty-five-year-old woman who tests positive for the BRCA-1 breast cancer gene and whose mother and sister both developed breast cancer before age forty has a RealAge that is seventeen years older. That is, her RealAge would be fifty-two. By knowing she has the gene, she can make choices that make her RealAge younger. The dilemmas involved in this scenario are extremely complex, and individual counseling is recommended.

Identifying cancer genes is a big step for science. Unfortunately, this research is still in the beginning stages. The more we understand about genetically inherited cancers, the more we will understand about cancers in general. For example, the recent identification of a specific mutation in a gene linked to an increased risk of colon cancer among Ashkenazi Jews has helped researchers identify a gene pathway that is believed to be implicated in as many as 90 percent of all cases of colon cancer. That discovery opens numerous doorways for treatment and prevention. There are numerous other examples. The more we learn, the better prepared we will be to stave off the ageing that cancer can cause.

What If You Get Cancer?

How Does It Affect Your RealAge?

No doubt some of you are cancer survivors and most of us know someone who is. How much effect does a positive diagnosis have on a person's RealAge? Well, that depends. Clearly, some cancers are much more harmful than others. They attack the body much more quickly and aggressively. On the other hand, some cancers grow slowly, resulting in little damage. The removal of a tumor, chemotherapy, radiation, and other therapies can often stop the spread of a cancer throughout the body. Some people have a tumor removed in their thirties and live until their eighties. The effect of the disease on your ageing depends on the type of cancer you have, how it is treated, and how long you are free from cancer after treatment.

Let's use the breast cancer example again. A fifty-eight-year-old woman who has had a malignant lump removed from her breast without indication of significant spreading in the lymph nodes has a RealAge of sixty-five. If that same woman undergoes chemotherapy and still shows no signs of tumor growth in the next five years, her RealAge will shift from being seven years older to being only two years older. In general, the longer a person goes disease-free after treatment, the less effect a cancer diagnosis has on his or her RealAge.

The best thing, of course, is to avoid cancer altogether, and that means avoiding cancer-causing substances and strengthening the immune system so it can act as it did in your youth and effectively scavenge early cancers. By becoming as young as you can be, your immune system will be in better condition and more able to wipe out any possible cancer cells in your body. Fortunately, there are foods, supplements, and behaviors that can help you keep your immune system young.

Let's consider some of those elements. Diet, vitamins, exercise, and preventing stress are all key ways of slowing ageing of the immune system. In fact, these are so important, I have devoted whole chapters to those topics. Here, though, let's consider three examples of immune system ageing— prostate cancer, skin cancer, and periodontal disease. As diverse as they are, they have something in common—the failure of the immune system.

Let's start with prostate cancer. Here are two things that may help men prevent it.

Just for Men: Tomato Paste and Green Tea Help to Keep You Cancer-Free

Ask any man what he fears most about ageing, and he may tell you heart disease or cancer, but, in his heart of hearts, what he fears most is impotence. Impotence is psychologically and emotionally devastating. Since virility is a sign of youthful manhood, losing the ability to perform is something that makes men feel most acutely that their bodies are failing and that they are getting old. There are four major causes of impotence: arterial disease, stress, psychological upsets, and prostate problems. Of the four, prostate enlargement and cancers are by far the most common—and predictable—reasons for the loss of sexual function.

The prostate is a small gland at the base of the penis. As men age, the prostate tends to become enlarged and often cancerous. In fact, most older men show signs of having microscopic cancers in their prostates. The enlargement, from cancers and other causes (called benign prostate hypertrophy when it is not associated with cancer), can be painful and uncomfortable. A swollen prostate cuts off urine flow, increases the need to urinate, and often makes urination painful. Sexual performance can become limited. And that ages us—physiologically and psychologically. Although drugs can be given to reduce the size of an enlarged prostate, they are not especially effective and have side effects, such as impotence or an increased risk of cancer. Fortunately, there are ways of preventing prostate cancer and the ageing it causes.

Prostate cancer is the most common cancer found in men. Some 250,000 new cases are diagnosed each year, and it causes 40,000 deaths annually— second only to lung cancer among cancer fatalities for men. More than 60 percent of men over age eighty will develop cancerous prostate cells. For those of us who plan to live into our eighties—healthily, heartily, vibrantly, and as young as sixty-year-olds—we need to be especially careful to protect ourselves from this kind of cancer. The best weapon against prostate cancer, or any cancer, is to avoid getting it in the first place.

Treatments for prostate cancer—surgery, chemotherapy, and radiation— are just as devastating as all cancer treatments but have an added side effect: Almost all the therapies are associated with a significant loss of sexual function in more than 50 percent of the cases. Despite this grim news, there is something that can give us hope—the tomato.

Tomatoes and Lycopenes

Studies have shown that the risk of developing prostate cancer is as much as one-third lower among men who frequendy eat foods containing tomatoes or tomato paste than among men who rarely eat such foods. Men who eat tomato products ten or more times a week have significandy lower levels of prostate cancer—a 34 percent reduction in severe metastatic prostate cancers—than do men who eat tomatoes less than twice a week.

The reason appears to be the antioxidant power of tomatoes. A substance found in tomatoes—lycopene—apparendy helps retard or reverse the ageing of cells in the prostate that can promote cancer growth. Lycopene is one of several kinds of carotenoids that are known for their antioxidant properties (see Chapter 8). Carotenoids, pigments found primarily in yellow, orange, and red fruits or vegetables, are similar to vitamins in that they help facilitate specific chemical reactions. Unlike vitamins, we do not require them to survive. A key function that carotenoids perform is to attach to free radicals, packaging them so they can be washed out of the body and preventing them from damaging our cells and chromosomes. Since the prostate is especially vulnerable to damage from environmental factors, it is especially vulnerable to damage from free radicals. Hence, the importance of the antioxidant powers of lycopene.

A study investigating a wide range of populations in Hong Kong, Tokyo, Milan, New York, Chicago, and Albuquerque, found that the incidence of microscopic prostate cancer was the same for all groups, no matter their geographic location or genetic heritage. The chances that these microscopic cancers would develop into full-blown prostate cancer varied wildly across locations, with the number of fatalities due to prostate cancer differing significantly. The areas of the world with the lowest levels of severe, or metastatic, prostate cancer are Mediterranean countries, especially Greece and Italy—where tomato-based foods are central to the diet. In areas where tomato-based foods are not common, the risk of cancer increased markedly.

A long-running question about prostate cancer has concerned the increased risk of the disease for African American men. It is interesting to note that studies have found that African Americans are less likely to eat tomato-based foods. Although no studies have been undertaken to show with certainty that dietary differences account for the higher incidence of prostate cancer for this population group, the data suggest that such could be the case.

Tomato paste, raw tomatoes, and cooked tomatoes all contain lots of lycopene. Our bodies, however, cannot absorb lycopenes except in the presence of fat. Drinking a glass of tomato juice by itself or eating slices of raw tomato without salad dressing does not provide us with lycopene. Some experts question whether we can absorb lycopene from raw tomatoes even in the presence of fat. Tomatoes cooked lightly in oil—as in tomato paste or pasta sauces—result in a two - to threefold rise in lycopene concentrations in the bloodstream the day after ingestion. In contrast, people who drink lots of tomato juice do not show this rise in lycopene-levels because the juice lacks the fats that help the body absorb the nutrients. Although slight cooking appears best, raw tomatoes with a little olive oil, sun-dried tomatoes in oil, and probably even tomato juice eaten with a bit of cheese or other fat may also increase lycopene levels.

Studies have found that most men get their lycopene from tomato sauce on pizza. Although that is certainly one way of getting lycopene, pizza with cheese, not to mention pepperoni and sausage, tends to be extremely high in saturated fats. Ways of getting tomato products without so much fat include eating tomato sauces on pasta, eating a roasted tomato with a drizzle of olive oil as a salad, eating tomato-based soups, putting salsa on meats or salads, and even eating ketchup. 

For Women

A diet rich in carotenoids—the antioxidants found in tomatoes and other red, yellow, and orange vegetables—has many beneficial effects for everyone. Therefore, even though women cannot receive the lycopene benefit for prostate cancer, they should still eat a diet heavy in carotenoid-rich fruits and vegetables. 

Lycopene appears to have other benefits as well. A 1997 reanalysis of the data gathered in the historic EURAMIC study found that men and women with the highest levels of lycopene in their bodies had the lowest risk of arterial ageing. Although there has only been one study to date, the reduction in mortality from atherosclerosis was 65 percent. Translated into RealAge terms, that would make ten helpings a week of tomato paste produce more than a five-year younger benefit for the average fifty-five-year-old man.

If you are trying to build up lycopene levels in your blood, do not eat potato chips or other foods containing the new fat substitute olestra (brand name, Olean). This fat 'fake' leaches fat-soluble vitamins, such as D and E, from your system and dramatically reduces the amount of lycopene in the body. One study found that eating just six olestra chips every day for a month reduced the amount of lycopene in the body by 40 percent, and eating sixteen chips a day reduced lycopene by as much as 60 percent.

Green Tea: A Cure for Prostate Cancer?

Another substance that appears promising in the prevention of prostate cancer is green tea. Several East Asian studies found that men who consume large amounts of green tea appear to have lower rates of prostate cancer. Studies at the University of Chicago have isolated the hydroxy '8' molecule in green tea that retards prostate cancer in laboratory animals. This molecule is reputed to be one of the most powerful antioxidants yet discovered, even more powerful than vitamins E and C. However, the green-tea molecule is notoriously fragile. The freezing and dehydration processes that imported green tea must undergo destroy the chemical compound that is linked to the reduction of the growth of prostate cancer cells. Unfortunately, to get any benefit from green tea, a person must drink as much as fifty cups a day. So far, there are no commercially available pills containing the green-tea extract in its proper form. While doubt remains, green-tea extract may well be an aid in preventing prostate cancer. Keep your eyes open for any new information on the subject. An extract supplement may be available soon if the studies continue to show promising results. Other preliminary research indicates that green tea—and black tea, too—may have other cancer-fighting abilities.

In both examples of the prevention of prostate cancer, a nutrient in our diet can affect our risk of getting cancer. Eating is one way we interact with our environment and one way we can lessen the impact of environmental factors on our risk of developing cancer. Another environmental cause is, as most of us know, sunshine. How exactly does the sun age you?