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How to Prevent Prostate Problems: A Complete Guide to the Essentials of Prostate Health
How to Prevent Prostate Problems: A Complete Guide to the Essentials of Prostate Health
How to Prevent Prostate Problems: A Complete Guide to the Essentials of Prostate Health
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How to Prevent Prostate Problems: A Complete Guide to the Essentials of Prostate Health

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The author presents valuable research material on every conceivable aspect of the prostate in a cogent and easily accessible narrative. This book defines exactly what the prostate is and how it is vulnerable to disease. Contains an excellent glossary of terms, a list of helpful resources, and an index.
LanguageEnglish
Release dateFeb 1, 2009
ISBN9781591205043
How to Prevent Prostate Problems: A Complete Guide to the Essentials of Prostate Health
Author

Frank Murray

Frank Murray is Associate Professor in Environmental Systems, Murdoch University, Australia,

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    How to Prevent Prostate Problems - Frank Murray

    Introduction

    As men age, many of us succumb to a number of prostate—not prostrate—irregularities, such as prostate cancer, prostatitis, and benign prostatic hyperplasia (BPH). Except for skin cancer, cancer of the prostate is the most common malignancy in American men, according to the National Cancer Institute, Bethesda, Maryland. Almost 219,000 men were diagnosed with prostate cancer in 2007, resulting in almost 27,000 deaths.¹

    The majority of men with low-grade, early prostate cancer—that is, confined to the gland—live a long time after diagnosis. Even without treatment, many of these men will not die of prostate cancer, but instead will live with the disease until they eventually die from some other, unrelated illness, the Institute said.

    While all men are at risk, the most common risk factor is age. Over 70 percent of men diagnosed with prostate cancer are over the age of sixty-five. African-American men have a higher risk of this cancer than other men. Dramatic differences in the incidence of prostate cancer are also seen in various countries, and there is some evidence that a less-than-perfect diet accounts for some of these differences. Genetics also appear to play a role, especially for families in which the diagnosis is made in men under the age of sixty. The risk of the disease rises with the number of close relatives who have this cancer.

    From 2000–2004, the median age of diagnosis for prostate cancer was sixty-eight years of age, the Institute added. This breaks down to 0.5 percent between thirty-five and forty-four; 8.4 percent between forty-five and fifty-four; 27.3 percent between fifty-five and sixty-four; 36.7 percent between sixty-five and seventy-four; 22.4 percent between seventy-five and eighty-four; and 4.7 percent from age eighty-five on.

    Based on cases diagnosed in 2000–2004 from seventeen geographic areas, the age-adjusted incidence of prostate cancer is 168.0 per 100,000 men annually. A further breakdown reveals these statistics: African-Americans (255.5 per 100,000 men); Whites (161.4); Hispanic (140.0); Asian/Pacific Islanders (96.5); and American Indian/Alaskan natives (68.2).

    The overall five-year survival rate for 1996–2003 from seventeen geographical areas was 98.4 percent, breaking down to 98.9 percent for white men, and 94.9 percent for African-Americans, the Institute said.

    It is estimated that one in six men will develop prostate cancer in their lifetime. As an example, 8.52 percent of men will develop prostate cancer between their fiftieth and seventieth birthdays.

    Since prostate cancer is a slow-growing malady, with proper medical intervention, people can live for many years. Some prominent prostate cancer survivors include Senator John Kerry (D., Mass.); Rudy Giuliani, former mayor of New York; General Norman Schwarzkopf; media mogul Rupert Murdoch; General Colin L. Powell; Joe Torre, former manager of the New York Yankees; actors Robert De Niro, Harry Belafonte, Jerry Lewis, and Mandy Patinkin.

    To save lives and detect prostate cancer and other prostate irregularities early on, many researchers recommend that men forty-five years and older should have a periodic digital rectal exam (DRE) and the prostate-specific antigen (PSA) blood test. PSA is a protein that circulates in the blood, and elevated levels of PSA may be a sign of prostate cancer.

    As for older men, many researchers suggest watchful waiting, in which the person’s condition is monitored, and treatment is not recommended until symptoms change. The reasoning for this is: a) the PSA test is not always accurate; b) anxiety over whether or not a man might have cancer could be too stressful for some men; and c) older men can often live with the cancer, but ultimately succumb to some other unrelated illness.

    Numerous studies have suggested that men with prostate cancer are often overtreated, which wastes resources and money, as well as needlessly subjecting men to the pain and risks of surgery or radiation, reported Denise Grady in the July 29, 2007, issue of The New York Times.²

    A 2006 study of men treated from 2000–2002 found that, among 24,405 men with cancers considered to be relatively low risk, 10 percent were overtreated with radical surgery, and 45 percent with radiation, she added.

    The surgeon’s expertise is crucial in treating prostate cancer, Grady continued. A study published in 2007 in the Journal of the National Cancer Institute found that the cancer was less likely to come back in men whose doctors had performed 250 or more operations. Their recurrence rate was 10.7 percent, compared with l7.9 percent of men whose doctors had performed the operation only ten times.

    Since doctors, urologists, and other health professionals continue to discuss which men should be tested for prostate problems, at which age, and so forth, this prompted Peter C. Albertsen, M.D., and Judith Fine, BA, of the University of Connecticut Health Center in Farmington, and James A. Hanley, Ph.D., of McGill University, Montreal, Canada, to discuss, in the May 4, 2005, issue of the Journal of the American Medical Association (JAMA) a study which documented twenty-year outcomes for a population-based cohort of 223 men diagnosed with localized (it did not spread to other areas of the body) prostate cancer between 1977 and l984. They noted a substantial increase in prostate cancer mortality among the forty-nine men who were alive more than fifteen years following diagnosis.³, ⁴

    In 1998, Albertsen, et al. published a competing risk analysis of 767 men, ages fifty-five to seventy-four, with clinically localized prostate cancer at diagnosis, who were treated with observation (watchful waiting) or androgen-withdrawal therapy alone.

    The purpose of that analysis was to provide an estimate of the natural progression of prostate cancer if treated conservatively, Albertsen said. Because these men have been followed up continuously by the Connecticut Tumor Registry, we had an opportunity to extend our follow-up to twenty years to determine whether prostate cancer mortality rates declined, remained constant, or increased after fifteen years.

    Albertsen added that extended follow-up of their competing risk analysis suggests that prostate cancer progression rates do not increase after fifteen years of follow-up. Therefore, men with low-grade prostate cancer have only a small risk of prostate cancer progression after twenty years of management by watchful waiting or androgen withdrawal therapy alone.

    He added that "these results do not support aggressive treatment of localized, low-grade prostate cancer. Men with poorly differentiated disease (Gleason scores of 7 to 8–10) have a high risk of death from prostate cancer. For example, only three men were alive after twenty years. Men with moderate grade disease (Gleason scores of 5–6) have an intermediate cumulative risk of prostate cancer progression after twenty years of follow-up.

    Our data provide what are likely overestimates of prostate cancer progression when men are treated by observation or androgen-withdrawal therapy alone, Albertsen continued. Only through randomized controlled trials designed to measure the efficacy of screening and treatment for prostate cancer can we answer questions concerning which patients may truly benefit.

    Commenting on the Albertsen, et al. study in the same issue of JAMA, Peter H, Gann, M.D., Sc.D., and Misop Han, M.D., of the Feinberg School of Medicine, Northwestern University, Chicago, Illinois, said the study reinforces the importance of Gleason scores in predicting outcomes for men with clinically localized disease. Beyond that, they added, interpreting the importance of these results for patients requires more subtle considerations.

    The true natural history of today’s cases of localized prostate cancer remains a mystery, Gann and Han continued. The most important answers to the most important questions are likely to come from clinical trials, such as PIVOT, which are comparing patients randomized to watchful waiting or surgery, and from PSA screening trials currently under way in Europe and the United States. Multivariable models for predicting pathological state before surgery, such as the Partin tables, are already used by clinicians and patients to assist in choosing therapy options for clinically localized disease.

    They went on to say that, over the next twenty years, there will be pronounced improvements in the ability of these models to predict not only true stage, but outcomes based on blood or biopsy samples available at diagnosis. These predictors will come from more detailed analysis of routine biopsy features, and also from the application of new molecular technologies. Indeed, one thing safe to predict is that, in twenty years, commentators discussing the natural history of prostate cancers diagnosed in the early twenty-first century will conclude that what happened in those cases is too difficult to interpret or altogether irrelevant.

    While the debate for testing, treatments, etc., continues, I hope this book will open your eyes as to what prostate and urinary problems arise as men get older, and what options they and their doctors have in dealing with the situation.

    By following the diet, lifestyle, and supplement recommendations in this book, you may be able to prevent or delay prostate problems. If you have to undergo treatment, the chapters on prostate cancer, prostatitis, and benign prostatic hyperplasia (BPH) can give you and your doctor the pros and cons of the various treatments, since many of them are very stressful and may actually not be necessary.

    Frank Murray • New York, NY

    1

    What Is the Prostate?

    The major internal male sex organs are composed of the two testicles (testes), with an epididymis, vas deferens, the seminal vesicles, Cowper’s glands, prostate gland, urethra, and the penis, according to the Columbia University College of Physicians and Surgeons Complete Home Medical Guide.¹

    The testes produce sperm and the hormone testosterone, while the sperm mature in the epididymis. The vas deferens are two firm tubes that extend from the epididymis to the prostate.

    The sperm travel through the tubes and are stored at their upper ends until they mix with the secretions of the seminal vesicles and prostate just prior to ejaculation, the publication reported. The exact purpose of the vesicles is unclear, but it is known that they contribute a portion of the ejaculate. The sperm actually account for only a tiny fraction of the seminal fluid or ejaculate.

    The Cowper’s glands, named after English surgeon William Cowper (1666–1709), are two small glands lying on either side of the urethra below the prostate gland. It is believed they secrete a small amount of clear, sticky fluid that is visible prior to ejaculation. This fluid often contains sperm, making withdrawal of the penis from the vagina prior to ejaculation an ineffective means of contraception.

    The urethra is the tube that goes from the bladder through one of the spongy cylinders in the penis and ends in a slit at the head of the penis. Urine and seminal fluid travel through the urethra at different times.

    The prostate gland is a walnut-sized structure situated deep in the lower abdomen beneath the bladder. During ejaculation it secretes a substance into the seminal fluid that is thought to stimulate the activity of the sperm. The gland may become a site of growths or infections, and since it is near the bladder and the urethra, any prostate disorder is likely to interfere with the normal flow of urine, reported The Physicians’ Manual for Patients.²

    Enlargement of the prostate is one of the most common problems that affect the gland. Other conditions include prostate infection, also called prostatitis, cancer of the prostate, and benign prostatic hyperplasia (BPH).

    It is estimated that 11 percent of men have never heard of prostate trouble, and perhaps an even larger number mispronounce it prostrate instead of prostate, said the Medical Care Yearbook.³

    The prostate is not a single gland but rather a collection of thirty to fifty small, gland-like clusters that are organized into several lobes held together by fibrous connective tissue. If the prostate resembles a doughnut, then the urethra runs through the doughnut hole. A valve allows urine—but not semen—to flow when the penis is flaccid. When the penis is erect, the valve blocks urine but permits semen to pass through.

    The prostate is almond-size in boys, but during puberty the male sex-hormone testosterone stimulates it to mature to the size of a walnut, and it produces seminal fluid. Unlike other glands, the prostate grows with age. In some men it can reach the size of an orange or grapefruit. However, around age fifty, prostate overgrowth (hypertrophy) causes noticeable problems in about 20 percent of men. By age fifty, that figure can reach to more than 50 percent.

    A prostatectomy is the surgical removal of the prostate gland. This procedure is usually performed when enlargement of the gland is causing obstruction to the flow of urine, reported Charles B. Clayman, M.D. The operation may also be performed to treat prostatitis or prostate cancer. The usual operation involves a transurethral prostatectomy, which is performed with a cystoscopy. If the gland is greatly enlarged, retropubic prostatectomy—which surgically removes the prostate through an incision made in the wall of the abdomen—may be necessary.

    When the catheter and drainage tube have been removed, the patient can begin to pass urine as the bladder fills in the normal way. In the beginning, urination may be frequent and sometimes painful. In some cases there is mild incontinence—inability to prevent the release of urine or feces—for several weeks. Patients are encouraged to drink lots of fluid to help wash out any remaining blood in the urine.

    Rarely, bleeding after the operation is severe, and blood transfusions may be required, Clayman said. Blood clots that may form within the bladder can be washed out through the catheter.

    A hospital stay of three to five days is usually necessary for transurethral prostatectomy, and between eight to ten days for the retropubic operation. After several weeks, patients can generally resume their regular activities, including intercourse.

    A prostatectomy may affect potency or sexual sensation in a small number of men. Most of the men are sterile following a prostatectomy, since semen is expelled backward into the bladder instead of being ejaculated. Seminal fluid in the bladder is said to be harmful, and it is excreted in the urine.

    The term prostaglandin is a misnomer, since it was initially given to substances which were originally thought to have originated from the prostate gland, reported Foods and Nutrition Encyclopedia.

    These hormone compounds—some sixteen prostaglandins have been identified—are made in various tissues of the body from arachidonic acid and other derivatives of linoleic acid. They are important in the control of blood pressure, pancreatic functions, the regulation of gastric secretions, the release of pituitary hormones, and smooth-muscle metabolism.

    These highly potent substances have been called local hormones or tissue hormones because they do their work near the areas in which they are produced, as distinguished from most circulating hormones, which aim at more distant targets, the publication added.

    2

    The Complex Case of Cancer

    Cancer is an ancient disease that was described by Hippocrates (c. 460–377 B.C.) and Galen (c. 130–201 A.D.) under various names. At the end of the nineteenth century, physicians were able, for the first time, to diagnose cancer in medical terms. But only in 1915, after two Japanese researchers, K. Yamagiwa and K. Ichikawa, had shown that continuous application of coal tar to rabbits’ skin produced a malignancy, were experimental studies on cancer begun, according to Mukti H. Sama, Ph.D.¹

    Cancer research was not especially active at the beginning of the twentieth century, probably because the mortality rate was not very high. For example, in 1900, cancer was only the ninth leading cause of death in the United States. By the 1950s, the mortality rate had doubled, and cancer emerged as the second leading cause of death. To date, over 250 kinds of cancers with different causes, symptoms, and degrees of lethality have been discovered, Sama added.

    Although there are many theories regarding the causes of cancer, the fundamental underlying theory is that the genetic material, the DNA of the cell, has been changed, Sama said. The various theories have attempted to explain how this change was brought about.

    For example, the DNA of a cancer cell is slightly different from that of a normal cell. This means that the sequence of the bases—adenine (A), guanine (G), thymine (T), and cytosine (C)—in a given strand of DNA is not the same. These sequences dictate the sequence of the transcribed messenger RNA, which, in turn, results in abnormal proteins in the cancer cells’ DNA sequence. These new proteins influence the mechanisms of growth control in such a way that cell division continues indefinitely.

    An important characteristic of a cancer cell is its lack of contact inhibition, Sama continued. Normal cells reproduce by dividing, but they stop dividing when the number of cells reaches a certain point. Exact control of cell division is a basic function of all multicellular organisms. The growth-control signal is thus transmitted by various proteins that interact with the protein receptors in the cell surface.

    The basic change in the DNA, known as mutation, can be caused by many factors, such as ultraviolet light, ionizing radiation, chemicals, free-radical scavengers, and viruses, Sama said. Mutation does not necessarily cause cancer. This occurs only if proteins that result from mutation affect cellular growth-control mechanisms.

    In the l930s and l940s, Charles B. Huggins (1901–1997), a Canadian-American surgeon, working in Chicago, Illinois, noted that the prostate gland—a common site for cancer—under the control of the male sex hormone secreted by the testes, produces regression in a high proportion of prostatic cancers by surgical castration, and later by medical castration that is accomplished by giving female sex hormones to the patients, reported Ewan Cameron, MB, and Linus Pauling, Ph.D.²

    Since prostate cancer was then almost untreatable, except by radical and debilitating surgery, this was a very significant therapeutic advance. Thus, the authors said they had clear examples that by either removing the source of, or medically suppressing, a particular hormone, regression of cancer in the target organ can be induced.

    Huggins found that using estrogen to block male hormones could also slow the growth of prostate cancer. Additionally, he showed that removing the ovaries and adrenal glands, which produce estrogen, could reverse tumor growth in some breast cancers. Drugs are now used to inhibit estrogen production. For his work, he shared a 1966 Nobel Prize with Payton Rous (1879–1970).³

    Huggins also pioneered orchiectomy (castration), which is performed for palliation or cure of prostate cancer.

    In spite of the numerous gadgets that today’s medicine has to image, diagnose, and track a tumor, there is an easier way to go about things, reported Alice Park in the June 15, 2007, issue of Time. She was discussing papers read at the American Society of Clinical Oncology (ASCO), which was held in Chicago in June 2007. Their answer to exposing a growing tumor’s secrets was to simply draw a little blood. Tests can detect proteins on cancer cells released by a tumor that is itself only dozens of cells large. Fortunately, most of these migrating cells die during their journey.

    Others are more menacing—pioneers programmed to send new growth in distant tissues, Park added. Either way, as epithelial cells—closely packed, multilayered cells of which most solid tumors are made—they are oddballs in their new fluid environment.

    Unfortunately, tests only reveal a certain amount of information. Suppose you could do more than collect the enemy cells; suppose you could, instead, interrogate them for specific information? That’s where the new tests come in.

    Researchers are starting to identify proteins on the surface of tumor cells that might signal a faster-growing, more aggressive type of cancer, Park continued. Other protein signatures may hint of a more advanced tumor that is poised to metastasize (move to other parts of the body). Both can help doctors craft more personalized therapies that match the right treatments to the right patients at the right time, thus improving effectiveness, lowering the costs of hit-or-miss treatments, and reducing toxic side effects.

    Added Gordon Mills, M.D., of the M.D. Anderson Cancer Center in Houston, Texas, We can look at tumors for changes at the DNA, RNA, and protein levels. It certainly gives us a way of looking at what is happening inside a tumor, and that’s very exciting.

    Currently, doctors collect a sample of the tumor tissue, a procedure that isn’t always possible if it is very small or inaccessible, or its location is not known, Park said. Tissue sampling can dislodge cells and cause them to spread the cancer. A blood draw is easy and simple and bypasses these risks. Doctors can now learn more about how treatment is progressing by tallying the number of circulating cancer cells and better understanding what that head count means.

    At the Chicago conference, researchers from the United States, United Kingdom, and the Netherlands reported that after about a month of treatment, men who had advanced prostate and colon cancers and lower circulating cell counts survived twice as long on average as those who had higher levels. More cells in the blood should suggest the drugs are not working and it is time for a different chemotherapy regimen.

    Added Mills, Such blood-based diagnostics may not yet have beaten cancer, but they are ‘the holy grail’.

    When a person is approached about being screened for cancer, it generates a certain amount of apprehension somewhat akin to the white coat syndrome, and it is, therefore, up to the clinician to assuage these fears.

    In a lucid article in the June 6, 2001, issue of the Journal of the American Medical Association (JAMA), H. Gilbert Welch, M.D., of Veterans Affairs Medical Center, White River Junction, Vermont, and the Dartmouth Medical School in Hanover, New Hampshire, pointed out how important it is to understand that cancer can appear in the interval between screening tests. These cancers are not detectable during an initial screening test, but are clinically obvious before the next test.

    Not surprisingly, interval cancers are the fastest growing tumors, Welch said. They are among the worst forms of cancer, more deadly than those detected by screening. Understanding that screening misses these cancers, it is important that patients do not give up on screening. If others develop cancer despite screening it is important because it invalidates a common belief that anyone who dies of cancer and was not screened would have been saved if only he or she had had a test.

    He goes on to say that physicians need to tell their patients that diagnostic tests are imperfect. Often, those with abnormal screening tests results do not have cancer, but before they are declared cancer-free, they may have to go through multiple tests, some of which are unpleasant and have serious complications. Additional testing may even become a regular event. Throughout the process, many will worry about whether or not they actually have cancer.

    Most physicians have developed some language to prepare patients for false-positive test results, Welch continued. But physicians are not as good at preparing patients for the reality that extra testing may become quite invasive and go on for a long time—perhaps indefinitely. More and more patients are undergoing colonoscopies every two to five years, undergoing additional pelvic examinations, colposcopies, cryoauterizations, and having repeated prostate biopsies. Patients should understand that more frequent testing can be a consequence of screening.

    This is the current harm of screening, he continued. Screening can detect pseudodisease, an abnormality that meets the pathologic definition of cancer, but either does not progress, or grows so slowly that an individual dies from another cause before the cancer ever reveals symptoms. Mounting evidence suggests that a cancer reservoir that is much larger than what is known to be clinically relevant exists in humans, especially for breast and prostate cancer. As screening tests become increasingly sensitive, the detection of pseudodisease is bound to become an increasingly common problem.

    As people become older, their competing risks for death increase, making pseudodisease more likely, Welch said. Given the common definition of cancer, however, the concept of pseudodisease is not familiar to most. But with the increasing detection of prostate cancer, internists and geriatricians have gotten some experience trying to describe it: Some men die from cancer, many more die with it.

    Discussing a patient’s concern about screening can feel ethereal and frequently conclude with sympathy, not an actionable plan, Welch added. Given the limited time for clinic visits, one service may compete with the other. However, the downside of screening is not frequently discussed, and the evidence that it exists is anecdotal. But it is definitely real, and the more time a clinician spends describing and communicating results and following up abnormal findings, the less time there is to spend with the patient’s concerns.

    The choice of screening hinges on the probability of various outcomes and how people feel about them, Welch said. The truth is that screening has multiple effects. A few people may have their lives saved, a few will die anyway. Many more will face testing cascades and uncertainty, some will be treated unnecessarily, and a few may die from treatment. Finally, all of them can be distracted from more important health problems. In short, for many, whether or not to be screened is a close call that needs to be weighed.

    Normally, cells grow and divide to form new cells as the body needs them, but when cells get old, they die, and new cells are needed to replace them. However, this natural process can sometimes go awry, and new cells form when the body does not need them. These extra cells can form a mass of tissue called a growth or tumor.

    Tumors Can Be Benign or Malignant

    Benign tumors are not cancer.

    • Benign tumors are rarely life-threatening.

    • Benign tumors can generally be removed, and they usually do not grow back.

    • Cells from benign tumors do not invade the surrounding tissues.

    • Cells from benign tumors do not spread to other parts of the body.

    Malignant tumors are cancer.

    • Malignant tumors are generally more serious than benign tumors, and they may be life-threatening.

    • Malignant tumors can often be removed, but they can grow back.

    • Cells from malignant tumors can invade and damage nearby tissues and organs.

    • Cells from malignant tumors can spread (metastasize) to other parts of the body. The cancer cells break away from the original (primary) tumor and enter the bloodstream or lymphatic system. The cells then invade other organs and form new tumors that damage these organs. The spread of cancer is called metastasis.

    Scientists in Europe and the United States have identified at least ten previously unknown gene variants linked to prostate cancer susceptibility, reported Joan Stephenson, Ph.D. Although researchers have not yet identified the specific genes flagged by these markers, some of the specific sites are possible candidates, including KLK3, the gene that decodes PSA; CTBP2 that is found in prostate tissue; and MSMB, a gene that encodes a protein produced by the prostate and is associated with a recurrence of the disease after a prostatectomy.

    3

    An Ounce of Prevention

    You may be able to reduce your risk of prostate cancer by changing the way you eat, according to Prostate Cancer: What You Need to Know Now, a publication of the American Cancer Society in Atlanta, Georgia. The Society recommends eating a variety of healthful foods, with an emphasis on plant sources, and limiting your intake of red meats, especially those that are high in fat or highly processed.¹

    They suggest that you eat five servings of fruits and vegetables daily. Beans, bread, cereals, grain products, pasta, and rice are also recommended.

    As discussed in Chapter 13, pink grapefruit, tomatoes, and watermelon are rich sources of lycopene, an antioxidant that helps to prevent damage to DNA and may help lower the risk for prostate cancer.

    Some studies have suggested that

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