Ronald W. Gumbs, Ph.D.

Do Cellphones Cause Brain Cancer?

2012-02-19T21:37:00.000-08:00

Do Cellphones Cause Brain Cancer?

Bruce Gilden/Magnum, for The New York Times

By SIDDHARTHA MUKHERJEE

Published: April 13, 2011

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On Jan. 21, 1993, the television talk-show host Larry King featuredan unexpected guest on his program. It was the evening after Inauguration Dayin Washington, and the television audience tuned in expecting politicalcommentary. But King turned, instead, to a young man from Florida, DavidReynard, who had filed a tort claim against the cellphone manufacturer NEC andthe carrier GTE Mobilnet, claiming that radiation from their phones caused oraccelerated the growth of a brain tumor in his wife.

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Bruce Gilden/Magnum, for The New York Times

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“The tumor was exactly in the pattern of theantenna,” Reynard told King. In 1989, Susan Elen Reynard, then 31, was told shehad a malignant astrocytoma, a brain cancer that occurs in about 6,000 adultsin America each year. To David Reynard, the shape and size of Susan’s tumor — ahazy line swerving from the left side of her midbrain to the hindbrain —uncannily resembled a malignant shadow of the phone (but tumors, like clouds, can assume the shapes ofour imaginations). Suzy, as she was known, held her phone at precisely thatangle against her left ear, her husband said. Reynard underwent surgery for hercancer but to little effect. She died in 1992, just short of her 34th birthday.David was convinced that high doses of radiation from the cellphone was thecause.

Reynard v. NEC — the first tort suit in the UnitedStates to claim a link between phone radiation and brain cancer — illustratedone of the most complex conceptual problems in cancer epidemiology. Inprinciple, a risk factor and cancer can intersect in three ways. The first isarguably the simplest. When a rare form of cancer is associated with a rareexposure, the link between the risk and the cancer stands out starkly. Thejuxtaposition of the rare on the rare is like a statistical lunar eclipse, andthe association can often be discerned accurately by observation alone. Thediscipline of cancer epidemiology originated in one such a confluence: in 1775,a London surgeon, Sir Percivall Pott, discovered that scrotal cancer was muchmore common in chimney sweeps than in the general population. The link betweenan unusual malignancy and an uncommon profession was so striking that Pott didnot even need statistics to prove the association. Pott thus discovered one ofthe first clear links between an environmental substance — a “carcinogen” — anda particular subtype of cancer.

The opposite phenomenon occurs when a commonexposure is associated with a common form of cancer: the association, ratherthan popping out, disappears into the background, like white noise. Thispeculiar form of a statistical vanishing act occurred famously with tobacco smoking and lung cancer. In themid-1930s, smoking was becoming so common and lung cancer so prevalent that itwas often impossible to definitively discern a statistical link between thetwo. Researchers wondered whether the intersection of the two phenomena wascausal or accidental. Asked about the strikingly concomitant increases in lungcancer and smoking rates in the 1930s, Evarts Graham, a surgeon, countereddismissively that “the sale of nylon stockings” had also increased. Tobaccothus became the nylon stockings of cancer epidemiology — invisible as acarcinogen to many researchers, until it was later identified as a major causeof cancer through careful clinical studies in the 1950s and 1960s.

But the most complex and most publicly contentiousintersection between a risk factor and cancer often occurs in the thirdinstance, when a common exposure is associated with a rare form of cancer. Thisis cancer epidemiology’s toughest conundrum. The rarity of the cancer provokesa desperate and often corrosive search for a cause (“why, of all people, did Iget an astrocytoma?” Susan Reynard must have asked herself). And when patientswith brain tumors happen to share a common exposure — in this case, cellphones— the line between cause and coincidence begins to blur. The association doesnot stand out nor does it disappear into statistical white noise. Instead, itremains suspended, like some sort of peculiar optical illusion that is blurryto some and all too clear to others. (A similarly corrosive intersection of arare illness, a common exposure and the desperate search for a cause occurredrecently in the saga of autism and vaccination. Vaccines arenearly universal, and autism is relatively rare — and many parents, searchingto explain why their children became autistic, lunged toward a common culprit:childhood vaccination. An avalanche of panic ensued. It took years of carefullyperformed clinical trials to finally disprove the link.)

The Florida Circuit Court that heard Reynard v. NECwas quick to discern these complexities. It empathized with David Reynard’ssearch for a tangible cause for his wife’s cancer. But it acknowledged that toolittle was known about such cases; “the uncertainty of the evidence . . . thespeculative scientific hypotheses and [incomplete] epidemiological studies”made it impossible to untangle cause from coincidence. David Reynard’s claimwas rejected in the spring of 1995, three years after it was originally filed.What was needed, the court said, was much deeper and more comprehensiveknowledge about cellphones, brain cancer and of the possible intersection ofthe two.

Allow, then, a thought experiment: what if SusanReynard was given a diagnosis of astrocytoma in 2011 — but this time, we armedher with the most omniscient of lawyers, the most cutting-edge epidemiologicalinformation, the most powerful scientific evidence? Nineteen years and severalbillion cellphone users later, if Reynard were to reappear in court, what wouldwe now know about a possible link between cellphones and her cancer?

To answer these questions, we need to begin with amore fundamental question: How do we know that anything causes cancer?

The crudest method to capture a carcinogen’s imprintin a real human population is a large-scale population survey. If acancer-causing agent increases the incidence of a particular cancer in apopulation, say tobacco smoking and lung cancer, then the overall incidence ofthat cancer will rise. That statement sounds simple enough — to find acarcinogen’s shadow, follow the trend in cancer incidence — but there are somefundamental factors that make the task complicated.

The most important of these is life expectancy,which is growing almost everywhere. The average life expectancy of Americanshas increased — from 49 in 1900 to 78 in 2011. Several cancers are strongly,often exponentially, age-dependent. An aging population will seem morecancer-afflicted, even if the real cancer incidence has not changed.

But what if we make an “age adjustment” for thepopulation and shrink or expand the cancer incidence to match the changes inage structure? To ask whether cellphones increase the risk of brain cancer,then, we might begin by turning to this question: Has the age-adjustedincidence of brain cancer increased in the recent past?

The quick answer is no. Brain cancer is rare: onlyabout 7 cases are diagnosed per 100,000 men and women in America per year, anda striking increase, following the introduction of a potent carcinogen, shouldbe evident. From 1990 to 2002 — the 12-year period during which cellphone usersgrew to 135 million from 4 million — the age-adjusted incidence rate foroverall brain cancer remained nearly flat. If anything, it decreased slightly,from 7 cases for every 100,000 persons to 6.5 cases (the reasons for thedecrease are unknown). In 2010, a larger study updated these results, examiningtrends between 1992 and 2006. Once again, there was no increase in overallincidence in brain cancer. But if you subdivided the population into groups, anunusual pattern emerged: in females ages 20 to 29 (but not in males) theage-adjusted risk of cancer in the front of the brain grew slightly, from 2.5cases per 100,000 to 2.6. These cancers appear in the frontal lobe — aknuckle-shaped area immediately behind the forehead and the eye. It isdifficult to imagine that cellphones caused these frontal-lobe tumors: how, orwhy, would a phone’s toxicity have skipped over the area nearest to it andcaused a tumor in a distant site? Most epidemiologists and biologists do notfind such a tissue-skipping mechanism plausible and most doubt that there isany causal link between frontal tumors and phones.

But a populationwide survey, you might argue, hasits limits. The carcinogenic effect of a phone might be so subtle that it neverregisters in such a survey. A phone may cause cancer after a long lag time —say, 20 years — and it may be too early to look for an effect in a generalpopulation. The survey data could be incomplete or of poor quality, thuslimiting an epidemiologist’s ability to ever find a discernible link.

Epidemiologists, fortunately, possess a morepowerful alternative to uncover a link between a risk factor and cancer.Consider the classic studies that finally revealed the association betweentobacco and lung cancer. In the late 1940s, Sir Richard Doll and Sir AustinBradford Hill, working in London, and Ernst Wynder and Evarts Graham, workingin St. Louis, began investigating whether tobacco smoking increased the risk oflung cancer.

Working independently, Doll and Hill, and Wynder andGraham, devised remarkably similar kinds of surveys to reveal a possible link.Using hospital records, they identified a “case” group (a cohort of men withlung cancer) and a matched group of men without lung cancer (a “control”group).

The case group and the control group were asked thesame questions, including how much and how often they smoked. By comparing theresponses of lung-cancer-afflicted men and nonafflicted men, the two teams ofresearchers stumbled on a striking association: men with lung cancer had a muchlonger and deeper history of smoking compared with men without lung cancer.

What if you perform a similar case-control studywith cellphones — comparing men and women suffering from brain cancer (cases)and men and women without brain cancer (controls) — looking at their pastcellphone use? In 2010, an enormous study, called Interphone, tried toaccomplish this task. Setting up the study took years: Interphone recruitedparticipants in 13 countries, ran for a decade and included 5,117 brain-tumorcases and 5,634 controls. The study was coordinated by the WorldHealth Organizationand financed primarily by the EuropeanUnion and cellphone companies, although by agreement industryrepresentatives did not have privileged access to results before publication.

Trials like Interphone are undertaken in the hopethat they cleanse the field of doubts. In fact, Interphone achieved just theopposite effect: it ignited even more puzzling questions. Over all, the studyfound little evidence for an association between brain tumors and cellphones.But when the two cohorts — cancer and no cancer — were subdivided according tothe frequency of cellphone use, bizarre results emerged. To start with, therewas an apparently decreased risk of brain tumors in regularphone users, compared with rare users or nonusers. In other words, regularcellphone use seemed to reduce the risk of brain tumors. In stark contrast,very high cellphone use (measured as a user’s cumulative call time) seemed toincrease the risk of a particular subtype of brain tumor. Needless to say, itis biologically implausible that these results are simultaneously true: how canregular cellphone use protect against cancer while frequent phone use increasesrisk? To most epidemiologists, including the authors of Interphone, the resultspoint to a systemic flaw in the trial.

Similar case-control studies have examined otherkinds of brain tumors, including a rare nonmalignant tumor called an acoustic neuroma. Here, too, the trials havebeen contradictory. Multiple studies found no association with cellphone use.In contrast, one study from Sweden found an increased risk in people who usedtheir phones for more than 10 years.

How can trials that seem so similar at face valuearrive at such disparate and contradictory results? The most likely commonproblem is bias — built into the very structure of these trials. In acase-control trial, patients are asked to remember their risk of exposure afterthe fact. In the Interphone study, for instance, participants were asked torecall the extent of their phone use years or even decades in their past. Andmemory, we now know, is a terribly slippery entity. A patient’s memory of hisor her past is a particularly charged and malleable thing; burned into David Reynard’smemory, poignantly, is the shape of the cellphone in his wife’s hand and theimprint of the cancer on her brain.

In fact, our memories turn out to be systematicallyfragile, especially when we are summoning our past to understand illness. In1993, a Harvard researcher named Edward Giovannucci set out to measure thisphenomenon. Giovannucci identified a cohort of women with breast cancer and an age-matched cohortwithout cancer, and asked each group about its previous dietary habits. Thesurvey produced a reliable and reasonable trend: women with breast cancer weremore likely to have consumed diets high in fat.

But the women in Giovannucci’s study had alsocompleted a dietary survey before their diagnosis of breast cancer. How did awoman’s memory of her diet compare with the actual diet that she recordedbefore her cancer diagnosis?

Giovannucci’s study illustrates the insidious natureof “recall bias.” In women with no cancer, there was no change between theactual and remembered diet. But women with breast cancer typically recalled amuch-higher-fat diet than they actually consumed. The diagnosis of breastcancer had not just changed a woman’s present and the future; it had alteredher sense of her past. Women with breast cancer had (unconsciously) decidedthat a higher-fat diet was a likely predisposition for their disease and(unconsciously) recalled a high-fat diet. It was a pattern poignantly familiarto anyone who knows the history of this stigmatized illness: these women, likethousands of women before them, had searched their own memories for a cause andthen summoned that cause into memory.

It is very likely that similar effects undid theInterphone trial: some men and women with brain cancer recalled adisproportionately high use of cellphones, while others recalleddisproportionately low exposure. Indeed, 10 men and women with brain tumors(but none of the “controls”) recalled 12 hours or more of use every day — anumber that stretches credibility. In a substudy of Interphone, researchersembedded phones with special software to track phone usage. When this log wascompared with the “recalled” usage, there were wide and random variations: someusers underreported, while others overreported use.

The trouble is that even the largest, longest,best-designed retrospective studies that rely on memory are likely to beriddled by recall bias. Typically, it is not the failure ofmemory that produces this bias, but its hyperactivity — its desire to explain theuncertainty of the present with the certainty of the past.

There are certainly methods in epidemiology tocounteract the biases created by selective memory: Interphone researchers couldhave initially identified a cohort of high-volume cellphone users and ofnonusers, and followed them over time to determine who developed or did notdevelop cancer. Such a study — called a “prospective trial” — would certainlyerase the biases of memory. But it would be logistically impossible to perform.Since the rates of brain cancer are small, about 6.5 cases per 100,000 persons,a trial of this design would need to follow an enormous cohort of cellphoneusers — hundreds of thousands of participants — to record even a few cancers.And where on earth would you find the nonusers for the study? In most nations, cellphoneusage is so common that finding 500,000 people who will not use phones for adecade is hard to imagine.

There are yet more powerful epidemiological methodsthat seem even more far-fetched. A trial that forcibly randomizes men and womento use cellphones or restrict phone use — a “randomized trial” — wouldcertainly guarantee the most bias-free result, but would trespass inviolableethical and practical concerns. Another study might try to minimize a person’sbiased memory of exposure by collecting actual data on phone use from phonenetworks (scanning phone minutes and call logs from real bills), but this wouldviolate privacy laws. Thus far, individual call logs — even anonymized logs —have not been made public to researchers.

What if we moved the studies from humans to animals?Benzene, benzopyrenes, methylcholanthrene and some aniline derivatives (amongmany other chemicals) were first discovered as cancer-causing agents usingmice, rats and rabbits. Decades before Doll and Hill’s elaborate studies ontobacco smokers in London, an Argentine biologist, Angel Roffo, “painted”rabbits with a grey-black solution containing distilled cigarette tar anddemonstrated that the smoky residue caused cancer.

Might an animal experiment identify the carcinogenicityof cellphone radiation that Interphone missed? Prototypical animal studies forcarcinogens involve exposing one group of animals to the suspected agent andcomparing it to the unexposed group. But as the 16th-century physicianParacelsus reminds us, “It is the dose that makes the poison.” Determining theappropriate amount to test and delivering it to the right part of an animal’sbody is often crucial to the experiment.

At face value, testing “radiation,” which ismeasured in standardized doses, would seem to make this simple. But allradiation is not created equal. The word “radiation” refers to energy thatemanates from a source — but the spectrum of radiant energy is broad. On thehighly energetic end of the spectrum is ionizing radiation — like X-rays orcosmic rays — that are so powerful they can tear away electrons from atoms andmolecules and penetrate barriers like the skull and the brain. On the way into— and through — the body, they deposit powerful bursts of energy, generatecorrosive chemicals, ruffle up DNA, kill cells and, most notably, mutategrowth-controlling genes to cause cancer.

Nonionizing radiation lies on the other end of theenergy spectrum. These rays can warm cells, boil water and stimulate chemicalreactions, but they cannot strip electrons away from atoms or damage DNA. Theyhave no capacity to mutate genes directly and thereby no simple and directmeans of initiating cancer. Radiation from microwaves, from cellular phones andfrom light bulbs are examples of nonionizing radiation.

All of this makes cellphone radiation a relativelyunlikely culprit as a mutation-causing agent. Nonetheless,biologists have exposed mice and rats to chronic nonionizing radiation(comparable to that emitted by phones) to determine whether it causes cancer.In rats prone to developing breast cancer, there was no acceleration of breastcancer. In another experiment, rats were treated with a chemical carcinogen inutero (to “prime” them to develop brain tumors) and then exposed to radiantenergy comparable to cellphone radiation for two hours per day, four days aweek, for 22 months. The experiment revealed no increased incidence of braintumors in rats. Nor was there any accelerated growth in previously establishedbrain tumors. From 1997 to 2004, six independent experiments on mice and ratsstudied the effects of chronic radiation on brain cancer. No experimentrevealed an increased risk of brain cancer.

But radiant energy need not penetrate the brain andmutate genes to have a biological effect on it. A cellphone user mightexperience changes in physiology that have nothing to do with the ionizingcapacity of radiation. Might a cellphone leave a physiological mark on thebrain through a yet unknown mechanism?

A recent study by Nora Volkow, published in TheJournal of the American Medical Association (JAMA) and reported in thisnewspaper on March 30, has raised this unusual possibility. Volkow is aninnovative brain researcher who is director of the National Institute on DrugAbuse in Bethesda, Md. She recruited 47 people and placed an “active” phonenext to one ear (the phone was on — generating radiation, but silent, so thatVolkow could eliminate the effects of sound and conversation). She then used aspecialized brain scanner capable of detecting alterations in glucose. Glucose— a sugar — is the metabolic fuel for the brain. When parts of the brain areactivated, brain cells begin to metabolize glucose at an increased rate.Volkow’s scanner was equipped to detect even marginal changes in glucose metabolism.

When Volkow compared subjects with phones turned onwith subjects who had their phones turned off, she found a striking pattern:there was a telltale sign of increased brain-glucose activity in the area ofthe brain immediately adjacent to the antenna of the phone.

But as Volkow points out, there is still a longconceptual leap from “increased brain-glucose activity” to “brain cancer.” Ourbrains are constantly altering the metabolism of sugar — the flux of glucosechanges when we remember Grandma’s house in Texas or listen to Bach or smellroses. When human beings dream during sleep, the increase in glucose metabolismin some parts of the brain is just as striking as the increase found inVolkow’s study with phones. “It’s not a dramatic increase,” she says. “When oureye responds to a visual cue, glucose metabolism in the brain increases muchmore dramatically” — and, surely, we do not think that visual stimulationcauses cancer. Her study proves, importantly, that cellphone radiation has abiological effect on the brain. But whether this effect is consequential —whether it causes cancer or, for that matter, protects against it — is entirelyspeculative.

The most exquisite — and arguably the most sensitive— means to identify a carcinogen is to study the effects of the substance noton humans or animals but on cells. In the 1970s, a Berkeley biochemist namedBruce Ames devised a cellular test to do just that. Ames’s test is based on aseries of simple principles. Normal cells in the body grow through celldivision, or mitosis, which is carefully regulated by genes. Certain genesaccelerate growth, while other genes dampen or stop it. Cancer originates whenthe “accelerator” genes are permanently activated or when the “brake” genes arepermanently damaged. Since genes are encoded by DNA, chemicals that mutate DNA— mutagens — can alter the growth-controlling genes and thereby cause cancer.Ames devised a special strain of bacterial cells that act as a “sensor” formutations and therefore can also detect mutagenic chemicals. Chemical mutagensare so commonly carcinogenic that versions of the Ames test represent the goldstandard by which most carcinogens are found.

Cellphone radiation is not a chemical, of course,but the rules about mutagenicity still apply (X-rays, for instance, are knownto cause cancer and are detectable by Ames’s test). Laboratory experiments thatlink phone radiation to DNA mutation using a version of the Ames test have beenlargely contradictory. In 2005, a panel of experts, including a biomedicalengineer, an epidemiologist, a genetic toxicologist and a radiation biologist,published a review of nearly 1,700 scientific papers on the cellular effects ofradiation emitted by phones. In the review of more than 50 experiments linking phoneradiation to DNA damage in animal or bacterial cells, evidence of damage hasbeen negative in more than two-thirds of the studies. Since nonionizingradiation cannot directly affect the structure of DNA, experiments linkingphone radiation to DNA damage are generally unconvincing. The most strikingstudy linking cellular phone radiation to DNA damage, published in 2005 byresearchers from the Medical University of Vienna, has recently been embroiledin even deeper scientific controversy: researchers studying the dataintensively have argued that the original study is fraudulent.

But it is possible for something to be a carcinogenwithout directly damaging DNA. Some chemicals might activate growth pathways orsurvival pathways in cancer cells (eventually damaging DNA and mutating genes —but indirectly). Exogenous estrogen, for instance, activates growth pathways in breastcells and can cause breast cancer but doesn’t damage DNA. Others may provokeinflammation, creating a physiological milieu in the body that allows malignantcells to grow and survive. Yet others — the class of substances that we knowleast about — might not damage DNA directly but chemically modify genes so thattheir regulation is changed. These substances are like the dark matter of thecarcinogenic world: they are barely visible to our current tests forcarcinogens and thus lie at the boundaries of the knowable universe. Cellphonesand their radiation have been tested for many of these properties — forinstance, their ability to chemically modify DNA without causing mutations —but evidence linking this form of radiation to such cellular changes remainslargely negative.

In the expert panel’s 2005 review, the authorssummarized the evidence: “There is little theoretical basis for anticipatingthat RF energy [from cellular phones] wouldhave significant biological effects at the power levels used by modern mobilephones and their base station antennas. The epidemiological evidence for acausal association between cancer and RF energy is weak and limited. Animalstudies have provided no consistent evidence that exposure to RF energy atnonthermal intensities causes or promotes cancer. Extensive in vitro studieshave found no consistent evidence of [DNA damage] potential, but in vitrostudies assessing the epigenetic potential of RF energy are limited. Over all,a weight-of-evidence evaluation shows that the current evidence for a causalassociation between cancer and exposure to RF energy is weak and unconvincing.”

The word “carcinogen,” it is believed, was firstcoined by the surgeon James Paget in an obscure passage of a lecture onsurgical pathology in 1853. Paget asked if there is “one material for cancer,one carcinogen,” that “may form different but closely allied compounds?”

Our vision of carcinogenesis has become vastly morecomplex since 1853. We now know that there is no “one cancer.” Breast, lung,prostate and blood cancer share a similarity — the uncontrolled growth of cells— but the specific genes and behaviors of these cancers are far from identical.

Nor is there “one material for cancer” — onearchetypal carcinogen. Agents that cause cancer are chemically diverse and cancer-specific.Estrogen can provoke cancer in the breast, but destroys prostate-cancer cells;vinyl chloride is exquisitely carcinogenic to the liver but not to the skin;chlorine and nitrogen mustard are both poison gases, but only one causesleukemia.

Notably, there is also no “one test” forcarcinogens. Scientific studies to capture the association between an agent andcancer cast an astonishingly wide net. On one end of that spectrum liepopulationwide human trials involving hundreds of thousands of men and women.On the other end are precise laboratory experiments that plumb the moleculardepths of cells and genes. The tests range from the telescopic to microscopic,from statistics to biochemistry — from observations of chimney sweeps tobacteria on a petri dish. Often one test must be corroborated by another.Asbestos and tobacco were identified by case-control studies and validated inanimal models. Estrogens were implicated by studies on human and animalphysiology and then found to be carcinogenic in prospective human trials.

Finding a carcinogen, in short, is not like solvinga mathematical equation, with a single formula and solution. It is more likesolving an epic detective case, with individual pieces of evidence that, takentogether, suggest a common culprit.

But thus far, this extraordinarily wide-cast net hasyet to find solid proof of risk for cellphone radiation: not a single trial ortest that has attributed carcinogenic potential has been free of problems. Populationwide studies have failed to demonstrate an increased incidence; retrospectivetrials have been contradictory and riddled with biases; animal studiesnegative; human physiological experiments inconclusive; cellular studiesinconsistent and weak. What is clearly needed, experts agree, is a single,definitive, unbiased study — “one trial,” to borrow Paget’s terminology.Logistically speaking, the simplest such human trial is a case-control studythat compares cancer patients with healthy patients, using phone-log data thatcompanies have thus far been reluctant to provide. The simplest animal studyinvolves subjecting rats and mice to long-term exposure to cellphone radiation.The National Toxicology Program has begun such a study. Cellphone radiationwill be turned on and off for 10-minute stretches for 20 hours each day. Thisexperiment — the closest we will get to making mice use actual cellphones — islikely to be published in 2014.

It is possible, of course, that even thesesophisticated experiments will be unable to determine the risk. The lag time ofcancer development with phone use may be 50 or 70 years — and cellphones havebeen around for only three decades or so. Yet even a slow-lagging cancer isunlikely to arise at a single point in time after exposure. Like most biologicalphenomena, cancer risk typically rides a statistical curve, with some patientsdeveloping cancer early, others peaking in the middle and yet others trailingoff decades later. Thus far, no such statistical curve has been evident forbrain cancer.

Might the cellphone industry have already performedsuch experiments and conspired to keep real data on brain cancers from us —just as the tobacco industry conspired to obfuscate real data on tobacco andcarcinogenesis in the 1950s? It’s possible, but there are important differencesin comparing these trials with the tobacco studies. With smoking, despiteactive attempts by the industry to stifle data, the epidemiological trials wereincontrovertibly positive, human physiological data markedly suggestive and animalstudies (including Roffo’s painted-rabbit experiment) striking.

As we await the definitive trial, then, it’sprobably wise to also start thinking differently about the cause of SusanReynard’s cancer. When a suspected cause for a devastating illness begins toslip away, there is often frustration and turmoil, paranoia and nihilism. In ashort story by LorrieMoore, the mother of a toddler with cancer rattles off a list ofpotential causes of her child’s illness — “giant landfills, agriculturalrun-off”; “lurid water”; “toxic potatoes”; “Joe McCarthy’s grave.”

The trouble with this kind of grasping is that it isindiscriminate. In truth, many substances of modern life do not — cannot —cause cancer. Some do, and it’s absolutely critical to identify and reduceexposure to them. Others don’t, and it’s absolutely worthwhile identifyingthese, so that we can focus on the real carcinogens around us. If we lumpeverything into the category of “potentially carcinogenic,” from toxic potatoesto McCarthy’s grave, then our scientific language around cancer begins todegenerate. The effect is like crying “wolf” about cancer: the publicprogressively numbs itself to real environmental toxins and becomes disinvestedin finding bona fide carcinogens.

To keep ourselves on the right path on environmentalcarcinogens, then, we need not just standards to rule carcinogens “in” but alsostandards to rule them “out.” The final, definitive trials on phone radiationmay settle this issue — but, as of now, the evidence remains far fromconvincing. Understanding the rigor, labor, evidence and time required toidentify a real carcinogen is the first step to understanding what does anddoes not cause cancer.

Siddhartha Mukherjee(smukherj2011@gmail.com) is an assistant professor of medicine in the divisionof medical oncology at Columbia University. He is the author of “Emperor of AllMaladies: A Biography of Cancer.” Editor: Ilena Silverman(i.silverman-MagGroup@nytimes.com).

Milk Intake in Early Life and Risk of Advanced Prostate Cancer

2012-01-02T11:00:00.000-08:00

Milk Intake in Early Life and Risk of Advanced Prostate Cancer

Sodium: Are you getting too much?

2012-01-02T10:27:00.000-08:00

Sodium: Are you getting too much?

By Mayo Clinicstaff

Original Article:http://www.mayoclinic.com/health/sodium/NU00284/?utm_source=Highlights&utm_medium=email&utm_campaign=HouseCall&pubDate=December%2028,%202009

Nutrition basics (18)

· Healthy diets (7)

· Healthy cooking (15)

· Healthy menus and shopping strategies (10)

· Nutritional supplements (2)

Sodium: Are you getting too much?

Find out how much sodium you really need, what high-sodium foods to avoid,and ways to prepare and serve foods without adding salt or sodium.

By Mayo Clinicstaff

You've been trying to eat less sodium — just a pinch of table salt on yourbaked potato and a dash to your scrambled eggs.

The main sources of sodium in the average U.S. diet.

But a pinch and a dash can quickly add up to unhealthy levels of sodium,especially when many foods already contain more than enough sodium. About 11percent of the sodium in the average U.S. diet comes from adding salt orother sodium-containing condimentsto foods while cooking or eating. But themajority of the sodium — 77 percent— comes from eating prepared or processed foods that contain the mineral. So even though you may limit the amount of salt you add to food, the food itself may already be high in sodium.

Are you getting too much? Here's where sodium sneaks into your diet and waysyou can shake the habit.

Sodium: Essential in small amounts

Your body needs some sodium to function properly. Sodium:
Helps maintain the right balance of fluids in your body; Helps transmit nerve impulses; Influences the contraction and relaxation of muscles

Your kidneys regulate the amountof sodium kept in your body. When sodium levels are low, your kidneys conservesodium. When levels are high, theyexcrete the excess amount in urine.

If your kidneys can't eliminate enough sodium, thesodium starts to accumulate in your blood. Because sodium attracts and holdswater, your blood volume increases. Increased blood volume, in turn, makes yourheart work harder to move more blood through your blood vessels, increasingpressure in your arteries. Certain diseases such as congestive heart failure,cirrhosis and chronic kidney disease can lead to an inability to regulatesodium.

Some people are more sensitive to theeffects of sodium than are others.People who are sodium sensitive retain sodium more easily, leading to excessfluid retention and increased blood pressure. If you're in that group, extrasodium in your diet increases your chance of developing high blood pressure, acondition that can lead to cardiovascular and kidney diseases.

How much sodium do you need?

Various organizations, including theNational Academy of Sciences' Institute of Medicine, havepublished recommendations on daily sodium limits. Most recommend not exceedingthe range of 1,500 and 2,400 milligrams (mg) a day for healthy adults. Keep inmind that the lower your sodium, the more beneficial effect on blood pressure.

If you are older than 50, are black or have a health condition such as highblood pressure, chronic kidney disease or diabetes, you may be more sensitiveto the blood pressure raisingeffects of sodium. As a result, aim for a sodium limit at the low end of therange recommended for healthy adults. Talk to your doctor about the sodium limit that's best for you.

Three main sources of sodium

The average U.S.diet has three main sources of sodium:

Processed and prepared foods. Most sodium in a person's diet comes from eating processed and prepared foods, such as canned vegetables, soups, luncheon meats and frozen foods. Food manufacturers use salt or other sodium-containing compounds to preserve food and to improve the taste and texture of food.
Sodium-containing condiments. One teaspoon (5 milliliters) of table salt has 2,325 mg of sodium, and 1 tablespoon (15 milliliters) of soy sauce has about 900 to 1,000 mg of sodium. Adding these or other sodium-laden condiments to your meals — either while cooking or at the table — raises the sodium count of food.
Natural sources of sodium. Sodium naturally occurs in some foods, such as meat, poultry, dairy products and vegetables. For example, 1 cup (237 milliliters) of low-fat milk has about 107 mg of sodium.

Be a savvy shopper: Find thesodium

Taste alone may not tell you which foods are high in sodium. For example,you may not think a bagel tastes salty, but a 4-inch (10-centimeter) oat-branbagel has 451 mg of sodium.

So how do you identify foods high in sodium? The best way to determinesodium content is to read food labels. The Nutrition Facts label tells you howmuch sodium is in each serving. It also lists whethersalt or sodium-containing compounds are ingredients. Examples of these compounds include:

Monosodium glutamate (MSG)
Baking soda
Baking powder
Disodium phosphate
Sodium alginate
Sodium nitrate or nitrite

How to cut sodium

You may or may not be particularly sensitive to theeffects of sodium. And because there'sno way to know who might develop high blood pressure as a result of ahigh-sodium diet, choose and prepare foods with less sodium.

You can cut sodium several ways:

Eat more fresh foods and fewer processed foods. Most fresh fruits and vegetables are naturally low in sodium. Also, fresh meat is lower in sodium than luncheon meat, bacon, hot dogs, sausage and ham are. Buy fresh and frozen poultry or meat that hasn't been injected with a sodium-containing solution. Look on the label or ask your butcher.
Opt for low-sodium products. If you do buy processed foods, select those that have reduced sodium.
Remove salt from recipes whenever possible. You can leave out the salt in many recipes, including casseroles, stews and other main dishes. Baked goods are an exception. Leaving out the salt could affect the quality as well as the taste of the food.
Limit your use of sodium-laden condiments. Salad dressings, sauces, dips, ketchup, mustard and relish all contain sodium.
Use herbs, spices and other flavorings to enhance foods. Learn how to use fresh or dried herbs, spices, zest from citrus fruit, and fruit juices to jazz up your meals.
Use salt substitutes wisely. Some salt substitutes or light salts contain a mixture of table salt (sodium chloride) and other compounds. To achieve that familiar salty taste, you may use too much of the substitute and actually not use less sodium. In addition, many salt substitutes contain potassium chloride. Though dietary potassium can lessen some of the harm of excess sodium, too much supplemental potassium can be harmful if you have kidney problems or if you're taking medications for congestive heart failure or high blood pressure that cause potassium retention.

Your taste for salt is acquired, so it's reversible. To unlearn this saltysavoring, decrease your use of salt gradually and your taste buds will adjust.Most people find that after a few weeks of cutting salt, theyno longer miss it. Start by using no more than 1/4 teaspoon (1 milliliter) ofadded salt daily, and then graduallyreduce to no salt add-ons. As you use less salt, your preference for itlessens, allowing you to enjoy thetaste of food itself.

· See Also

HandScheduled

Section Focus

True or False: Prostate Cancer Growth Is Faster in Black Men?: Johns Hopkins Health Alerts

2011-12-31T09:08:00.000-08:00

True or False: Prostate Cancer Growth Is Faster in Black Men?: Johns Hopkins Health Alerts

Prostate cancer prevention: What can men do? by Mayo Clinic staff

2011-03-31T13:59:00.000-07:00

Cancer risk: What the numbers mean

Take the time to understand what cancer risk is and how it's measured. This can help you put your own cancer risk into perspective.

By Mayo Clinic staff

You might wonder what your chances are of developing cancer. But cancer statistics can be confusing. News reports make it sound as if nearly every day something is found to dramatically raise your risk. Sorting through all the information and figuring out what's valid and what isn't can be tricky.

What is risk?

When scientists talk about risk, they're referring to a probability — the chance that something may occur, but not a guarantee that it will. As an example of probability, if you flip a coin, there is a one in two chance, or a 50 percent chance, that the coin will land heads up.

Risk estimates for cancer and other diseases are determined by studying large groups of people to discover the probability that any given person or category of people will develop the disease over a certain period of time, and to see what characteristics or behaviors are associated with increased or decreased risk.

How is risk expressed?

	Absolute risk
	Relative risk

Risk is generally divided into two categories:

Absolute risk
Absolute risk refers to the actual numeric chance or probability of developing cancer during a specified time period — for example, within the year, within the next five years, by age 50, by age 70, or over the course of a lifetime.

One type of absolute risk is lifetime risk, which is the probability that an individual will develop cancer over the course of a lifetime. For instance, an American man's absolute risk of developing prostate cancer in his lifetime is about 17 percent. Put another way, about 17 out of every 100 men will develop prostate cancer at some time in their lives. And 83 out of every 100 men won't develop prostate cancer.

Keep in mind that lifetime risk isn't the risk that a person will develop cancer in the next year or next five years. An individual's cancer risk has a lot to do with other factors, such as his or her age. For instance, a woman's lifetime risk of developing colon and rectal cancer is just over 5 percent, or about 523 cases per 10,000 women. But her risk of developing colon and rectal cancer before the age of 40 is 0.07 percent, or about seven cases per 10,000 women.

Relative risk
Relative risk gives you a comparison or ratio rather than an absolute value. It shows the strength of the relationship between a risk factor and a particular type of cancer by comparing the number of cancers in a group of people who have a particular exposure trait with the number of cancers in a group of people who don't have that trait.

For instance, relative risk might compare the lung cancer risk for people who smoke with the lung cancer risk in a similar group of people who don't smoke. You might hear relative risk being expressed like this: The risk of lung cancer for men who smoke is 23 times higher than the risk for men who don't smoke. So the relative risk of lung cancer for men who smoke is 23.

Relative risk is also given as a percentage. For example, the risk of lung cancer for men who smoke is 2,300 percent higher than it is for men who don't smoke. Keep in mind that when you hear about relative risk, there's no upper limit to the percentage increase in risk. Most people think 100 percent is the highest possible risk, but that isn't true when talking about relative risk.

A relative risk of 100 percent means your risk is twice as high as that of someone without that risk factor. A 200 percent relative risk means that you are three times as likely to develop that condition.

Risk seems greater when put in terms of relative risk. A 100 percent increase in risk may seem enormous, but if the risk began as one in 100 people, the risk is increased to two in 100.

continued:

Cancer risk: What the numbers mean

Where do cancer risk statistics come from?

Most information about cancer risk and risk factors comes from epidemiologic studies, which are studies that focus on large, well-defined groups of people. Cancer researchers have identified many of the major environmental factors that contribute to cancer, including smoking for lung cancer and sunlight for skin cancer. But uncovering more subtle cancer risks has proved more difficult.

Many studies of cancer risk factors rely on observational approaches. In these studies, researchers keep track of a group of people for several years without trying to change their lives or provide special treatment. This can help scientists find out who develops a disease, what those people have in common and how they differ from those who didn't get sick.

How do cancer risk statistics relate to you?

Risk statistics can be frustrating because they can't tell you your own specific risk of cancer. Just because studies have found that men have a nearly 50 percent chance of developing cancer in their lifetimes doesn't mean that your risk, if you're a man, is 50 percent. Your individual risk is based on many different factors, such as your habits, your family history of cancer and the environment in which you live.

Even then, the combination of risk factors might not apply directly to you. Cancer is highly individualistic. You can have two people with the same age, sex, race, socioeconomic status and comparative lifestyles and still have totally different disease experiences. Risk statistics are helpful in general statements such as "exercising regularly tends to coincide with a reduced risk of chronic diseases, such as cancer." But exercising regularly won't guarantee that you won't get cancer.

Talk with your doctor about your risk of cancer. He or she can review what elements in your life may increase your risk. You can then discuss what you can do to help lower this risk.

Keep cancer risk statistics in perspective

You might hear a news report about a study that seems to indicate you may be at increased risk of a particular type of cancer. Don't jump to conclusions based on this one report. Take a step back and think about what the risk really means.

Observational studies aren't foolproof. Researchers agree that one study by itself isn't authoritative. This is why you sometimes see studies with seemingly contradictory results. Scientists tend to weigh the evidence of many research studies over time to better determine whether a finding is true. News reports, though, often focus on each new study in isolation, rather than as a part of an evolving picture. This can sometimes cause unnecessary alarm or confusion.

When reading about cancer risk statistics, pay attention to these details:

§ Who's being observed? A news report may say a certain activity increases the risk of cancer for a group of people. But who was being observed in the study? Pay attention to the ages of the people and their characteristics. For instance, some people are genetically predisposed to certain types of cancer.

§ How many people were studied? In general, studies involving thousands of people are more accurate than are those that examine a small group of people.

§ Have similar studies been done? The findings of one study are more reliable if they're similar to findings by other studies.

News reports that focus on alarming statistics, such as a 300 percent increase in risk, but don't give you much context aren't very helpful. If you're concerned about the risk, gather more information.

Question

Pomegranate juice: A cure for prostate cancer?

Is it true that pomegranate juice may slow the growth of prostate cancer? How much should I drink?

Answer

from Erik Castle, M.D.

Some research suggests that drinking pomegranate juice may slow the progression of prostate cancer.

For example, in one study, the length of time it took for prostate-specific antigen (PSA) to double after surgery or radiation for prostate cancer was significantly longer in men who drank 8 ounces (237 milliliters) of pomegranate juice daily for up to two years. A longer PSA doubling time indicates that the cancer may be progressing less rapidly. Other studies have found that certain compounds in pomegranate juice inhibited growth of prostate cancer cells in the laboratory.

Although these results are encouraging, they're only preliminary. Clinical trials are under way, and it's too early to say if pomegranate juice can definitely slow the growth of prostate cancer. It's also unclear whether drinking pomegranate juice alters the course of prostate cancer overall so that men live longer or better.

If you choose to drink pomegranate juice, talk with your doctor first. Although pomegranate juice is generally safe, there is evidence that it affects the metabolism of several prescription medications, including the blood thinner warfarin (Coumadin) and some drugs used to treat high blood pressure and high cholesterol.

Prostate cancer prevention: What you can do

Your odds of prostate cancer prevention may be increased by exercising and eating a low-fat diet rich in fruits, vegetables and fish. Maintaining a healthy weight also can help.

By Mayo Clinic staff

There's no sure way to prevent prostate cancer — but you can make diet and lifestyle choices that might aid in prostate cancer prevention.

While any man can get prostate cancer, it's most common in older men, in men with a family history of prostate cancer and in black men. Although age, genetics and race are factors you can't change, there are some factors you can control that may enhance prostate cancer prevention.

Prostate cancer is complicated, and researchers are still trying to understand its causes and determine which prostate cancer prevention strategies are safe and most effective.

Following these guidelines may help lower your risk of prostate cancer. These steps may also help prevent other cancers and health conditions such as heart disease.

Nutrition and preventing prostate cancer

So far, research does not support definite nutritional guidelines for prostate cancer prevention. However, you can reasonably act on these suggestions:

§ Eat sensibly. Eat moderate-sized portions and keep your calories under control.

§ Choose balanced meals. Prostate cancer rates vary greatly from one country to another, with the highest rates appearing in countries where people tend to eat a lot of fat. A diet high in saturated fats (such as animal fats found in red meat) may pose the greatest risk.

§ Eat a variety of fruits and vegetables. A diet high in fruits and vegetables has been linked to a lower risk of various kinds of cancer. Foods high in folate — a B vitamin found in spinach, asparagus and some beans — may be helpful. Also, eating vegetables with diindolylmethane — a nutrient found in cruciferous foods such as broccoli, kale and cabbage — might protect against prostate cancer. Studies show mixed results about whether lycopene — an antioxidant found in tomatoes — lowers prostate cancer risk.

§ Choose healthy foods. Opt for whole-grain foods, such as brown rice, quinoa and whole-wheat bread. Limit sweets and salt.

§ Drink alcohol in moderation. Generally, this means no more than two drinks a day for men. Studies show that regular heavy drinking increases the risk of aggressive prostate cancer.

Experts are still studying other foods to see whether they help prevent prostate cancer. While the verdict's still out, eating more of these foods probably won't hurt — and may help prevent cancer and other health problems:

§ Eat foods rich in omega-3 fatty acids. While a diet high in most kinds of fat is linked to a higher risk of cancer and other health problems, there is an exception. Omega-3 fatty acids — a type of fat found in cold-water fish such as salmon, herring and mackerel — may reduce the risk of certain cancers. Study results are mixed, and some researchers say eating these fats has no effect on cancer. But these fats are still a healthy addition to your diet.

§ Eat soy products and legumes. Soybeans and other legumes contain phytoestrogens, which are plant-based chemicals that behave like the hormone estrogen in the human body. These chemicals might help to prevent prostate cancer. In fact, one possible explanation for lower rates of prostate cancer in Asian men is that they eat more soy protein.

§ Drink green tea. Green tea contains antioxidants such as polyphenols that may help prevent certain cancers and other health problems.

§ Get enough vitamin D. Not many foods contain vitamin D, but fish liver oil, cheese and egg yolks contain some. Check with your doctor to see if you need a vitamin D supplement. Some studies suggest that vitamin D may help prevent prostate cancer.

Obesity and prostate cancer

Researchers have not established a direct link between obesity and incidence of prostate cancer. However, obesity might affect levels of hormones related to prostate cancer risk. It may also increase the risk of dying of prostate cancer.

Strategies for preventing obesity include:

§ Following guidelines for a healthy diet

§ Meeting with your doctor to develop a plan for physical activity

§ Doing some form of aerobic exercise for 30 minutes or more daily

continued:

Prostate cancer prevention: What you can do

Drugs to prevent prostate cancer

Current research does not support the routine use of any drug to prevent prostate cancer, but several medications show potential benefits, including statins, aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil, Motrin, others). Researchers are also studying certain drugs that affect testosterone levels. While these medications may help prevent prostate cancer, they can also cause side effects and are not generally recommended for routine use in preventing prostate cancer.

Selenium and vitamin E

Some nutrition research had suggested that daily doses of the mineral selenium, vitamin E or both may have helped to prevent prostate cancer. But further study has shown these supplements have no effect on prostate cancer. In some cases, these supplements may cause side effects or lead to other health conditions.

Before using any supplement, talk with your doctor. This is particularly important if you're taking other over-the-counter or prescription medications. Taking vitamins, herbal medicines or nutritional supplements can pose health risks, especially in high doses. Some may even increase the risk of prostate cancer.

Prostate cancer risk: A common-sense perspective

Prostate cancer is the second most common cause of cancer death in men, exceeded only by lung cancer. Even so, prostate cancer affects far more men than it eventually kills. According to the American Cancer Society, about 1 in 6 men in the United States will be diagnosed with prostate cancer during their lifetime. Yet only 1 in 35 men in the U.S. will die of the disease.

Why does the number of prostate cancer cases exceed the number of deaths by such a large ratio? One answer is that prostate cancer generally progresses more slowly than many other types of cancer. Many men live with it for years. Many survive disease-free after treatment. And others refrain from treatment while closely monitoring the cancer's progression — an approach known as "watchful waiting."

To keep your risks in perspective, stay in regular contact with your doctor about your prostate health. Ask about prevention strategies that make the most sense for you, given your current health and medical history.

An annual prostate checkup can't reduce your risk of cancer, as perhaps a healthy diet and exercise can. But if prostate cancer does develop, a digital rectal exam (DRE) and a prostate-specific antigen (PSA) test may discover the problem in its earliest stage, when treatment can be most effective.

Definition

By Mayo Clinic staff

Prostate cancer

Prostate cancer is cancer that occurs in a man's prostate — a small walnut-shaped gland that produces the seminal fluid that nourishes and transports sperm.

Prostate cancer is one of the most common types of cancer in men. Prostate cancer usually grows slowly and initially remains confined to the prostate gland, where it may not cause serious harm. While some types of prostate cancer grow slowly and may need minimal or no treatment, other types are aggressive and can spread quickly.

Prostate cancer that is detected early — when it's still confined to the prostate gland — has a better chance of successful treatment.

Symptoms

· Mayo Clinic services

· Diagnosing prostate cancer at Mayo Clinic

· Prostate cancer treatment at Mayo Clinic

· Mayo Clinic research

· Mayo Clinic Cancer Center

References

DS00043

Feb. 3, 2010

© 1998-2011 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "MayoClinic.com," "EmbodyHealth," "Enhance your life," and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.

Symptoms

By Mayo Clinic staff

Prostate cancer may not cause signs or symptoms in its early stages. Prostate cancer that is more advanced may cause signs and symptoms such as:

§ Trouble urinating

§ Decreased force in the stream of urine

§ Blood in your urine

§ Blood in your semen

§ Swelling in your legs

§ Discomfort in the pelvic area

§ Bone pain

When to see a doctor
Make an appointment with your doctor if you have any signs or symptoms that worry you.

Ask your doctor about the benefits and risks of regular prostate cancer screening. Medical organizations differ on their recommendations for prostate cancer screening, but many advise men in their 50s to discuss the issue with their doctors.

Causes

By Mayo Clinic staff

	Prostate gland
	Prostate cancer

It's not clear what causes prostate cancer. Doctors know that prostate cancer begins when some cells in your prostate become abnormal. Mutations in the abnormal cells' DNA cause the cells to grow and divide more rapidly than normal cells. The abnormal cells continue living, when other cells would die. The accumulating abnormal cells form a tumor that can grow to invade nearby tissue. Some abnormal cells can break off and spread (metastasize) to other parts of the body.

Risk factors Symptoms

Risk factors

By Mayo Clinic staff

Factors that can increase your risk of prostate cancer include:

§ Older age. The risk of prostate cancer increases with age. Prostate cancer is most common in men over 65.

§ Being black. Black men have a greater risk of prostate cancer than do men of other races. It's not clear why this is.

§ Family history of prostate cancer. If men in your family have had prostate cancer, your risk may be increased.

§ Obesity. Obese men diagnosed with prostate cancer are more likely to have advanced disease that's more difficult to treat.

What is your lifetime risk of prostate cancer and can prostate cancer be prevented?

2011-03-31T13:50:00.000-07:00

What Is Risk?

email this page

Researchers describe risk as the estimated chance of getting a disease during a certain time period, such as within the next 10 years, or during your lifetime. For example, you might hear a statement “A man’s risk of developing prostate cancer is 17 percent during his lifetime.”

For information about the statistical terms used to express risk and other statistical measures of cancer, see the Glossary of Statistical Terms.

Find out more:
How most people think about risk	How doctors think about risk

Test your knowledge of risk:

For men in the U.S., the lifetime risk of prostate cancer is nearly 17 percent. What does this mean? Click on your choice:
In general about 17 of every 100 males in the United States will be diagnosed with prostate cancer during their lifetime. This is the absolute risk of prostate cancer for U.S. males. Every man in the U.S. has a 17 percent chance of dying from prostate cancer. If a man is over 40, his chance of getting prostate cancer in the next year is almost 17 percent.

African American men have a relative risk of 1.2 for diagnosis of prostate cancer when compared to White men. What does this mean? Click on your choice:
The risk of a diagnosis of prostate cancer is linked to where African American men live. Overall, African American men are more likely to be diagnosed with prostate cancer than White men. Fewer African American men than White men will be diagnosed with prostate cancer.
	Prostate Cancer - Step 1: Find Out About Prostate Cancer Risk	email this page
	What are the known risk factors for prostate cancer? No one knows the exact causes of prostate cancer. Doctors can seldom explain why one man develops the disease and another does not. However, it is clear that prostate cancer is not contagious. No one can "catch" this disease from another person. Research has shown that men with certain risk factors are more likely than others to develop prostate cancer. These risk factors are:

Age

Race/Ethnicity

Family history

Find out more:
What is the prostate? Things to know about prostate cancer	Prostate cancer statistics	Changes in the prostate

Understanding Prostate Cancer Risk Tool
Check the risk factors that apply to you to build your own list. Then go to Step 3 to learn what you can do to reduce your risk for factors in your list. After you build your list, you can print it out and take it with you to your doctor.

Prostate Cancer Risk Factor

How Will I Know?

Does This Risk Factor
Apply to Me?

Age

Age is the most important risk factor for prostate cancer. The chance of getting prostate cancer increases with age. If you are less than age 40, your chances of developing prostate cancer are low (1 in 19,299). After age 40, the risk rises. If you are age 40 to 59, your risk is 1 in 45. Iif you are age 60 to 79, your risk is 1 in 7.

Yes

Race

If you are African American, you are at highest risk for prostate cancer—it tends to start at younger ages and grows faster than in men of other races. Your risk is 60 percent higher than White men. If you are White, you are at the second highest risk for developing prostate cancer. If you are Hispanic or Native American, you are at the third highest risk. If you are Asian American, you are at the lowest risk.

Yes

Family history of prostate cancer

If you have a father or a brother with prostate cancer, your risk of developing it increases 2 to 3 times that of men without family involvement. If you have a mother or a sister with breast cancer, your prostate cancer risk may increase slightly. About 5 to 10 percent of prostate cancer cases are believed to be due mainly to high-risk, inherited genetic factors or prostate cancer susceptibility genes.

Yes

Prostate Cancer Risk Action Tool
Below are risk factors for prostate cancer. Select the ones you want to work on and to put on your risk reduction list. After you build your list, you can print it out and take it to your doctor to discuss your action plan.

Prostate Cancer Risk Factors	Action List	Select Items To Put On My Risk Reduction Action List
Age	You cannot change your age, but if you know that the risk of prostate cancer increases as you grow older, you can be alert for prostate cancer symptoms and follow your doctor’s instructions for screening. See the links in the blue area above for more information about prostate cancer screening and symptoms.
Race	If you are African American, you should be particularly alert to the symptoms of prostate cancer because your risk is 60 percent higher than that of Whites. If you are White, you have the second highest risk. The risk is lower in all other racial groups, but all groups should be alert to the symptoms. All groups should follow their doctors’ instructions for screening. See the links in the blue area above for more information about prostate cancer screening and symptoms.
Family history of prostate cancer	You can consider genetic counseling. Talk with your doctor about the need to see a genetic counselor if you have prostate cancer in your family. See Elements of Cancer Genetics Risk Assessment and Counseling.

Prostate Cancer - Step 4: Ask Your Doctor About Prostate Cancer Risk
You and your doctor need to work as a team to reduce your cancer risk. Here are some tips to help you talk with your doctor about risk.

Know your risk factors and take your risk factor list with you to the doctor's office.
Prepare your list of questions before your visit (see below).
Know what behaviors you are willing to change.
Take one step at a time-be realistic about what you can do.
Add your concerns to the doctor's intake form if they are not listed.

email this page
Read the Doctor's Comments

Questions For Your Doctor
Click on the questions below that you would like to ask your doctor. Take your list when you visit your doctor.

	Do you think I should be worried about prostate cancer?
	What puts me at risk for prostate cancer?
	No one in my family has had prostate cancer. Does that mean I won't get it?
	Here is my family history. How might this affect my risk for prostate cancer?
	What can I do to maintain good prostate health?
	What screening tests do you recommend? How often?
	Are there any other things I can do to reduce my risk for prostate cancer?
	If I have a prostate problem that is not prostate cancer, will it affect my risk of prostate cancer in any way?

Prostate Cancer — Step 5: Find More Information	email this page
Use this step to check out additional information on prostate cancer. It is important to know that there is still much to be learned. Some aspects of prostate cancer are still controversial. Researchers are conducting clinical trials to find more definitive answers.

NCI Web Site Topic Page for Prostate Cancer

Cancer Topics: Prostate Cancer
Main page for prostate cancer on the NCI Web site.

Overviews

What You Need To Know About Prostate Cancer
Detection, symptoms, diagnosis, and treatment of colorectal cancer.

NIH Senior Health: Prostate Cancer
Web site that features authoritative and up-to-date information in a format tailored to older adults.

Understanding Prostate Changes: A Health Guide for Men
Covers the spectrum of prostate conditions (both noncancerous and cancerous) that occur with age. Provides information about symptoms, treatment options, and types of tests that detect these conditions.

Prevention, Genetics, Causes

Information related to prevention, genetics, and risk factors for prostate cancer, including two major clinical trials and genetic counseling information.

Prostate Cancer (PDQ®): Prevention
[ patient ] [ health professional ]
Expert-reviewed information summary about factors that may influence the risk of developing prostate cancer and about research aimed at the prevention of this disease.

Genetics of Prostate Cancer (PDQ®)
Discusses family history of prostate cancer and the inheritance of prostate cancer risk.

Search: Cancer Genetics Services Directory
Database of professionals who provide services related to cancer genetics.

Screening and Testing

Information about methods of cancer detection, including new imaging technologies, tumor markers, and biopsy procedures.

Prostate Cancer (PDQ®): Screening
[ patient ] [ health professional ]
Expert-reviewed information summary about tests used to detect or screen for prostate cancer.

Early Prostate Cancer: Questions and Answers
A fact sheet that describes risk factors for prostate cancer, and symptoms and treatment options for localized disease. Discusses available screening tests.

The Prostate-Specific Antigen (PSA) Test: Questions and Answers
A fact sheet that defines PSA and screening tests for prostate cancer and describes the benefits and limitations of the test.

Report from Large NCI Study Suggests PSA Testing Could Be Done at Longer Intervals for Men Who Choose To Test
Many men who choose to get a prostate-specific antigen test may not need to repeat the test as frequently as previously thought, according to data from the Prostate, Lung, Colorectal and Ovarian trial.

Some Men with Low PSAs Have Prostate Cancer
Article released from the NCI Press Office, 5/26/2004.

Treatment

Various treatment options available to men with prostate cancer.

Clinical Trials

Prostate Cancer Trial Results
Summaries of newsworthy clinical trial results.

Search for Clinical Trials
Search tool for clinical trials that are open to participants by type of cancer, stage/subtype of cancer, type of trial, and location of trial.

Research

What You Need To Know About Prostate Cancer: The Promise Of Cancer Research
Research being conducted on prevention, screening, and treatment of prostate cancer.

Cancer Research Portfolio
Search for research projects currently under way, by type of research, type of cancer, and participating institutions.

Statistics

Prostate Cancer Trends, 1973-1995
A comprehensive population-based evaluation on the demographic and clinical features of prostate cancer cases.

Other Resources

Staying Healthy
Behaviors you can change to live a healthier lifestyle.

Get More Information From the National Cancer Institute
How to get additional information from the National Cancer Institute.

Your Disease Risk: Cancer
An interactive tool from the Harvard Center for Cancer Prevention that estimates your risk of cancer and provides tips for prevention.

Dr. Gabriel Cousens' Reverse Diabetes Program - Tree of Life Rejuvenatio...

2011-03-29T19:20:00.000-07:00

@ronaldwgumbs is Popeye and does not appreciate radiation in spinach

2011-03-21T17:54:00.000-07:00

By LAURAN NEERGAARD, AP Medical Writer Lauran Neergaard, Ap Medical Writer – Mon Mar 21, 5:18 pm ET

WASHINGTON – Radiation-tainted spinach from Japan's damaged nuclear reactors may sound scary, but here's a reality check: Even if any made it to stores there, you'd have to be Popeye to eat enough to worry.
With some fallout found in an increasing number of foods, Japan's government is taking steps to stop contaminated products from reaching consumers — and the U.S. and other countries are double-checking imports.
The Chernobyl disaster made clear that radiation from food can be a real risk: Thousands of cases of thyroid cancer after the 1986 reactor explosion there are blamed on the Soviet Union's failure to stop children in the region from drinking milk contaminated with radioactive iodine — children who also weren't given a thyroid-protecting drug, potassium iodide.
Japan's earthquake-damaged reactors haven't leaked nearly as much radiation as Chernobyl, and aren't expected to — and this time around, people are being warned, food is being tested and there's potassium iodide in the high-risk zone.
Japan has banned sale of milk, spinach and a few other products in regions from the leaking power plant toward Tokyo after discovery of higher-than-allowed levels of radiation in a range of foods. On Monday, the World Health Organization said Japan should act quickly to ensure that no contaminated foods are sold — as a precaution against long-term risk to nearby residents who otherwise might repeatedly consume large amounts of those products.
Still, international scientists say risk from food in Japan so far is low, especially outside the disaster zone — and in the U.S. in particular because it imports very little food from Japan.
Besides, there was radiation in food well before Japan's earthquake and tsunami.
"The world is covered in cesium-137 from the atomic weapons tests of the `50s and `60s," says nuclear physicist Patrick Regan of the University of Surrey in England.
"There is radioactivity in all food. It's really a matter of saying how much," agrees University of New Mexico radiologist Dr. Fred Mettler, who studied the health effects of the Chernobyl disaster. Here are questions and answers about the situation:
Q: What's the danger?
A: Radioactive iodine, from food or the air, can build up in the thyroid, leading to thyroid cancer years later. Young children and pregnant women are at greatest risk. Thyroid cancer is one of the least fatal cancers if treated promptly.
Radioactive cesium can build up throughout the body, is harder to eliminate and high levels are thought to be a risk for various other cancers.
But it takes quite high exposure to harm, says Mettler: In contaminated villages around Chernobyl, thyroid cancer was documented. But if there was an increase in any other cancer, it was too small to detect, he says.
Q: In what foods in Japan have these radioactive elements been found?
A: Iodine has been found mostly in milk and spinach, but also in chrysanthemum greens, leeks and a few other foods. Cesium also has been found in some vegetables. Levels found so far range from trace amounts to milk with iodine levels five times the acceptable limit, and in spinach, iodine levels 27 times the ceiling. Officials soon will test seafood.
Q: If you ate that, what would it mean?
A: You'd have to eat 2 pounds of the most contaminated spinach to absorb about as much radiation as you'd get from a CT scan of the head, says Dr. Clifford Chao, radiologist-in-chief at New York-Presbyterian Hospital.
People who drank milk with the highest measured levels of iodine for two weeks would absorb less than a year's worth of natural background radiation, according to a report from British environmental radiation group, Mike Thorne and Associates Ltd. But infants would absorb more than adults.
Q: What about breastfeeding?
A: Radioactive iodine could be in breast milk if nursing mothers in Japan were exposed; potassium iodide comes in doses for infants, too, if needed.
Q: What's being done to make sure contaminated foods don't reach consumers outside of Japan?
A: China, South Korea and a number of neighboring Asian countries have ordered radiation monitoring of food imports from Japan.
"There is no risk to the U.S. food supply," the U.S. Food and Drug Administration said Monday.
Foods from Japan make up less than 4 percent of all U.S. imported foods, but the FDA said it would "be paying special attention" to imports from the earthquake-affected area.
Q: How does radiation get into food anyway?
A: Fallout can land on crops in fields and wash into the soil to be soaked through the roots. Livestock can eat contaminated animal feed. It's possible seafood could be affected from contaminated water, although in the ocean "dilution would be huge," Mettler says.
Q: What about canned or other foods stored before the earthquake — can residents eat that?
A: The WHO says radioactivity cannot contaminate sealed packaged foods, and that cropland can be covered with tarps and livestock brought into barns and fed clean feed.
Q: How long will radiation be a food threat?
A: Radioactive iodine decays quickly, with a half-life of eight days, meaning the length of time it takes for half of it to break down harmlessly. "In a couple of months, the iodine is a non-issue," says Mettler.
Cesium, however, can stay in soil for 30 years. But animals intended for slaughter can be given clean feed for a few months until cesium in their bodies drops to safe limits, he says. Also, the radiation stays only in the top inches of soil so deep plowing can make a field safe to use.
Q: Wait a minute, the U.S. and other countries irradiate certain foods to kill bacteria. How is that different?
A: No radioactivity is left in irradiated foods because the energy used, from such sources as X-rays and electron beams, is too low. The FDA, World Health Organization and other authorities have repeatedly found the process to be safe.
___
EDITOR's NOTE — Lauran Neergaard covers health and medical issues for The Associated Press in Washington. AP Medical Writer Margie Mason in Hanoi, Vietnam, contributed to this report
BLOGGER's NOTE - I eat large quantities of spinach as a part of a plant-based diet to prevent cancer. If there is radiation in spinach, then all other plants have been exposed. This is especially troubling because radiation increases the risk of getting cancer. I'm still concerned about plutonium in my urine, stools, and blood.

You have come a long way baby, or Have you?

2011-03-20T22:42:00.000-07:00

Why Do We Let Them Dress Like That?

Women of a liberated generation wrestle with their eager-to-grow-up daughters—and their own pasts

The Wall Street Journal is troubled that sex is prevalent among the youth of today, and asks:

"Why have we let them dressed that way?"

Some more fashion for male chauvinist rabbits

2011-03-20T22:25:00.000-07:00

Is this the beginning of the end or the end of the beginning of the sexual revolution?

2011-03-20T22:20:00.000-07:00

How to talk to Republicans, if you have to?

2011-03-20T13:22:00.000-07:00

Dear Illogical and Irrational Republicans:
   Did you know that President Clinton had created 22 million jobs, jobs, jobs with a GOP congress that was focused primarily on his demise? This illogical and irrational GOP obsession with his sexual appetite for oral sex ignored the fact that the Republican leaders enjoyed fellatio from their mistresses, instead of wives.
   Are you aware that President Clinton also found time to balance the budget, even producing a surplus?
   President George Bush created less than 1 million net jobs, started two wars without providing the funding, combined with an unfunded prescription benefit for seniors with the intent to privatize social security.
   What is wrong with Republicans? You talk constantly about not raising taxes and balancing the federal budget. Is it that you are all hypocrites or that you are filled with fecal matter and your rectal orifices are polluting the planet, while ignoring facts, such as global warming. Go and detoxify your filthy bodies. Purge evil from your deranged minds and tortured souls.
   I understand why you hate the current occupant of the White House and your current fascination with one, Sarah Palin. But it is sad that intelligent bloggers like Charles Krauthammer fear him because of the strength of his intellect, his love for his wife and children, and that he has the potential to transform this nation so that it can successfully compete with the Chinese, Indians, Japanese, and Koreans.
   Does Rep. Paul Ryan know that a tax on the the multi-frequency trading in derivatives ($600 trillion) at a rate of 0.01% would raise $600 billion dollars annually, transferring wealth from the Wall Street Pigs to the Suckers on Main Street? But President Obama does not believe this and neither does the GOP (correct me if you do) or the American people.
   What is it about the following chart that you fail to comprehend?

Bladder Cancer Prevention

2011-03-18T09:47:00.000-07:00

Johns Hopkins Health Alert

Cancer Prevention -- Protecting Your Bladder

Comments (0)

Johns Hopkins Health Alerts | Healthy Living After 50 |
Reduce Your Risk for Bladder Cancer

Bladder cancer is common, it is a major public health concern, and it is strongly linked to cigarette smoking.
Bladder cancer isn’t nearly as well known as lung cancer, but it should be: Bladder cancer is common, it is a major public health concern, and it is strongly linked to cigarette smoking.
Most people diagnosed with bladder cancer are aged 60 or older. Carcinogens in the urine increase the risk of bladder cancer. Cigarette smoking is strongly implicated; other risk factors for bladder cancer include chronic bladder infections and treatment with cyclophosphamide (a chemotherapy medication). People regularly exposed to hair dyes in their occupation (such as hair dressers) are at increased risk for bladder cancer, but no association has been proved for people who dye their hair.
You can take these steps to lower your risk of bladder cancer:
Don’t smoke. Smokers and former smokers (the risk never declines to completely normal) are more than twice as likely to develop bladder cancer as people who have never smoked. It is thought that cancer-causing compounds in tobacco smoke are absorbed into the blood and eventually collect in the urine, where they damage the cells lining the bladder. However, giving up cigarettes does not seem to produce as dramatic a drop in risk for bladder cancer as for lung cancer and heart disease.
Drink enough fluid. Adequate intake of water and other fluids promotes urination and help to flush carcinogens from the bladder. The American Cancer Society recommends drinking several glasses of water or other nonalcoholic beverages a day.
Eat plenty of cruciferous vegetables. A diet that routinely includes several weekly servings of broccoli, cabbage, cauliflower and other cruciferous vegetables appears to be protective.
Limit exposure to workplace chemicals. Chemicals used in the making of dyes, rubber, leather, textiles, printing materials, and paint products have been implicated in bladder cancer.
Treat bladder infections. People with chronic or frequent infections have higher rates of bladder cancer than those who are not prone to such infections.

Johns Hopkins Health Alerts | Healthy Living After 50 |
Reduce Your Risk for Bladder Cancer

Posted in Healthy Living on August 31, 2006

Medical Disclaimer: This information is not intended to substitute for the advice of a physician. Click here for additional information: Johns Hopkins Health Alerts Disclaimer

Cancer

2011-03-18T09:06:00.000-07:00

Johns Hopkins Health Alerts Topic Page:

Johns Hopkins Health Alerts Cancer Information Home Page

View All Health Alerts • View All Special Reports

Cancer is a group of many related diseases that begin in cells, the body’s basic unit of life. To understand cancer, it is helpful to know what happens when normal cells become cancerous.
The body is made up of many types of cells. Normally, cells grow and divide to produce more cells only when the body needs them. This orderly process helps keep the body healthy. Sometimes, however, cells keep dividing when new cells are not needed. These extra cells form a mass of tissue, called a growth or tumor. Tumors can be benign or malignant.
Benign tumors are not cancer. They can often be removed and, in most cases, they do not come back. Cells from benign tumors do not spread to other parts of the body. Most important, benign tumors are rarely a threat to life.
Malignant tumors are cancer. Cells in these tumors are abnormal and divide without control or order. They can invade and damage nearby tissues and organs. Also, cancer cells can break away from a malignant tumor and enter the bloodstream or the lymphatic system. That is how cancer spreads from the original cancer site to form new tumors in other organs. The spread of cancer is called metastasis.
Most cancers are named for the organ or type of cell in which they begin. For example, cancer that begins in the lung is lung cancer, and cancer that begins in cells in the skin known as melanocytes is called melanoma. When cancer spreads (metastasizes), cancer cells are often found in nearby or regional lymph nodes (sometimes called lymph glands). If the cancer has reached these nodes, it means that cancer cells may have spread to other organs, such as the liver, bones, or brain.
When cancer spreads from its original location to another part of the body, the new tumor has the same kind of abnormal cells and the same name as the primary tumor. For example, if lung cancer spreads to the brain, the cancer cells in the brain are actually lung cancer cells. The disease is called metastatic lung cancer (it is not brain cancer).
At Johns Hopkins Health Alerts, you will find articles on more than a dozen kinds of cancer, including cancers of the: prostate, colon, stomach, bladder, thyroid, cervix, and esophagus.

Additional information about Cancer can be found in the BOOKSTORE .

Enlarged Prostate (BPH) and Prostatitis

2011-03-18T08:54:00.000-07:00

Johns Hopkins Health Alerts Topic Page:

Enlarged Prostate (BPH) and Prostatitis Topic Page

View All Enlarged Prostate Health Alerts • View All Enlarged Prostate Special Reports

The prostate is a gland located at the base of a man’s bladder, behind the pubic bone and in front of the rectum. This gland, which is roughly the size and shape of a small crab apple, weighs only about an ounce in young men. It surrounds the urethra, the tube that carries urine away from the bladder and transports semen during ejaculation. A good way to envision the prostate is as an apple with the core removed, with the urethra passing through the middle.

The prostate’s primary function is to produce prostatic fluid, a component of semen. Also, during ejaculation, smooth muscles in the prostate contract to help propel semen through the urethra. Technically the prostate is not part of the urinary system. But because of its location and relationship to the urethra, the prostate can (and often does) affect urinary function.

What is Enlarged Prostate—Also Known as Benign Prostatic Hyperplasia (BPH)? When a man reaches his mid-40s, the area of the prostate that encircles the urethra begins to grow. This overgrowth of prostate tissue is called benign prostatic hyperplasia, or BPH. With continued growth, the expanding prostate may constrict the urethra, causing symptoms such as difficulty starting urination or a weak urine stream. BPH occurs in approximately 31 percent of men between the ages of 50 and 59, 36 percent of men age 60 to 69, and 44 percent of those age 70 and older. Not all of these men experience urinary tract problems related to BPH, but many do. Although BPH can cause a number of bothersome symptoms, it is not life threatening.

What is Prostatitis? Also known as inflammation of the prostate, prostatitis is common and often frustrating. It can cause pain in the lower back and in the area between the scrotum and rectum (the perineum) and may be accompanied by chills, fever, and a general feeling of malaise. Nearly half of all men will develop prostatitis at some point in their lives.

How Johns Hopkins can help. If you or someone you care about has BPH or prostatitis, obtaining accurate information is an important part of the treatment plan. Johns Hopkins Medicine is ideally positioned to provide you with timely, authoritative information and advice on conditions affecting the prostate. Johns Hopkins is ranked No. 1 in Urology by U.S. News and World Report's annual Rankings of American hospitals—and No. 1 overall.

At Johns Hopkins Health Alerts, H. Ballentine Carter, M.D., Director of Adult Urology at the Johns Hopkins University School of Urology, and his colleagues discuss the prevention, diagnosis, and daily management of BPH and prostatitis.
You’ll find articles on: BPH drugs and sexual dysfunction, combination therapy for BPH, medications for chronic prostatitis, the importance of a BPH-friendly diet, overactive bladder, and much more.

Prostate Disorders

2011-03-18T08:43:00.000-07:00

Johns Hopkins Health Alerts Topic Page: Prostate Disorders

View All Prostate Disorders Health Alerts • View All Prostate Disorders Special Reports

Prostate cancer: After skin cancer, prostate cancer is the second most common cancer in American men and is second only to lung cancer as a cause of cancer deaths. In 2009, an estimated 192,000 men were diagnosed with prostate cancer, and about 27,000 died of the disease.

The good news is that reliable diagnostic tests and numerous treatment options are available, and death rates from prostate cancer are on the decline. Nearly 100 percent of men are still alive five years after a prostate cancer diagnosis, about 93 percent are alive 10 years after diagnosis, and approximately 79 percent are alive 15 years after diagnosis.

Although the symptoms of prostate cancer are similar to those of benign prostatic hyperplasia (BPH), the conditions are not related. Having BPH neither increases nor decreases a man’s risk of prostate cancer. In addition, it is possible for a man to have both conditions at the same time.

For more information on BPH and prostatitis, go to the Enlarged Prostate and Prostatitis Topic Page.

How Johns Hopkins can help. If you or someone you care about has been diagnosed with prostate cancer, obtaining accurate information is critically important. Johns Hopkins Medicine is ideally positioned to provide you with timely, authoritative information and advice on the full range of your prostate cancer treatment options. Johns Hopkins is ranked No. 1 in Urology by U.S. News and World Report's annual Rankings of American hospitals—and No. 1 overall.

At Johns Hopkins Health Alerts, H. Ballentine Carter, M.D., Director of Adult Urology at the Johns Hopkins University School of Urology, and his colleagues discuss the prevention, diagnosis, and daily management of prostate cancer.

You’ll find articles on: the value of the PSA velocity test, the Gleason score, quality of life issues after prostate cancer treatment, new screening tests, choosing the right treatment for your prostate cancer, the role of the pathologist, the TMN prostate cancer staging system, and much more.

Harmless Virus Could Be an Answer to Cancer

2011-03-15T23:12:00.000-07:00

You'd think that infecting a cancer patient with a virus would be the last thing a doctor would want to do. But what if it was a virus that attacks and kills cancer cells? That's exactly the premise that led to the founding of Oncolytics Biotech (ONCY), a Calgary-based biotechnology company. It's about to begin Phase 3 trials that could pave the way for a marketable cancer treatment based on this technology in two years, says CEO Dr. Brad Thompson (pictured) in an interview with DailyFinance.
"We're working on a product that is widely applicable to quite a few indications of cancer and is based on a naturally occurring virus that's commonly found in the environment and that happens to have a preference of growing in cancer cells as opposed to growing in normal tissue."
It's called a reovirus (short for Respiratory Enteric Orphan virus), and it's a type which most people pick up by age 12 through inhalation or contact that causes few or no health problems. But when the virus enters cancer cells, it kills them.
On-Off Switch
Viruses, naturally, prefer cells that can't fight them off. And these cancer cells all have a common characteristic: They have a certain growth pathway, called the Ras pathway, turned on. "If a cell doesn't have that pathway turned on, nothing happens, so it's like an on-off switch for the virus's growth," Thompson explained. In the human body, very few normal cells have that Ras pathway turned on, and those die in the same amount of time the virus takes to kill them, so the body is not affected. "And that's where the story would end if only these few cells had the Ras pathway turned on all the time," Thompson added. "But it happens to be the state in most cancers."
"When the Ras pathway is turned on, it turns off the virus defense mechanism in the cell so the virus can go in and replicate itself," Thompson continued. It keeps replicating until its host -- the cancer cell -- is overwhelmed and dies, which happens within three days.
"Anywhere between two-thirds to 75% of the primary carcinomas -- ovarian, prostate, non-small cell lung cancer and so on -- actually have that pathway turned on," Thompson said. "In metastatic disease, which spreads beyond the primary tumor, it's between 95% to 100% that have the Ras pathway. So you have a disease that has this pathway, and a virus that for other reasons requires that pathway to grow."
Infecting the Cancer
That's where Oncolytics and its drug, Reolysin, come in play. Reolysin is "a variant of the virus we found in nature," explained Thompson. The treatment "is rather straightforward," he said. It involves five days of intravenous injections, and the side effects are few: Most commonly, patients run a small fever and feel a little tired.
Once the virus has killed the cancer cells, "the body actually clears the virus pretty effectively," Thompson explained, because the body mounts a normal immune response to the infection. "Normally, the latest we ever find the virus in the body is a couple of weeks after the first injection, and then it's completely gone," he says.
The company was founded in 1998 after several scientists at a virology lab in the University of Calgary started having problems growing the virus. As they screened it against established cells they found the correlation with the Ras pathway. "And then this little light bulb went on. Somebody said, wait a minute, that can be useful in oncology," Thompson tells.
Thompson lost his mother and an uncle to cancer, and himself got melanoma. "Right after that, while the surgery was still healing in my leg, I got a call from a colleague of mine in the Alberta government asking me whether I would talk to this group of researchers at the University of Calgary who were working on a virus. I had very heightened sensitivity to cancer at that time and had expertise in the area. So I got a close look at it, and that's how I got involved in it."
"That's how Oncolytics started," he added. "In less than a year, we went public, cross-listed and did six financings."
Phase 3 Clinical Trial
The company has completed about a dozen early-phase clinical trials so far, and has seven to eight ongoing for a broad range of cancers, including melanoma, lung and ovarian. But the real test will be the upcoming Phase 3 clinical trial for head and neck cancer.
The study is designed to combine Reolysin with the standard chemotherapy care for head and neck. In earlier studies, the response rate to the treatment was 42% when Reolysin was added to common therapy, much higher than the average 10% response rate for the disease.
If that response rate holds up, no doubt patients would be eager for the drug to reach the market. "We could be selling product by 2012, if everything lines up properly," said Thompson. "The sad part about head and neck patients is that you know very quickly whether your product works on them or not. The patients we're looking at have a median life expectancy of 4.5 months, so you don't have to wait much to know whether your product had benefit for the patients."
What's Next?
"The real question for us is what comes after that," Thompson added. "We're probably going to have to go after something that has a much larger market than head and neck and will also be a much larger clinical program than head and neck."
"Oncology is a very competitive, crowded space," Thompson acknowledged when asked about competitors. But he added that Oncolytics is looking at diseases that aren't getting much attention elsewhere. This also seems to be good news for patients with those diseases.
For now, Oncolytics has no bigger-company partners, which is rare for a biotech in advanced stages of clinical trials. But Big Pharma has shown interest. "There are very few unpartnered Phase 3 oncology products. So we have certainly raised the interest of a number of our big pharma colleagues." But Oncolytics claims to be in no hurry and prefers to partner when it's best for the company and shareholders. Thompson indicates that a partnership could be announced by the end of the Phase 3 study.
Like all small biotechs, Oncolytics is facing challenges, most notably the possibility that its experimental drug will not work in late-stage trials despite positive early indications. But if anything, it's encouraging to see companies always in a quest to find improved treatments for a deadly disease.

Melly Alazraki

Stock Market Writer and Analyst

Balancing the budget without confiscating super-rich people’s money.

2011-03-12T00:56:00.000-08:00

Video: Why can’t we balance the budget by confiscating super-rich people’s money?Michael More's Solution

Congratulations on your excellent analysis and commentary.

Here is one of many plausible solutions for balancing the budget and gradually reducing the national debt.

We can eliminate the debt problem by taxing the trading of derivatives ($600 Trillion/ year) and other credit default swaps, which caused the Great Recession in 2008. Analyze that,

Now do the math. A tax of 0.1% generates $600 Billion. In 10 years, this generates $6 Trillion.

These instruments, which Warren Buffet called weapons of financial destruction, are traded daily by this chemist, as well as by many filthy rich hedge fund managers in multi-frequency trades with very fast computers. As you know and Mad Money Jim Cramer will confirm, we do not create liquidity or jobs or provide capital to the economy; we only feed at the decadent trough that is Wall Street, while anally raping the ignorant suckers on Main Street.

It is a closely guarded secret that is perfectly legal, and it is engaged in by only a few of the 400 billionaires, including Mr. George Soros, who made $1.8 Billion in 2010.

With respect to Medicare, I will present some ideas in my next post.

The History of Prostate Cancer: Can it be prevented?

2011-03-11T18:34:00.000-08:00

In modern societies, cancer, in general, is second only to cardiovascular disease as a cause of death. The history of this disorder has the potential to improve our understanding of disease prevention, etiology, pathogenesis and treatment. A striking rarity of malignancies in ancient physical remains indicates that cancer was rare in antiquity, and so poses questions about the role of carcinogenic environmental factors in the industrialized societies. Although the rarity of cancer in antiquity remains undisputed, the first published histological diagnosis of cancer in an Egyptian mummy demonstrates that new evidence is still forthcoming.

In light of the fact that March is Prostate Cancer month, the following is restricted to cancers of the prostate, in particular, and specifically on prevention. And since I am neither a physician nor an expert, I refer the reader to these books, the covers of which are illustrated below.

Man to man: After you have read these books and consulted with a urologist, please return to this blog, and
we will talk some more. In the meantime, a recent photograph of me with my bother is attached.

The Gumbs Brothers

Studentlifeguru's Blog

2011-03-06T23:25:00.000-08:00

Studentlifeguru's Blog

World Travel Guide | Where I've Been

2011-03-06T23:23:00.000-08:00

World Travel Guide | Where I've Been

Nutrition Facts: An interactive guide to food labels - MayoClinic.com

2011-03-06T23:17:00.000-08:00

Nutrition Facts: An interactive guide to food labels - MayoClinic.com

Dietary fiber: Essential for a healthy diet - MayoClinic.com

2011-03-06T23:16:00.000-08:00

Dietary fiber: Essential for a healthy diet - MayoClinic.com

What the World Eats, Part I

2011-03-06T23:15:00.000-08:00

What the World Eats, Part I

Bat Crisis: White-nose Syndrome

2011-03-06T23:13:00.000-08:00

Bat Crisis: White-nose Syndrome

Pesticides Reduction

2011-03-06T23:11:00.000-08:00

Pesticides Reduction

Joel Fuhrman, M.D.: Heart Health: How You Can Prevent and Reverse Heart Disease

2011-01-07T13:14:00.000-08:00

Joel Fuhrman, M.D.: Heart Health: How You Can Prevent and Reverse Heart Disease

Feed Our Vets - Home

2010-12-31T05:45:00.000-08:00

Feed Our Vets - Home

National Center for Complementary and Alternative Medicine [NCCAM]

2010-12-24T09:41:00.000-08:00

The budget for this branch of the NIH must be increased in order to lower the cost of health care in the nation. Please ask your representatives in Congress to support increased clinical studies on prevention using alternative medical approaches. I am particularly interested in seeing more studies of plant based foods in preventing chronic diseases.

About NCCAM [NCCAM]

Join Natalie Portman and support Village Banking - FINCA

2010-12-24T09:23:00.000-08:00

Join Natalie Portman and support Village Banking - FINCA

Holiday drinks: Good cheer, but watch the calories - MayoClinic.com

2010-12-23T08:44:00.000-08:00

Holiday drinks: Good cheer, but watch the calories - MayoClinic.com

Arsenic - Drinking Water Contaminants, Facts/Removal Methods

2010-12-22T14:54:00.000-08:00

Arsenic - Drinking Water Contaminants, Facts/Removal Methods

Ronald W. Gumbs, Ph.D.

Do Cellphones Cause Brain Cancer?

Milk Intake in Early Life and Risk of Advanced Prostate Cancer

Sodium: Are you getting too much?

Nutrition basics (18)

· Healthy diets (7)

· Healthy cooking (15)

· Healthy menus and shopping strategies (10)

· Nutritional supplements (2)

Sodium: Are you getting too much?

How much sodium do you need?

Three main sources of sodium

Be a savvy shopper: Find thesodium

How to cut sodium

· See Also

True or False: Prostate Cancer Growth Is Faster in Black Men?: Johns Hopkins Health Alerts

Prostate cancer prevention: What can men do? by Mayo Clinic staff

continued:

Cancer risk: What the numbers mean

Where do cancer risk statistics come from?

How do cancer risk statistics relate to you?

Keep cancer risk statistics in perspective

Question

Pomegranate juice: A cure for prostate cancer?

Is it true that pomegranate juice may slow the growth of prostate cancer? How much should I drink?

Answer

from Erik Castle, M.D.

continued:

Prostate cancer prevention: What you can do

Drugs to prevent prostate cancer

Selenium and vitamin E

Prostate cancer risk: A common-sense perspective

Definition

Living with cancer newsletter

· Mayo Clinic services

· Mayo Clinic research

Symptoms

Living with cancer newsletter

Causes

Living with cancer newsletter

Risk factors

Living with cancer newsletter

What is your lifetime risk of prostate cancer and can prostate cancer be prevented?

Dr. Gabriel Cousens' Reverse Diabetes Program - Tree of Life Rejuvenatio...

@ronaldwgumbs is Popeye and does not appreciate radiation in spinach

You have come a long way baby, or Have you?

Why Do We Let Them Dress Like That?

Women of a liberated generation wrestle with their eager-to-grow-up daughters—and their own pasts

Some more fashion for male chauvinist rabbits

Is this the beginning of the end or the end of the beginning of the sexual revolution?

How to talk to Republicans, if you have to?

Bladder Cancer Prevention

Cancer Prevention -- Protecting Your Bladder

Johns Hopkins Health Alerts | Healthy Living After 50 |Reduce Your Risk for Bladder Cancer

Johns Hopkins Health Alerts | Healthy Living After 50 |Reduce Your Risk for Bladder Cancer

Cancer

Johns Hopkins Health Alerts Cancer Information Home Page

Enlarged Prostate (BPH) and Prostatitis

Enlarged Prostate (BPH) and Prostatitis Topic Page

Prostate Disorders

Harmless Virus Could Be an Answer to Cancer

Balancing the budget without confiscating super-rich people’s money.

The History of Prostate Cancer: Can it be prevented?

Studentlifeguru's Blog

World Travel Guide | Where I've Been

Nutrition Facts: An interactive guide to food labels - MayoClinic.com

Dietary fiber: Essential for a healthy diet - MayoClinic.com

What the World Eats, Part I

Bat Crisis: White-nose Syndrome

Pesticides Reduction

Joel Fuhrman, M.D.: Heart Health: How You Can Prevent and Reverse Heart Disease

Feed Our Vets - Home

National Center for Complementary and Alternative Medicine [NCCAM]

Join Natalie Portman and support Village Banking - FINCA

Holiday drinks: Good cheer, but watch the calories - MayoClinic.com

Arsenic - Drinking Water Contaminants, Facts/Removal Methods

Johns Hopkins Health Alerts | Healthy Living After 50 |
Reduce Your Risk for Bladder Cancer

Johns Hopkins Health Alerts | Healthy Living After 50 |
Reduce Your Risk for Bladder Cancer