What follows are a few articles cobbled together from the internet. If I were a bookie, from the little I have read, I'd reckon that some if if not all Leukaemias were triggered by viruses. This does not divorce the cluster from the nuclear plant. It does not seem unreasonable to suppose the cluster incidence may have something to do with radiation, perhaps by lowering resistance or mutation.

The first question we should ask is.

The mechanics of pain and suffering may be fascinating, but it strikes me that the argument is polarised here. A bit like two people arguing about what makes gunpowder dangerous, one person claiming sulphur is the villain, and the other shouting 'charcoal charcoal'.

Whether it's dangerous or not, what the fuck do we want a nuclear power station for anyway?

Promoting Professor Leo Kinlen’s population mixing and an as yet unidentified virus as causing the Sellafield leukaemias, local pressure group CORE (Cumbrians Opposed to a Radioactive Environment) has questioned the credibility of ‘eminent’ cancer specialist Sir Richard Doll for his current acceptance of an unsubstatiated theory which he has twice rejected in the past. A CORE spokesperson said today: "This is another orchestrated attempt to shift attention away from radiation, particularly with part privatisation coming on. It is unscientific to concoct a computer programme to make a hypothetical theory fit. Sir Richard Doll’s support for the Newcastle research makes its validity even more suspect. His view has littlfe credibility with us." CORE campaigner Janine Allis-Smith, whose son developed leukaemia, wrote to Sir Richard Doll in 1989, when a viral cause was first suggested and before he agreed to be a BNFL witness to testify against Cumbrian leukaemia victims. As a then Director of the Imperial Cancer Research Fund and a member of the United Kingdom Coordinating Committee for Cancer Research (UKCCCR) that received £3 million from BNFL, the CEGB and the UK Atomic Energy Authority for research into the cause of childhood leukaemia, he replied: "I am personally far from convinced that a virus plays any part in the production of childhood leukaemia in this country, but the idea is scientifically attractive ...... because it could explain some of the epidemiological findings. Only one factor is firmly established as a cause of childhood leukaemia: namely radiation."

Child leukaemia linked to infection

There is a glut of leukaemia cases around Sellafield

Childhood leukaemia is likely to be caused by an infection, according to a study by researchers from Newcastle University.

The study, to be published in the British Journal of Cancer on Monday, also found that clusters of cases around industrial sites are the result of "population mixing" - with newcomers' children more at risk than those born to locals.

Childhood leukaemia is extremely rare and scientists have been investigating the higher incidence of the disease near sites such as Sellafield nuclear reprocessing plant in Cumbria, northern England, for around 20 years.

The study found in Cumbria that around half of all cases of two childhood cancers - acute lymphoblastic leukaemia (ALL) and the related disease Non-Hodgkin's Lymphona (NHL) - could be linked to an infection caused by outsiders moving into the rural community.

Researchers Heather Dickinson and Louise Parker studied the records of 119,539 children born in Cumbria between 1969 and 1989.

They found that youngsters were much more likely to develop either ALL or NHL if both their parents were born outside Cumbria.

"All children, whether their parents are incomers or locals, are at a higher risk if they are born in an area of high population mixing," Dickinson said in a statement issued by the Cancer Research Campaign, which publishes the British Journal of Cancer.

"But children of incomers seem particularly at risk because they are potentially being exposed to more new infections," she added.

Sir Richard Doll, the renowned cancer expert who first linked tobacco with lung cancer, said childhood leukaemia appeared to be "an unusual result of a common infection".

"You would get an increased risk of it if you suddenly put a lot of people from large towns in a rural area, where you might have people who had not been exposed to the infection," he said.

He added that the study supported a theory developed by Professor Leo Kinlen of Oxford University that childhood leukaemia was caused by infections introduced into a community by migrant workers.

Responding to the findings, Prof Kinlen said the next challenge was "to identify the infective agent, and at the moment scientists have little idea what it could be".

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19 March 1999

Radiation Protection - Science in Crisis
Flaws in NRPB modelling
There are two strands to the Low Level Radiation Campaign's case:

• the scientific basis of radiation protection standards is fundamentally flawed, particularly for internal radiation from radionuclides which, following inhalation or ingestion, become incorporated into body tissue.
• there is a lot of evidence of health effects associated with low levels of radioactive pollution, and that these effects are greater than predicted or explained by official models of radiation hazard;

The Health section of this site deals with the health aspects.

This section concentrates on the flawed basis of standards handed down by the International Commission on Radiological Protection (ICRP).
It is not intended to be an exhaustive review of everything that is wrong:-
we are not discussing, for example, Professor Alice Stewart's analysis of the range of radiation sensitivity in human populations, nor the large uncertainties in "critical group" modelling.
These are important, but there is something still more fundamental:-
ICRP's scientific model, which is used as the basis of radiation protection almost everywhere,

• is based on studies which are completely silent on the health effects of internal contamination
• is an averaging model, which is inappropriate -- like saying that the energy you receive from warming yourself at an open fire could just as safely be absorbed by means of taking one of the burning coals and swallowing it.

In August a paper re-examining leukaemia in children near BNFL's Sellafield reprocessing plant concluded that the risk to children arose not from parental radiation exposure but from the mixing of populations that resulted from people moving to work in this previously isolated area. So strong was this conclusion that the eminent epidemiologist Sir Richard Doll commented that the cause of such childhood leukaemia is now clearly established as infection (of unknown origin) and not paternal or environmental radiation exposure.

Medical Opinion

Does this mean that we should avoid moving town and meeting newcomers during the early part of our children's life?

This might be a natural conclusion to draw from this report when it is read in isolation. However, a number of factors should be considered before acting in this way. Firstly, only one in 1800 children gets leukaemia so the risk to them is low, overall. Secondly this report focuses on only one factor that contributes to leukaemia.

There is other strong scientific evidence that there are several other steps needed to develop leukaemia. Finally, moving home and meeting newcomers is not the only way in which your child can be exposed to new viruses. Indeed meeting new viruses is part of normal development of the immune system for us all and keeps the majority of us well in our later lives. It is impossible to protect your child from exposure to viruses whilst giving them a normal healthy upbringing.

This report's conclusions will be used to develop new research aimed at trying to unravel the steps in the process leading to leukaemia but it is only one piece of the jigsaw. Whether this will lead to ways of preventing leukaemia remains to be seen.

Dr. David Walker - Medical editor

Every day we are all exposed to viruses and bacteria, mostly through contact with other people. Only rarely do these infections make us ill because our bodies, through the immune system, are able to fight them off. We are best at fighting off germs our bodies have met before. However, when we meet new germs - which can happen when we meet people from other parts of the country - our bodies are not so able to fight them and they can make us ill.

Acute lymphoblastic leukaemia (ALL) is a cancer of the white blood cells and is the commonest childhood cancer. Non-Hodgkinís lymphoma (NHL) is a cancer of the lymph glands but is in many ways similar to ALL. Both white blood cells and lymph glands are part of the body's immune system and are involved in the fight against infection.

Since the beginning of this century it has been suspected that infections may cause leukaemia, but since people with leukaemia are more susceptible to infections, it has not been clear whether infections are the cause or the result.

In 1983, a cluster of cases of ALL and NHL was discovered in children living in Seascale, the village close to the Sellafield nuclear reprocessing plant - since 1950 there had been more than 10 times the number of cases expected. A government committee, set up to investigate the phenomenon, reported in 1984 that there was no evidence that the cases were linked to radiation from Sellafield.

In 1988, professor Leo Kinlen of the University of Oxford put forward the theory that in rare cases exposure to common infections through population mixing might result in childhood leukaemia and lymphoma. He suggested that there was so much population mixing when construction workers and nuclear staff moved into the Sellafield area that this could have caused the excess of ALL and NHL in Seascale children. He has produced more than ten scientific papers which have helped support his population mixing theory.

"We made a detailed study of children born in Cumbria by looking at the records of 119,539 children born there between 1969 and 1989. These children were followed up to see whether those who developed ALL or NHL had anything in common. Strikingly, we discovered that child higher risk because they are potentially exposed to more new infections. We also discovered that young children, whether their parents were incomers or locals, were more at risk if they were born into an area where a high number of residents were newcomers.

We made a computer model of how ALL and NHL were linked to population mixing which showed that the Seascale cluster could have been predicted due to the unusual amount of population mixing there. Eight out of ten children born in Seascale were to parents who had moved into Cumbria from outside. Our model predicted that population mixing could have led to the 8 cases of ALL and NHL in Seascale children".

Although we are now confident that ALL/NHL can be caused by an unusual response to infection, children with the disease are not infectious and can't spread the disease to others. ALL and NHL are not diseases that can be caught. Professor Kinlen of Oxford University says: "The challenge now facing researchers is to identify the infective agent and at the moment scientists have little idea what it could be."

Our report of our study was published recently and, in an accompanying editorial, internationally renowned cancer expert, Sir Richard Doll, says: "The time has now come when Kinlen's hypothesis of population mixing as a cause of childhood lymphoblastic leukaemia can be regarded as established".î

• Funded by the North of England Childrenís Cancer Research Fund
• British Journal of Cancer: Vol 8, issue 1, Sept 1999

By Philip E. Ross

IN 1983 BARRY MARSHALL, AN INTERNIST FROM PERTH, Western Australia, discovered that a spiral bacterium called Helicobacter pylori causes most stomach ulcers. It turns out it also causes most cases of stomach cancer. His discovery was a monumental step forward in medicine, taking patients from the realm of pallitative treatments that left them ill into the territory of cures. Now doctors test ulcer patients for the bacterium and treat those who have it with powerful doses of antibiotics like Omeprazole, Clarithromycin and Amoxicillin.

The nagging question is why it took so long for doctors to accept Marshall's discovery. For years the medical establishment laughed off Marshall's theory, even after he demonstrated it by drinking H. pylori and giving himself ulcers, and even after other labs replicated his experimental results. Although that had happened by 1986, "they didn't start treating for H. pylori for another nine years," Marshall says, still amazed by it all. "Hundreds, even thousands of people must have died from ulcers who wouldn't have."

Could the medical establishment be making the same mistake about other chronic diseases--such killers as heart disease, cancer, diabetes, multiple sclerosis and Alzheimer's? It is taken as a given among both doctors and scientific researchers that the causes of these ailments are genetic or environmental or both. That's where almost all of the research money is going. We're spending at least $2 billion a year looking for genes that cause cancer, Alzheimer's, heart disease and obesity. A large part of the $150 billion a year this country spends fighting pollution is aimed at removing trace toxins that are suspected of contributing to cancer. There is no question that genes and environment contribute to chronic diseases. But what if bugs start the process for some or many of these diseases? Are we perhaps looking in the wrong places for cures and preventive measures? Is it possible that, for some future generation of patients, cancer, Alzheimer's or obesity will be attacked with a vaccine?

The question is not as far-fetched as it seems. Consider the matter of cervical cancer, which every year is diagnosed in perhaps 179,000 American women and kills 4,200. The evidence that there is something infectious about this disease goes back a long way--to 1832. It was then that Rigoni Stern noted that celibate women almost never came down with this cancer. (He compared incidence of the disease in nunneries with incidence in the general population.) The observation came long before Louis Pasteur even elucidated the germ theory of disease, and it went nowhere for 151 years.

Then in 1983--coincidentally the year that Barry Marshall made his medicine-shattering discovery about ulcers--Harald zur Hausen of the German Cancer Research Center in Heidelberg proved that human papilloma virus could cause cervical cancer. It has since become clear that the virus is to blame for virtually all cases of this cancer. It is still true that genes and environment play a role in this killer. But there is no question that preventing the viral infection would all but eliminate the cancer.

The medical establishment didn't welcome zur Hausen's theory. "To convince scientists, as well as pharmaceutical companies, took a long time," he says with a sigh. What a tragedy. Imagine that the germ theory of cervical cancer had caught on in Pasteur's day and that scientists spent the next century striving to find a vaccine against the virus. We might have won this part of the war on cancer by now.

The germ theory has had an irregular string of victories in medicine. In 1854 an astute doctor noted a pattern in cholera cases that made it clear a waterborne pathogen was the cause; in 1865 Joseph Lister cut mortality by keeping operating rooms antiseptic; in the 1890s it dawned on the world that malaria, far from being due to the "bad air" that its name implies, was due to bugs. The early successes were followed by a long stretch in this century when there weren't many stunning surprises regarding the connection of infectious agents to disease. After all, it doesn't take a genius to see that measles spreads. Making the connection when there is a long lag time between infection and disease, though, is hard. Cervical cancer comes 30 years after a woman contracts the virus from a perfectly healthy man, and it doesn't develop in every woman who gets the virus.

The science of infectious disease may be moving faster now. We have new tools for distinguishing microbes, for finding subtle clues to cryptic infections and for devising antimicrobial drugs that might, by ameliorating an illness, show that it must therefore be infectious in origin.

Could heart disease be related to a slow-moving infectious agent? No question that heredity and diet play a role in the clogging of arteries. But maybe a bug starts the inflammatory process that swells the lining of an artery. Some circumstantial evidence points to Chlamydia pneumoniae, a common denizen of the lower respiratory tract. Pfizer, Hoechst Marion Roussel, and Abbott Laboratories are each testing proprietary antibiotics against the bacterium in the hope that the drugs will reduce heart attack rates.

Hoechst is also testing whether a war against C. pneumoniae can help asthma patients. Zur Hausen says an experimental vaccine against human papilloma virus--and thus cervical cancer--may reach the market within three years. It might also be effective against nonmelanoma skin cancer, which zur Hausen has recently linked to the same virus.

Other diseases, at earlier stages of investigation, are on the list of suspects for infectious causation. Among them: breast and ovarian cancers, multiple sclerosis, juvenile diabetes, reactive arthritis, Alzheimer's, even obesity, and the list grows by the year.

"There have been many, and there will be more, for when you look, you find," says Anthony Fauci, the famed National Institutes of Health virologist. Fifteen years ago, he notes, most doctors doubted that viruses played any role in cancer; now the consensus is that they cause around 20% of cases. "And it will turn out to be a lot more than that," Fauci says.

"People talk about our bodies' exposure to pesticides and chemicals--they're nothing compared to microbes," says Julie Parsonnet, an infectious diseases specialist at Stanford University Medical School. "Your gut is loaded with bacteria; your genitourinary tract, your skin, your mouth, your eyes. Our bodies contain at least ten times more microbial cells than human ones--we are walking petri dishes, more microbe than man--and our relationship to microbes may be responsible for a huge amount of disease."

When the prevalence of a disease is highly localized, you can tease out the microbial actors all the more easily. That was true of Burkitt's lymphoma, rare everywhere but in Africa, where it is the leading cause of cancer death in children. It turns out the cancer develops only if you are simultaneously infected with Epstein-Barr virus (a ubiquitous bug best known for causing mononucleosis) and malaria, which in its severest form is mainly found in Africa.

Another local detective story was recently reported in the British Journal of Cancer. Scottish researchers found that a cluster of cases of childhood leukemia was heavily weighted with children who had recently moved to the area. That statistical clue is evidence of an infectious cause.

When no clear pattern of infection can be seen on the disease map of the world or in special populations, then it can be tough to demonstrate that a given germ, even if found often in the tissues of patients, is the cause of their ailments.

The best example of such a hard case is C. pneumoniae and heart disease. The bacterium is found more often in the plaque that hardens arteries than in corresponding places in people whose arteries are clear. Is the bug a culprit or a bystander?

Serious people doubt that it is a culprit. Paul Ridker of Brigham & Woman's Hospital in Boston says it's no surprise to find Chlamydia in the inflamed tissue surrounding plaque. These bacteria live inside white blood cells--that's how they evade the rest of the immune system--and when the white cells rush off to help orchestrate the inflammation, the Chlamydia could just be hitching a ride. Nor is it a surprise that people who have already had heart attacks have a lot of Chlamydia antibodies--such people are weakened, and thus more likely to get infections. He said his group at Harvard followed healthy people for years and found that the ratio level of their antibodies to Chlamydia did not predict their risk of having a heart attack.

Proponents of the other side of the debate say that our tools for measuring infection were designed to detect acute infections, where the immune response is very strong. They may not work on low-level, chronic infections that hide from the immune system in white blood cells or other sanctuaries. They also argue that lab animals fed a high-fat diet could develop atherosclerosis faster if they were also infected with C. pneumoniae.

"We are walking petri dishes, more microbe than man.

"There are many things that can cause inflammation," says Michael Dunne, director of clinical studies for infectious diseases at Pfizer. "But I think it is likely that infection is driving the atherosclerotic process." In a 3,500-patient study due to end late next year, Pfizer is giving three-month courses of its Zithromax antibiotic to half the patients and placebos to the other half. If it works, maybe we'll all end up taking the pills.

Firm evidence connecting bugs to chronic diseases once thought to be wholly environmental or genetic is still pretty scarce. But there is some fascinating evidence--or speculation, perhaps we should say--from the budding field of Darwinian medicine. The reasoning is as follows. A chronic ailment like schizophrenia or cancer cannot be genetic in origin, because it confers a disadvantage in the competition to reproduce. If schizophrenics are even a bit less likely to have children than sane people, then the schizophrenia gene should die out over time. Indeed, it takes just a slight evolutionary unfitness--a 1% drag on reproduction--for a moderately rare gene to become extremely rare over the course of a few thousand years of human evolution. So if you see a disease that has afflicted mankind for a long time and confers any evolutionary disadvantage, you should suspect a bug.

Paul Ewald, a professor of biology at Amherst College, is the pioneer of this view of microbial disease. He came to the field from evolutionary biology proper--in his case, the study of birds. He shifted his focus when a bad case of diarrhea had him wondering what the damned germ could possibly be getting out of his misery. Answer: the chance to spread itself into the water supply.

Purify the water, as we have done in this country for generations, and you break the chain of infection. Ewald wondered what would happen then--could the guilty microbe evolve into a more benign form, in an attempt to linger longer in the host?

Theory said that it should, and practice has confirmed that it does. "The second most successful vaccine of all time is the one against diphtheria, because they made the vaccine from the bacteria's toxin," Ewald says. "Not on purpose--they just noticed that the toxin makes a great antigen [target for the immune system to attack]. The organisms in the wake of that vaccine are as mild as can be--people are getting the diphtheria organism all the time without knowing it."

The crude Darwinian approach practiced by prior generations of doctors assumed that all germs evolved to coexist happily with their hosts, Ewald notes, not considering that bugs could easily evolve the other way, toward nastier disease. He thinks such a swing toward virulence explains the terrible influenza pandemic of 1919, which killed more people than World War I.

Normally, flu, like any other disease transmitted through the air, requires a more-or-less ambulatory host. You can feel bad, of course, but not so bad that you stay home in bed, where you can't cough on strangers. Change the equation, and you may well change the virus (one of the most mutable known). Ewald thinks that conditions on the Western Front aided this process, shoving what was perhaps a worse-than-usual bug in a truly diabolical direction.

Soldiers with flu would have been stuck in their trenches until practically keeling over. These bad cases would get sent to a clinic, where their uncommonly intense infections would spread to others. The sickest of that bunch would then be removed to hospitals further back, and the process of selection would continue. Result, according to Ewald: the most virulent strain of flu ever seen. About 20 million died.

Selection effects also explain why the infections acquired in hospitals are so tough, Ewald says. Hospital workers spread germs from patient to patient, carrying strains that, because they prostrate a patient, would not have succeeded in spreading in the general population. Mosquitoes do much the same thing; they make deadly infections more feasible on the evolutionary plane.

A chronic infection, which goes on for an entire lifetime, would tend to spread in a different manner. It might travel via sexual contact, or from mother to child at birth, or during nursing. Because new hosts don't crop up very often in these scenarios, such a bug couldn't be all that virulent--it has to keep its host alive (and perhaps feeling good and looking marriageable)to maximize its own chances of getting into another host.

"Sexually transmitted pathogens may cause a lot more problems than we're yet aware of.

"Evolutionary theory leads me to conclude that sexually transmitted pathogens cause a lot more problems than we are yet aware of," Ewald says. "They must survive a long time in the host, hidden from the immune system; the only ones that survive will have figured out that trick. They may hold down their damage in the short run, but chances are that in the long run they'll muck something up. One way to reproduce is to stay inside the cell, wait until it divides, and divide with it--HTLV [the AIDS virus] and human papilloma virus do that. But how to get the cell to divide? By mucking up its mechanism, and that moves you one stage closer to cancer."

So maybe there are lots of slow-acting infectious agents that, for their own evolutionary purposes, lurk inside our cells and cause havoc over long periods. If that is the case, it is time to repeal the four postulates of Robert Koch. This famous 19th-century bacteriologist set a high standard for proving that a disease is caused by a microbe. First, he demanded, find epidemiological statistics consistent with infection; then isolate the suspected causative organism; then produce the same disease in an experimental animal by injecting the organism; then retrieve the organism from the animal. The rules worked for acute diseases. But with cryptic infections lasting decades, involving organisms that are often hard to culture in test tubes or in animals and that affect people very differently because of the intercession of genes and behavior, the chain of causation can get unmanageably complex. In the new realm of chronic disease, declares Ewald, you should start off assuming that a microbe is not merely a possible villain, but the likeliest one.

Ewald credits this sharpening of his thesis to his unorthodox collaborator, Gregory M. Cochran, a Ph.D. in physics who researches optics for the military and works on evolutionary biology as an avocation. "I consider him a genius," Ewald says.

Ewald first crossed paths with Cochran a couple of years back, when Ewald served as one of the three referees for a paper Cochran had submitted to a scientific journal. Cochran argued--and still does--that homosexuality probably has to be infectious in origin because it is widespread, of ancient duration and very bad for the reproductive success of the affected person. Any gene for the behavior, therefore, should have become very rare long ago.

The other two referees were appalled; Ewald was intrigued, although he, too, rejected the paper on technical grounds. In his notes to the author he offered to collaborate with him on similar research topics. So far they have published two academic papers; others are forthcoming.

Applied to the matter of homosexuality, Cochran's view of genes and germs is rank speculation and without practical application anyway. But it is useful if only as a mental exercise that leads to a change in thinking about disease causation. Ewald and Cochran argue that researchers should at least give germs equal standing with other unproved theories when they tackle ailments like psychosis and diabetes. Cochran sums up the new germ theory this way: "Big, old diseases have to be infectious."

Schizophrenia is very common--1% of the population has it--widespread, ancient and costly from a Darwinian point of view. Heredity clearly plays some role in susceptibility to the affliction. Could that be the whole explanation? Defenders of the pure-gene view have to come up with some way around the matter of reproductive fitness. They argue that the underlying factors for the disease may have provided our Stone Age ancestors with some unspecified advantage in surviving to adulthood. But Cochran says there is no particular reason to believe this story.

"Besides, it's so bad for your fitness it should have disappeared very, very recently, let alone a long time ago--things move fast when you have fitness differential that big," he says. He cites, as an example of recent evolution, the steep decline in the frequency of the gene for sickle-cell anemia among African-Americans, compared with what you'd expect to find, given the percentage of their African ancestry and the prevalence of the gene in Africa. There is a simple reason why the sickle-cell gene has not disappeared in Africa; people born with one copy of this gene have only slight anemia, but they do have an increased ability to survive malaria infections. Thus, offsetting the genetic pull toward elimination of the gene--namely, that children born with two copies of the gene die young in Africa--is an evolutionary pull in favor of the gene.

"The gene for sickle-cell anemia provides a very expensive defense against malaria--it kills children born with two copies of it--and in America you have no such threat to defend against," Cochran notes. "If it started out with a gene frequency of 20%, the highest you get in Africa, and you put it in a nonmalarial area, it should drop to a third that in ten generations. This changes fast."

If schizophrenia imposes a similar cost, and offers no offsetting gain, why hasn't the genetic propensity to get it dropped to the low, low level you'd expect to find from random mutations? Could it be that it's caused by a bug? Remember that it's hard for humans to outevolve microbes, given that microbes go through more generations in a day than we do in a century.

"Big old diseases have to be infectious."

The first of Koch's demanding postulates has already been satisfied for schizophrenia: It turns out to be significantly more common in children born in winter months, when infections are most common, even though symptoms do not normally develop until late adolescence. Many have sought a microbe perpetrator, without success, but Cochran can at least spin a plausible scenario.

"Maybe an infection cuts back on certain connections among neurons in the brain of the newborn, and later, in late adolescence, when many connections are pruned back, you find that you're a quart low," he says. "The same is true of postpolio syndrome--you recover from paralysis, and then, in your late 60s, you're short of motor neurons."

Following this line of reasoning, Ewald and Cochran began to question a tenet of Darwinian medicine that argued that we get chronic illnesses today because our bodies are adapted to Stone Age environments. Back then, any gene that helped get us from birth through reproductive age would have been favored even if that same gene imposed health disadvantages at age 60.

But in the view of Ewald and Cochran, that argument, while important, cannot be the whole story. "We see a lot of old people who are doing well in old age, and that suggests that there is enough genetic variability for evolution to work with," Cochran notes. "Suppose you get hit by a falling boulder and grandpa takes in your kids and raises them, and suppose there's a famine, and a certain percent of the people are going to die. The question is, who? Having a grandfather around could help just enough to make the difference." And if your grandchild survives, so do your genes.

Does this mean that our inherited genes and the environment we now enjoy don't matter? Not at all--it only means that they are not necessarily more important than microbes. As zur Hausen points out, everyone with cervical cancer has the human papilloma virus, but not everyone with the virus develops the cancer. What's more, women infected with human papilloma virus are more likely to progress to cervical cancer if they smoke.

No modern illness is more often attributed to Stone Age genes in a Jet Age body than obesity; yet even here, certain microbes may be the real problem. Five different viruses have been implicated in obesity in animals, and one--adenovirus 36--has been found in both humans and animals.

Nikhil Dhurandhar, an obesity specialist at Wayne State University, discovered the virus originally in chickens, who were getting fat before dying of their illness. He found that in chickens, rodents and monkeys, adenovirus 36 caused increases in body fat and--peculiarly enough--decreases in the level of cholesterol and triglycerides in the blood.

He found that antibodies to the virus showed up five times more often in the obese people than in lean ones from the same states (Florida, Wisconsin and New York). On top of that, the obese people who have been infected by the virus had lower cholesterol and triglyceride levels than the other obese people did. The National Institutes of Health is funding a three-year investigation.

A confirmation of Dr. Dhurandhar's theory would suggest that we are barking up the wrong tree in obesity treatments. Instead of filling people up with phentermine and fenfluramine, maybe we should be looking for a vaccine or an antiviral drug.

What's the payoff if this new way of looking at chronic illness proves correct? First off, it would explain a number of medical puzzles. We know that poorer, less-educated people suffer from more infections; this could be why they have more heart disease and cancer, even after you take into account smoking and other risk factors.

Second, it could suggest new places to look for the causes of old diseases. For example, there ought to be a lot more sexually transmitted microbes than we know about, and many dismissed as benign may turn out to be pernicious. We could even reexamine our study of the human genome to find whether subtle genetic variations affect our resistance to particular infections.

Scientists now think they know what protease precipitates Alzheimer's. They don't yet know what gives rise to this enzyme or how to respond with a treatment. It could be that a protease inhibitor will prevent the disease; or it could be that an antimicrobial will be the answer.

The new germ theory of disease suggests new priorities in drug research. The challenge of AIDS has shown us how far science can go in devising antivirals, if the will is there. Maybe we will want to develop more antivirals against what have until now seemed to be innocuous acute infections but may well turn out to be the precursors of long-term disease. Work on a vaccine against Epstein-Barr virus has so far been motivated by a desire to head off mononucleosis; maybe the work would have gone faster if we'd known the virus also causes cancer. Maybe specialists in all diseases should consider the possibility that germs could be the problem.

"From when I was in medical school until now, we've made very little advance in understanding high blood pressure," says Barry Marshall. "Millions of people are taking medication every day of their life to control this problem, yet it's quite possible somebody could make a breakthrough tomorrow, just as I did with H. pylori, and explain it."

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