Wednesday, August 13, 2008

BOOK REVIEW of Hyping Health Risks By Geoffrey C. Kabat


Does the wearing of shoes with heels cause schizophrenia? That was the contention made in 2004 by a Swedish physician in Medical Hypotheses, a scientific journal that specializes in out-of-the-box thinking. "Heeled footwear," the physician observed, "began to be used more than 1,000 years ago, and led to the occurrence of the first cases of schizophrenia." As heeled shoes sprinted across the world, he said, so did the incidence of the disease. He called for epidemiological studies to check his hypothesis.

It is possible that some epidemiologist somewhere is crunching heeled-shoe data and preparing a paper on the subject. And if such a paper appears, the media will treat it with sober regard -- assuming that it confirms the doctor's wild idea. A Nexis survey of newspaper headlines from the past week finds epidemiological studies playing a role in all sorts of claims: that sleep apnea increases the risk of early death; that thunderstorms provoke asthma attacks; that cellphones might cause cancer; that flu shots may not help the elderly; that consuming fruit drinks increases the risk of diabetes in women. Some of these reports may turn out to be important but most will amount to a kind of scientific noise, adding to our uneasy sense that, in the modern world, danger lurks on every side.

In "Hyping Health Risks," Geoffrey Kabat, an epidemiologist himself, shows how activists, regulators and scientists distort or magnify minuscule environmental risks. He duly notes the accomplishments of epidemiology, such as uncovering the risks of tobacco smoking and the dangers of exposure to vinyl chloride and asbestos. And he acknowledges that industry has attempted to manipulate science. But he is concerned about a less reported problem: "The highly charged climate surrounding environmental health risks can create powerful pressure for scientists to conform and to fall into line with a particular position."

Mr. Kabat looks at four claims -- those trying to link cancer to man-made chemicals, electromagnetic fields and radon and to link cancer and heart disease to passive smoking. In each, he finds more bias than biology -- until further research, years later, corrects exaggeration or error.

In the 1980s, some women on Long Island thought they noted a high incidence of breast cancer in their community and charged that man-made chemicals were to blame. In 1993, a tiny, overhyped study, examining the blood of Long Island women, announced that it had found a strong association between DDE, a metabolic molecule derived from the pesticide DDT, and breast cancer. Alarmed activists persuaded Congress to fund a massive epidemiological study devoted to the causes of breast cancer among women on Long Island.

In 2002, the Long Island study found no association between cancer and blood levels of DDE or other synthetic chemicals, including PCBs. That same year the American Cancer Society reported that 22 studies could find no association between breast cancer and compounds like DDE and PCBs. "The politicization of breast cancer," Mr. Kabat notes, "led initially to the carrying out of the studies based on weak hypotheses and inadequate methods, which were greatly oversold."

In 1979, a small study suggested that electromagnetic fields (EMF) from power lines and home appliances might cause cancer, especially in children. In 1989, Paul Brodeur played up these findings in the New Yorker and charged industry with a coverup. Mr. Kabat explains in detail how several epidemiologists slanted their studies so that, he believes, they could justify further funding for their EMF research. Indeed, epidemiologists kept torturing weak data with sophisticated statistical techniques, trying to force electromagnetic fields to confess to murder. They never did. Physicists eventually showed the biological implausibility of the EMF claim. One physicist, Mr. Kabat says, "likened concern over weak EMF from power lines to the fear that leaves falling from trees could fracture a person's skull."

In the 1990s, EPA regulators were eager to charge that residential exposure to radon -- a gas that arises naturally from certain geological formations -- was a major cause of lung cancer. They pointed to several studies to make the case and proposed a host of expensive regulations. It turned out that 90% of the lung cancer that the EPA's studies attributed to radon was actually associated with cigarette smoking.

Finally, Mr. Kabat takes up the vexed case of passive smoking. He shows how anti-smoking activists, in collusion with EPA regulators, steam-rolled over evidence that passive smoke is a very minor cause of chronic lung disease. An irritant, yes, but a death sentence for bystanders, no. The EPA's 1992 meta-analysis -- the source for anti-smoking regulations ever since -- simply tossed out studies that failed to show an association between cancer and passive smoking.

I know whereof Mr. Kabat speaks. In 1992, as the producer of a PBS program, I interviewed an epidemiologist who was on the EPA's passive-smoking scientific advisory board. He admitted to me that the EPA had put its thumb on the evidentiary scales to come to its conclusion. He had lent his name to this process because, he said, he wanted "to remain relevant to the policy process." Naturally, he didn't want to appear on TV contradicting the EPA.

Mr. Kabat himself got burned by activist fury when, in 2003, he and a colleague published a study using 40 years of American Cancer Society data. The study found "no evidence of an elevated risk of coronary heart disease or lung cancer" in the nonsmoking spouses of smokers. Activists attacked the study before publication by saying that Mr. Kabat had been funded by tobacco money. In fact, only the last seven years of data collection had been funded by a research center supported largely by tobacco companies. Mr. Kabat was not prepared for this kind of scientifically irrelevant and dishonest assault. But some good came of it: It provoked him to write this book.


Breakthrough curbs cancer cells

Australian scientists are hoping to cure leukaemia, asthma and rheumatoid arthritis after their breakthrough discovery of how to stop killer blood cells growing. The team has unlocked the secrets behind the protein which controls the way the blood cancer cells spread when it is damaged - and have found a way to stop its deadly process.

Work is now starting to design a drug to prevent the damaged proteins operating, effectively stopping the cancer as well as asthma and inflammatory diseases such as rheumatoid arthritis.

After spending a decade uncovering the structure of the receptor protein, which sits on the surface of white blood cells, lead researcher Professor Michael Parker, of Melbourne's St Vincent's Institute, said scientists could now build a drug to attach itself to the protein and stop it sending messages into the cells telling them to multiply unchecked. "If we can stop the signal for the proliferation of uncontrolled growth of the cells then we can stop the leukaemia in its tracks," he said.

Working with molecular biologists at Adelaide's Hanson Institute, the Melbourne scientists used X-ray and synchrotron imaging to build an image of the structure of the protein for the first time, hoping to find a way to block its process. The GM-CSF hormone - which controls the production of blood cells in the body - works by attaching itself to the receptor proteins, which then send a message into white blood cells telling them to multiply. When damaged, the protein's messages cause an over-production of cells or cells which persist too long, resulting in diseases such as leukaemia as well as some inflammatory conditions.

The major breakthrough came when the researchers realised the proteins linked together to form networks on the surface of white blood cells after being activated by the hormone, and that by stopping the networks forming they could also stop the growth.

While the drug development phase has only just begun, Professor Parker said it would be easier to target a protein on the surface of the cell rather than trying to come up with a molecule to break its way into the centre of the cell.


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