Junkfood Science: When media shapes perceptions

April 09, 2007

When media shapes perceptions

A story in the news this weekend perfectly illustrates how easy it is to manipulate our perceptions of risk. A close look gives us a few new skills to add to our critical thinking arsenal, too.

The BBC reported Saturday that “Fat hormone boosts colon cancer:”

A chemical produced by fat cells makes colon cancers grow faster, a US study has suggested. The British Journal of Surgery study could help explain why severely overweight people appear to be at far greater risk of the disease.

A team at the University of California, San Diego found that the hormone leptin triggered increased growth in human colon cancer cells.

Obese people are up to three times more likely to develop colorectal cancer....

Dr Kim Barrett, who led the research, said: "These results may explain why obesity increases a person's risk of colonic cancer....Obesity is increasing...

News of the discovery of “the culprit between obesity and colon cancer” made its way around the world from Romania, Australia, to Kazakhstan. Just like the game of telephone, by the time it reached India, it was “Obese people face more risk for cancer of colon.”

And the All Headline News release — “Obesity Linked with Development of Colon Cancer” — also found it’s way from San Diego to Washington, DC.

Let's look at another side of this headlining story and three key things to consider anytime we hear of a new medical discovery.

Key # One

Similar media stories told us of a study finding the same thing back in January.

Wow, so there must be a lot of research confirming that obesity increases the risk for colon cancer.

Not so fast....it was the same study reported again!

This is happening increasingly more often. Those trying to persuade us of something know that the more often we hear a claim, the more apt we are to believe it to be true. And the more times a study is reported, the larger body of evidence we believe exists.

With growing numbers of journals rushing to release some studies early online and then in print months later — as in this study published online in January and in print this month in the British Journal of Surgery — the more we are vulnerable for falling for this. Each release generates more news. The studies being blitzed to media attention might ideally be those of the most urgent public and medical importance but, instead, are not infrequently ones benefiting a certain interest or viewpoint and accompanied by press releases.

Studies may also be presented at meetings, sometimes again and again, with some eventually being published. And each time, those may also make the news. This study was presented in 2005 at the Annual Meeting of the American Gastroenterological Association in Chicago.

The effectiveness of this technique doesn’t just occur by saturating consumer media, but even medical journals. The same study or subtle variations of it can appear in different journals and in various forms. It succeeds in giving the impression that a hypothesis has been replicated and confirmed, or of growing consensus. This technique is also one of the reasons why tallying the number of published papers for a certain claim does not equal more or better quality evidence. This study had also been published in abstract form in Gastroenterology in 2005.

Key # Two

You don’t actually believe that a single reporter took a moment to do a lick of fact checking, do you?

When we hear a health claim, we can first ask ourselves if it makes any logical sense based on real life and actual health statistics. It would have taken a mere minute to confirm the National Cancer Institute’s statistics on cancer rates. With incidences of obesity rising, if obesity caused the development of colorectal cancer, then we should see correspondingly rising rates of colorectal cancer.

The NCI of the National Institutes on Health recently released its report, “Annual Report to the Nation on the Status of Cancer, 1975-2003.”

It stated that the incidences of colon and rectal cancers (even despite increased surveillance) have been dropping among both men and women. That alone suggests the opposite of what these recent stories have been trying to convince us of!

A simple search of the medical literature reveals that cancer registries in the United States have continued to find that “obesity is associated with lower incidence rates of colorectal cancer,” as researchers at the Kansas Cancer Registry reported in the journal Cancer this past fall. The most significant factors associated with higher incidences of colorectal cancer were such things as old age, male gender, under educated, and sedentary smokers.

A study of over 3,000 adults who had received colonoscopies at 13 Veterans Affairs medical centers across the country, sought unsuccessfully to identify lifestyle risk factors for advanced colorectal cancer in asymptomatic people. It found no association with body mass index or cholesterol levels, nor tenable odds ratios for alcohol consumption, whole grains, vitamin D, etc. “Further study is needed to determine if lifestyle changes can moderate the risk of colorectal cancer,” they concluded.

Key # Three

You are not a petri dish or test tube found in a laboratory. And while we’re at it, you are not a lab rat or fruit fly or some other nonhuman species — not technically. We are best waiting until scientists have tested something on actual people and credibly shown something to be clinically meaningful before we react. Hypotheses based in the laboratory don’t always play out in real life, as we’ve seen with countless nutritional studies. Science in progress and years away from giving us reliable solutions, is better left to scientists to sort out before we jump to conclusions or change our diet or lifestyle.

While leptin — a recently discovered hormone produced by fat cells and cancer cells is believed to play various roles in fat storage, anorexia, depression, fertility and other metabolic functions — has been a popular target for pharmaceutical research, they’re just beginning to better understand it. Leptin researchers already had a false start when they believed it to be a possible weight loss drug based on rat studies, but it didn’t prove to work that way in people.

In this preliminary study, they looked for possible effects on a cellular level in a test tube and said what they saw in three colon cancer cell lines treated with leptin “could provide a link between obesity and colonic cancer and may represent a target for anticancer drug development.” The intricacies of oncological pharmaceutical development is beyond what most of us can grasp and we’ll save it for the experts. But French researchers appear to have already published research looking further and found that while “leptin acts as a growth factor on [human] colon cancer cells in vitro, it does not promote tumour growth in vivo.” They concluded that their findings “do not support a pivotal role for hyperliptinaemia in intestinal carcinogenesis.”

“In vivo” means in an actual living organism, whereas “in vitro” means in the laboratory.

Even when the French researchers increased the leptin levels more than four times in animal studies, there was no increase in tumor numbers or sizes, and leptin even reduced the development of precancerous tumors in the colon. In other words, they’ve found no support for leptin as causing colon cancer.

Scientists are still trying to thrash out the hows and whys of the development of colon cancers and while clinical studies are increasingly finding “improper” diet unrelated, there is also no good data looking at body fatness alone, especially in the absence of high insulin levels or insulin resistance which is seen among thin people, too. Much of the research being funded is still on molecular and cellular levels, according to Sharon E. Fleming, a professor at the University of California, Berkeley. Interestingly, in 1999 researchers at the University of California, San Francisco, reported that the protein beta catenin, activated by a mutated gene, is almost certainly what causes most colon cancers. They reported that their research “should fuel ongoing efforts by pharmaceutical companies to develop ways to block beta catenin.”

The bottom line is that we all support scientists working towards effective treatments or cures for cancers, and most of us realize those are years away. But to get there, research needs to move forward based on its efficacy, not other, less productive, agendas or ideologies.

How often is the public privy to the early trials-and-errors of investigations in laboratories, let alone for them to receive this degree of media attention? Almost never. Clearly, the media headlines this weekend considerably overstated the conclusions of this study and its importance for consumers. And while it certainly gained notice for the researchers, important for getting funding, we can ask ourselves how was this story helpful and what service did it provide the public? Was it in any way news we could use?

In fact, the degree of media attention given this investigation and its claims that fat leads to colon cancer appears to have served only one actual function:

It added yet another threat to heighten the perception that obesity is a disease with deadly consequences.

© 2007 Sandy Szwarc

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