Are Parasites in Charge?

Parasites can influence the behavior of the organisms they inhabit.

For example, mice infected with the protozoan Toxoplasma gondii, the organism that causes toxoplasmosis, become lethargic and lose their fear of cats, the primary host of the parasite

Clearly, in a cat-infested environment, such mice don't last very long. And the cats that eat the infected mice become infected themselves and then spread the eggs (oocysts) through their feces.

The behavior modification caused by other parasites in other organisms are even more bizarre.

So, could human behavior also be influenced by some of the parasites we all carry? Some people think yes.

Our guts are filled with bacteria. Many of these bacteria are beneficial. For example, gut bacteria produce most of the B vitamin biotin that we need. Other bacteria can cause obvious harm, for example, gut inflammation, pain, and diarrhea. The diarrhea benefits the bacteria because it increases the probability that other people will come in contact with the abundant fluid and become infected themselves.

Effects on behavior could be more subtle. We know that animals infected with rabies virus behave differently. They become more aggressive and tend to bite. Because the virus colonizes the salivary gland, such bites pass the infection on.

But why am I babbling about all this, interesting though it might be?

It's because I'm wondering if it's gut bacteria that program some people to eat more than normal, causing obesity. Why would the bacteria do that? Well, the more you eat, the more food there will be in the gut, which means the more the bacteria could grow.

There is some evidence that gut bacteria are related to obesity: overweight people tend to have different types of bacteria than normal-weight people. And some animal studies showed that transferring the gut bacteria from mice prone to metabolic syndrome into normal mice caused the normal ones to develop metabolic syndrome too.

So this idea that gut bacteria are associated with obesity is not new. Whether the bacterial population causes the obesity or the obesity provides a gut environment friendly to certain types of bacteria, or perhaps both in a vicious circle, has not yet been definitively proved.

A recent study reported at the Stockholm meeting of the European Association for the Study of Diabetes showed that transplanting fecal matter from thin people into obese people with prediabetes did not result in any weight loss. However, the recipients did see their insulin resistance decrease.

Clearly, obesity, type 2 diabetes, and gut populations are related somehow. One possibility is that certain bacteria are especially efficient converters of food and fiber into compounds that can easily be taken up in the gut, essentially adding calories to whatever we eat.

But I'm wondering if there's more than a metabolic effect. I wonder if the gut bacteria, like the parasites that change behavior in mice and spiders, are subtly changing the behavior of their hosts.

If the bacteria made the hosts feel sluggish, they wouldn't want to move around a lot and burn off calories. If the bacteria made the hosts hungry all the time, they would eat more than they needed to maintain their weight.

The bacteria could then happily munch on the extra calories, rapidly multiply, and infect other people.

Is this really true? No one knows. But the idea intrigues me.

Popular Press Spins

When I was in graduate school, way back in the 1960s, almost every news report about some scientific finding ended by trying to explain why this finding would help to cure cancer. This was the era of the War on Cancer, and scientists hoped that relating their research to curing cancer would increase their chances of getting big research grants.

In the virus course I took with Jim Watson, the exams usually included a question in which we had to explain why some newspaper report of a scientific finding was wrong, that it actually would have nothing to do with cancer. They were fun questions.

Today, instead of trying to show how new studies can help to cure cancer, most popular press stories I see suggest that the findings provide a new target for new drugs, probably hoping to increase their chances of getting funding from drug companies.

Many of the stories appearing in popular science releases like Eurekalert and Science Daily are written by PR people at the institutions where the research is done. Their goal is to call attention to their institutions, professors, and funding sources as well as to the research itself. As a result, usually more than half of the articles is garbage.

When I was a newspaper editor, we'd get tons of press releases like this, and part of our job was to rewrite them without the self-promoting garbage. But these science news sites don't do this. Most of them simply print the press releases verbatim; you can read exactly the same stories on myriad sites.

An example from Science Daily:

"Researchers at the University of Edinburgh report a new experimental compound that can improve memory and cognitive function in aging mice. The compound is being investigated with a view to developing a drug that could slow the natural decline in memory associated with aging.

"With support from the Wellcome Trust Seeding Drug Discovery award, the team has identified a preclinical condition that they hope to take into human trials within a year."

Note that in the first two paragraphs they've mentioned the institution, the potential for drug development, and the funding source. They haven't mentioned what we all want to know: what this compound is. You have to slog through a lot of other boring stuff before they'll reveal that. Some stories even list all the researchers, their degrees, and their positions at the university before they'll tell you what the new finding actually was.

Here's another one:

"University of Michigan scientists have identified events inside insulin-producing pancreatic cells that set the stage for a neonatal form of non-autoimmune type 1 diabetes, and may play a role in type 2 diabetes as well. The results point to a potential target for drugs to protect normally functioning proteins essential for producing insulin."

In this case the PR people managed to make the institution the first word of the article.

You may say, "So what!" and that's partially true. We just have to learn to skim most of these articles to get to the crux of the story. And these popular press releases are important in alerting us to new journal articles that we'd probably never know of otherwise. Most of the press releases do have links to the original articles, although in many cases we can only read the abstracts unless we want to pay.

But I think the important thing is to remember that these articles are written by PR people whose goal is different from our goal. Their goal is to publicize their institution and overemphasize the importance of the research there. Our goal is to understand as completely as possible how good the evidence supporting the claims in the summary article is.

Whenever possible, I try to get the full text of an important article. I don't make the effort for what I consider less important ones. Time is not infinite. I once spent 2 days researching the science behind a story about using lettuce and some complex molecular biology to give people insulin by eating lettuce. Most of the popular press summaries didn't really understand what the research showed.

But if I spent 2 days researching every article I read, I wouldn't be able to read very many, and in the long run I'm hoping that having a surface acquaintance with a lot of research will be more useful than having an in-depth acquaintance with just a little.

I'm sure most of you are already aware of the way the press spins news about science research. But it never hurts to examine it again.

It's a reader-beware situation out there.