“Mr. Osborne, may I be excused? My brain is full,” a student with a particularly tiny head asks his classroom teacher in a classic Far Side comic by Gary Larson. The deadpan answer to this question would be, “No, your brain is almost certainly not full.” Although there must be a physical limit to how many memories we can store, it is extremely large. We don’t have to worry about running out of space in our lifetime.

The human brain consists of about one billion neurons. Each neuron forms about 1,000 connections to other neurons, amounting to more than a trillion connections. If each neuron could only help store a single memory, running out of space would be a problem. You might have only a few gigabytes of storage space, similar to the space in an iPod or a USB flash drive. Yet neurons combine so that each one helps with many memories at a time, exponentially increasing the brain’s memory storage capacity to something closer to around 2.5 petabytes (or a million gigabytes). For comparison, if your brain worked like a digital video recorder in a television, 2.5 petabytes would be enough to hold three million hours of TV shows. You would have to leave the TV running continuously for more than 300 years to use up all that storage.

The brain’s exact storage capacity for memories is difficult to calculate. First, we do not know how to measure the size of a memory. Second, certain memories involve more details and thus take up more space; other memories are forgotten and thus free up space. Additionally, some information is just not worth remembering in the first place.

This is good news because our brain can keep up as we seek new experiences over our lifetime. If the human life span were significantly extended, could we fill our brains? I’m not sure. Ask me again in 100 years.

The connection between gut bacteria and obesity has gained some weight, with new findings demonstrating links in mice among immune-system malfunction, bacterial imbalance and increased appetite.

Mice with altered immune systems developed metabolic disorders and were prone to overeating. When microbes from their stomachs were transplanted into other mice, they also become obese.

“This supports the notion that some of the increase in obesity may be because of changes to gut bacteria,” said Andrew Gewirtz, an Emory University immunologist and co-author of the study, published March 4 in Science.

The findings are the latest in a growing body of research about the long-unappreciated role of bacteria in our bodies. Bacterial cells actually outnumber human cells in the body: From an outside perspective, people are not so much individual organisms as symbiotic human-bacteria collectives.

Disturbances to internal bacteria have been linked to asthma, cancer and many autoimmune diseases. Gut flora have also been linked to obesity. In 2006, researchers led by Washington University microbiologist Jeffrey Gordon documented bacterial changes in the stomachs of mice who became obese on high-fat diets.

When transplanted, their gut bugs turned other mice obese, suggesting that altered bacteria were not only an effect of weight gain, but a cause. The Science findings complement those, but also emphasize the immune system’s role and the possibility of appetite change.

“The reason why people are eating too much may not simply be because unhealthy food is cheap and available, but that their appetites may be driven by changes in gut bacteria,” said Gewirtz,

In the Science study, Gewirtz and Emery microbiologist Matam Vijay-Kumar studied a strain of mice deficient in TLR-5, a gene that’s required for immune systems to recognize many types of bacteria.

They found that TLR-5–deficient mice are about 20 percent heavier than regular mice. They overeat, have high blood pressure and high cholesterol, and are insulin-resistant. In humans, that constellation of conditions is known as metabolic syndrome, and in both people and mice leads to obesity and diabetes.

Earlier research had found unusual patterns of bacteria in the guts of those mice. When the researchers transferred bacteria from the stomachs of TLR-5–deficient mice to mice without gut bacteria, the recipients started to eat more, and soon developed metabolic syndrome.

“It’s a really exciting paper. It confirms and supports a lot of the findings we’ve had, and adds in the interaction between gut bacteria and the immune system,” said Peter Turnbaugh, a systems biologist who moved from Jeffrey Gordon’s lab to Harvard University. “It’s been thought for a long time that maybe the immune system is an important regulator of what’s in the gut.”

How gut bacteria produce metabolic changes isn’t known. They may process nutrients directly, or alter the activity of metabolism-regulating genes.

Mice used in the research are not considered exact models of bacteria and obesity in humans. Instead they’re models of these sorts of relationships likely to exist in people. Gewirtz’s team is now investigating whether people with metabolic syndrome have unusual gut bacteria.

The findings don’t suggest obesity is literally contagious, said Turnbaugh. But they do raise the possibility of altering the composition of gut bacteria, either directly or — more realistically — by learning what sort of environmental and lifestyle factors produce obesity-causing bugs.

One possible culprit is the ubiquitous presence of antibiotics, both prescribed and in the environment, said Gewirtz.

“It may be that an unintended consequence of this has been the upset of bacterial populations that are promoting obesity and metabolic syndrome,” he said.

Image: Left, regular and TLR-5–knockout mice. Right, a comparison of their insulin-producing islet cells./Andrew Gewirtz

Female short-nosed fruit bats in China’s Guangdong Province show their preference for certain males by fellating them, according to an October journal article. Researchers observed that licked males were able to copulate longer, thus improving the likelihood of insemination. (The scientists also confirmed that bats mate while upside down.)

[Chronicle of Higher Education, 10-29-09]

Removing part of the brain can induce inner peace, according to researchers from Italy. Their study provides the strongest evidence to date that spiritual thinking arises in, or is limited by, specific brain areas.

To investigate the neural basis of spirituality, Cosimo Urgesi, a cognitive neuroscientist at the University of Udine, and his colleagues turned to people with brain tumours to assess the feeling before and after surgery. Three to seven days after the removal of tumours from the posterior part of the brain, in the parietal cortex, patients reported feeling a greater sense of self-transcendence. This was not the case for patients with tumours removed from the frontal regions of the brain.

“Self-transcendence used to be considered just by philosophers and crank new age people,” says co-author Salvatore Aglioti, a cognitive neuroscientist at the Sapienza University of Rome. “This is the first really close-up study on spirituality. We’re dealing with a complex phenomenon that’s close to the essence of being human.”

The authors pinpointed two parts of the brain that, when damaged, led to increases in spirituality: the left inferior parietal lobe and the right angular gyrus. These areas at the back of the brain are involved in how we perceive our bodies in spatial relation to the external world. The authors of the study in the journal Neuron1, say that their findings support the connection between mystic experiences and feeling detached from the body.

“The most surprising part was the rapidity of the change,” says Urgesi. “This discovery shows that some complex personality traits are more malleable than previously thought.”

Reasoning Project