People facing weight problems often know why. That weakness for donuts in the morning, that meatball sandwich at work, or that dead-tired feeling that makes you wince at any activity but channel surfing.
Sure, most of the nation needs to eat less and move more. But is that the only reason America is so fat?
As more scientists and sociologists look at our bulging waistlines, some unusual explanations for the nation's weight gain in the last 30 years are popping up.
As recently as last week, research has questioned whether bacteria, our genes or wine could be influencing weight gain.
In 2008, the National Health and Nutrition Examination Survey estimated that 33.8 percent of adults in the United States were obese.
But the rates aren't creeping up evenly. Obesity rates for men jumped nearly 5 percent since 2000, from 27.5 to 32.2 percent of all men reportedly obese. Women's obesity rates gained two percentage points in the last eight years, from 33.4 to 35.5 percent.
Considering the poundage, it's no wonder why some think there's an environmental explanation for our fat. Following are three scientific findings that hint it isn't completely an individual's fault he or she is overweight.
People always love to pin weight on hormones, big bones, or genes. But bacteria?
A professor of pathology at Emory University thinks the idea that gut bacteria influences some people's weight gain is not as crazy as it sounds.
The concept starts with the findings that about 8 percent of the population is genetically deficient in a protein called Toll-like receptor 5 (TLR5), which helps the immune system regulate bacteria in the gut. According to associate professor Andrew Gewirtz, of Emory University, an additional half of a percent of people are completely without the TLR5 protein.
Gewirtz studied mice that lacked the TLR5 gene and found a connection between bacteria and fat. The mice born without TLR5 formed a bacteria colony that either irritated their stomachs, or made them eat 10 percent more than other mice.
These mutated mice often weighed 20 percent more than normal mice, and were more likely to be insulin-resistant -- a precursor to diabetes. Even when scientists withheld food to make sure the genetically mutated mice never got fat, the mice still grew up with insulin problems, according to a study by Gewirtz and lead author Matam Vijay-Kumar in ScienceExpress.
When researchers transferred the gut bacteria from the mice with the genetic mutation into healthy mice, then the healthy mice started gaining weight too. It turned out normal mice could catch the hunger-inducing bacteria that TLR5 failed to regulate.
Of course, what happens in mice doesn't always happen in humans. But Gewirtz says his results are leading to questions about the human population that's missing TLR5.
"We are currently assessing how many people with this deficiency are obese," said Gewirtz.
Since our genes haven't changed much in the last 50 years, but some bacteria that we carry have, Gewirtz wonders if, like mice, people without TLR5 are transferring bacteria that lead to weight gain.
"In humans this type of transfer of intestinal bacteria to a person who has no intestinal bacteria is a process that happens at birth," said Gewirtz.
What to make of this study?