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?
"It's interesting," said Keith Ayoob, an associate professor at Albert Einstein College of Medicine in New York City. "But it's a long way from saying this happened in mice, and that explains the obesity epidemic in this country."
Ayoob, who counsels families to help children lose weight, says he'd rather look at individual eating habits while he waits for researchers to examine Gewirtz' work.
Until then, "I would say a lot more research is needed."
There's no doubt that some families are naturally thin, and others are naturally husky.
But new research out of Stanford University has indicated that even the success of a diet could be predicted by your genes.
Recently Waltham, Mass.-based Interleukin Genetics, Inc., paid for DNA testing of 138 women who had taken part in a diet study in 2007. In the previous study women were assigned to a low-carb, low-fat or general diet.
Stanford researchers then compared the women's weight loss success with their genetic profile of three genes that show a pattern for metabolizing fats and carbohydrates, according to the Associated Press.
They found that if women's genes indicated they would metabolize fats better, they lost more weight on a low-fat diet than a low-carb diet. The reverse was true for women whose genes indicated they metabolized carbs better, Mindy Dopler Nelson, a nutritional biologist at Stanford University, reported at an American Heart Association conference last week.
Women whose diets matched their genes lost 10 more pounds over a year compared to women on mismatched diets, Nelson reported.
So is it really a question of finding your genetic diet match?
Ayoob had a cheaper solution while more studies examine the link.
"The smartest thing to do is look at where the excess is in your diet," said Ayoob.
Frequently patients coming to Ayoob need help kicking obviously bad habits that lead to weight gain. For example, Ayoob said, some people have a weakness for sugary drinks. Others, he said, miss breakfast and then have a problem gorging and snacking through the day.
"You want to be comfortably hungry when you eat," said Ayoob. "When you're starving you're going to make poor choices."
If your gut bacteria or your genes are not at fault, how about looking at your circle of friends as a source of obesity?
In 2007, an article in the New England Journal of Medicine used 30 years of data on 12,000 people to show obesity and weight loss may actually be contagious -- things that spread among people who know each other.
"They key idea is that people are influenced by the behavior and actions of those around them. This applied to something that people may not have thought of, which is body size," said Dr. Nicholas A. Christakis, author of the recent book "Connected," which looks at how various phenomena from depression to obesity spreads through society.
Over the three decades, Christakis showed how obesity in one person in a circle of friends statistically meant more people in their circle of friends would become obese. The same was true of weight loss.
"We're not saying we found the cause of the obesity epidemic. We're not," said Christakis. "Social networks have a general property that they magnify what they are seated with."
While Christakis could show an obesity epidemic spreading through friend networks, he could only make an educated guess why.
"One possibility is that you start doing things -- certain behaviors that I copy," said Christakis.
So if one friend starts serving beer and cookies all the time, perhaps another friend will pick up the habit. Or if one friend joins a running club, perhaps another friend will join it too.
Christakis said another possibility is that "What's spreading between people is an idea, or a norm."
For example, if most people a person associates with are overweight, then that person's idea of "normal weight" is likely to be bigger than what is actually healthy.
Ayoob says this finding rings true with studies and his experience counseling families.
"I've had parents request evaluations because they think their children are too thin. But they're at the 50 percentile of the estimated height and weight for their age," said Ayoob. The children were smack in the middle of weight for their age, but they are "only thin compared to other children in the household who are obese."
Large or small portion sizes may also spread as social "norm," Ayoob said. If mom always served three scoops instead of two, chances are the children will grow up reaching for more.
"Social networking does not cause obesity," said Ayoob. "But I think it's a marker for a lifestyle."