The problem of obesity has become a major focus in public health. Since 1980, the numbers of obese people have doubled and approximately one-fifth of the population is now classified as obese. The explosion in the prevalence of the disease, which is not only characterized by increase body mass but also higher risk for other chronic diseases such as diabetes, cancer, and cardiovascular disease, has both personal and economic consequences. In response, there has been a major focus in research to understand how this condition occurs and more importantly, how to prevent and possibly cure it.
Since the mid-2000s, part of that focus has involved the study of the role of germs in the development and prevention of massive weight gain.
In 2004, the first study to show a link between germs and obesity revealed a surprise: Obesity may not be entirely linked to increased food intake. When mice raised without exposure to germs in their intestines were introduced to the microbiome of normal mice, their weight gain exploded even though they didn't eat more food. A deeper look at the process revealed that certain microbes sent signals from the gut to the liver to start storing fat.
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While this was an apparent accusation of germs as the cause of weight gain, the tone was tempered based on historical perspective. In a world where food is scarce, this action of germs would be beneficial, but when food is readily available, the microbes don't know any better and perform the same actions, with obesity being an inadvertent consequence. The study suggested that both food intake and the presence of germs in the gut were responsible for weight gain.
A few years later, in 2008, the focus took a turn as other researchers found that obesity was linked to the immune system. The evidence suggested that the work of microbes sending signals to the liver caused inflammation in reaction to the production of fat. This would start a cycle in which the body would continue to store more fat and the inflammation would continue. While the germs may start the fat storage process, the inflammation took it to pathogenic levels.
This revelation opened the door to the investigation of certain microbial species that were known to prevent inflammation. By extrapolation, it was thought that these good germs could help to prevent and possibly resolve the disease. This sparked a hunt for the right microbes to help maintain a healthy body weight and keep inflammation at bay.
Over the last five years, these good bacteria have been identified, and to no one's surprise, most are already known as probiotics. When these bacteria are maintained in the gut, there appears to be -- at least in mice -- a reduction in the levels of inflammation and, as a consequence, a reduction in obesity. In humans, the data is sparse though there has been progress made in revealing that we too may benefit from these good germs.
But earlier this week, a group or researchers based out of the University of Maryland School of Medicine published an article that takes the concept of using germs to combat obesity to the extreme. Instead of using the usual probiotics, the research team investigated the use of the basis of an unappetizing childhood song: worms; or more specifically, a microscopic worm known as a nematode.
Today, nematodes are best known as a natural means to control insects, but in the field of health, they remain an enigma. There are a number of pathogenic worms that can cause burdensome infections with long term consequences. But in the same context of acne, where strain differences can mean the difference between a good and bad germ, several strains of these worms have shown to be beneficial to the human condition. Their magic is based on their ability to control inflammation to ensure that there is no hyperactivity. As a result, these worms have been used to help conditions such as asthma, chronic diarrhea, and inflammatory bowel disease.
The University of Maryland researchers' method was fairly simple: feed both healthy and obese mice a good strain of worm and look for any body weight changes. The results, however, revealed that unlike the study from 2004, which directly linked the gut microbes to the liver, the actual process of weight gain (and loss) required a middleman -- the immune system. When fed the worms, the mice lost weight, but the worms had no effect on the liver. Instead, as expected, the nematodes controlled inflammation; as a consequence, the liver halted the cycle of sending out the signals to store fat.
The data, while both interesting and very preliminary, suggests obesity might very well be an autoimmune condition caused by an imbalance in the microbiota of the gut. Germs, therefore, can be a help or hindrance depending on what resides in the gut and how it affects the immune system. Good germs will help to keep obesity down while bad germs could lead to increased weight gain even without eating more.
Over the coming years, inflammation will continue to be a major focus in obesity research, and options for controlling weight gain -- including probiotics, proper diet and exercise -- will continue to be recommended in the hopes of reversing the current trends. Our understanding of obesity continues to grow and soon we may fully understand how this morbid disease occurs. But even without a proper explanation, the work to stop this epidemic, whether it be germy, wormy or otherwise, will go on.