Scientists have known for more than century that the human digestive system (“the gut”) harbors bacteria. For the most part, scientists assumed (since the bacteria were there all the time) that the bacteria were generally harmless but not particularly important. It’s only in the last decade or two that research began to show that not only do we carry bacteria, but also it has important roles to play in health.
A new piece of research along this line, a study by a consortium of researchers led by Dr. Jeffrey Gordon of Washington University (St. Louis, Missouri), discovered that transplanting the human gut bacteria from lean and obese twins had a corresponding effect on mice.
Why mice? The experiment involved mice genetically and environmentally reared so they have no digestive bacteria of their own – a blank slate, of a kind. This is not a condition that can be replicated ethically with people.
In order to control the human contribution, the researchers identified pairs of human twins where one was lean and the other obese. This ‘leveled the genetic playing field,’ since twins for the most part have identical genetic backgrounds.
The researchers transplanted the bacteria from the fat twins and the lean twins into the bacteria-free mice and observed – the mice with the bacteria from the obese twins grew fat (about 15-17% more body fat); the mice with bacteria from the lean twins stayed lean (or lost weight). This more or less confirmed many other studies suggesting that obesity (or leanness) has some relationship to gut bacteria.
Given the understanding that the bacteria play a role in food digestion – especially for fats and carbohydrates, two big contributors to obesity – the various studies considered it likely that the microbiome of the gut, collectively, might play a role in the development of obesity.
However, intuitive as it might be, it has been difficult to pin down the correlation. That’s why the experiment with the mice is being hailed as an important finding.
The researchers then went one step further, something they call “The Battle of the Microbiota.” They placed mice with the “lean bacterial biome” in the same cage with the mice with the “obesity biome.” They also included a fresh set of mice without a digestive biome. Over time, the mice traded bacterial content through eating each other’s feces (which caged mice readily do). The question was, would one set of bacteria take over, or would the bacterial families mix?
Somewhat to the researchers’ surprise, the bacteria from the lean twins took over in mice that started with the obesity biome and they began to lose weight. The obese mice also began to lose the metabolic abnormalities associated with obesity. This appeared to provide evidence that not only was the type of bacteria in the biome tied to leanness and obesity, but that the balance favors leanness.
Of course, as is usually the case in science, there is correlation but a more elusive causation. As the researchers pointed out in their findings, the mice were given standard mice-food pellets, which are very lean (all vegetable, no fat). So as a follow-up, the researches compensated by developing their own mouse food, with controlled amounts of fat mixed in with the vegetable material.
They repeated their ‘mixed cage’ experiment, this time providing two types of food – one loaded with fat and the other with mostly vegetable content. This time the mice with the obesity biome retained their biome and remained fat. These mice lost the obesity biome only when they were exposed to bacteria from a lean biome and they were fed a diet low in fat.
While this kind of result is ‘highly suggestive’ (low fat diets are better, and maybe with a shot of ‘lean biome bacteria’), it really opens more questions for the scientists. The challenge now is to tie the effects from the two kinds of biome to specific bacteria. This will not be easy. The human gut contains more than a 100 trillion (yes, trillion) bacterial cells from literally hundreds of species. Sorting them out and then identifying the bacteria most involved with obesity will take some time – perhaps decades.
In the meantime, this and other studies have opened the door on a hot new topic for both medicine and medical quackery – fecal transplants. Even in the absence of specific knowledge for which bacteria are doing what, there is a movement in the medical industry to experiment with transplanting the digestive biomes from person to person.
This is risky. Not only because scientists don’t yet know what bacteria are involved, but mainly because the human system is so complex, so sensitive to a wide variety of genetic and environmental factors, that not only are outcomes unpredictable, so is safety. Then too, most of the research is based on rodent experiments, which is obviously not the same as developing results with people. The safe and sensible path to learning about the influence of digestive biomes is through years of hard work and many clinical trials. Unfortunately, there are many people with serious obesity problems and an entire industry developing to promise them relief. Fecal transplanting, as distasteful as that may sound, is likely to become not only topical but headline news in the near future.