The new clue to obesity may be surprising to you.While
overeating, inactivity and genetics are key players in the path to
obesity, but there may be a surprising, hidden cause that's also to
blame. (Hint: it's in your stomach-and it's not that cheeseburger you
ate for lunch.)
More than a
third of adults
in the US are obese, according to the Centers for Disease Control and
Prevention. As these rates escalate, researchers are working to figure
out obesity's causes in the hopes of developing more effective and less
invasive treatments than doctors currently are relying on.
Recent research shows a surprising obesity predictor: intestinal
bacteria. In 2010, Andrew Gewirtz, Ph.D., now a professor at Georgia
State University's Center for Inflammation, Immunity & Infection,
led a seminal study in this particular field. He and his team found that
mice without a gene for toll-like receptor 5 (TLR5), a gene which helps
cells control and detect bacteria, ate about 10 percent more than
normal mice. Given limited food, mice without TLR5 still had insulin
resistance, and when given high-fat diets, they gained more weight and
developed diabetes and fatty liver disease.
In short, an inability to detect the presence of bacteria led mice to develop
metabolic syndrome-that
dangerous cocktail of obesity, insulin resistance, elevated
triglycerides and elevated cholesterol, which puts people at risk for
type 2 diabetes, heart disease and certain kinds of cancer.
How does this work? TLR5 detects flagellin, a component of bacteria's
flagella, which propel their movement. If there's no TLR5, which acts
like a sort of "border patrol", bacteria has the ability to multiply
without inhibition.
Surprisingly, the composition of one's intestinal bacteria is not only
a matter of genetics. When Gewirtz and his colleagues transferred the
intestinal bacteria of TLR5-deficient mice to healthy mice, they
exhibited the same dangerous eating behaviors and associated weight
gain. "What this means is that when you transfer bacteria from one group
of mice to another, you can transfer this predisposition for obesity
and its related metabolic diseases," says Gewirtz.
So, what does this mean for us? "While adult humans may not
efficiently transfer bacteria to each other, transmission to a newborn
baby is very efficient," explains Gewirtz. "Thus, what our results may
mean to humans is that the bacteria one acquires from their early
development, especially their parents, may have a big impact upon one's
tendency to develop obesity and/or type 2 diabetes over a lifetime."
Another study conducted by Mihai Covasa, Ph.D., and his colleagues at
the French National Institute for Agricultural Research (INRA) has
confirmed and built on these findings. The researchers bred
obesity-prone and obesity-resistant rats-the former weren't actually
obese, but actually came from a lineage of rats that had a tendency to
gain weight and fatten quickly when fed high-fat foods. The researchers
extracted microbiota from the rats' feces and implanted them into the
stomachs of mice that had been germ-free since birth. For eight weeks,
adequate time for the maturation of the intestinal microflora, the mice
ate either a regular or a high-fat diet.
The results? The mice implanted with the obesity-prone gut bacteria
ate more and gained more weight and fat-regardless of whether they were
fed a high- or low-fat diet-compared to all other groups.
The upshot is that proneness to obesity can be inherited not just
genetically, but also by simply transferring intestinal bacteria such as
from parent to child. Also, the composition of your microbiota is
controlled by a variety of factors, your environment and antibiotics, as
well as your diet. "Diet can affect bacteria, but bacteria can affect
appetite," notes Gewirtz. "So it's an interrelated factor." When
discussing obesity, he says, "Most people have focused on diet and
lifestyle or lack of exercise, but this is another potential
contributor."
That said, there's no clear-cut cause-and-effect here-and researchers
are still trying to unravel how those changes in gut bacteria could
influence obesity in humans. "We speculate that those changes do
influence obesity in humans," he says, "but it is indeed not established
fact."
So what is in a bacterial profile that could make people prone to
obesity? Could it be the amount of bacteria, or are there specific
bacteria that present a problem? Both Drs. Covasa and Gewirtz say there
are a lot of unknowns here and that the answer is not so simple.
Preliminary findings, according to Covasa, show that obese individuals
may have reduced microbial diversity. And Gewirtz's follow-up work has
indicated that the issue is largely a matter of bacteria's instability.
In healthy mice, the composition of intestinal bacteria doesn't change
frequently, but in obesity-prone mice, the population shifts from week
to week.
The current research is on mice, not humans, but Gewirtz and his team
have found preliminary indications that their findings apply to us, too.
A certain percentage of people are TLR5 deficient, and thus far, it
looks as though they may be prone to obesity, just like mice. But only
one in 250 people are TLR5-deficient-a tiny percentage of the obese
population-so the point isn't to show that TLR5-deficiency is a
significant cause of obesity, but rather that the mouse work applies to
humans. The research is also meant to show that something that alters
humans' bacterial composition can affect their metabolism.
One thing you shouldn't take away from these findings is the idea that
if you have this or that bacterial profile, you're screwed. Both
Gewirtz's and Covasa's research has shown that, no matter what your
intestinal bacterial profile, you do have to eat more for the adverse
metabolic effects to take hold.
Right now, some doctors rely on invasive gastric bypass surgery to
treat obesity; these findings indicate that there might be another way.
The end goal is to isolate just what a healthy bacterial profile looks
like and, if possible, which types of bacteria are particularly
important. From there, researchers could develop a way of manipulating
obese people's microbiota to potentially decrease their proneness to
metabolic syndrome-and protect their health.
Are
you afraid of being away from your mobile phone? You may have (dun dun
dun!) Nomophobia:
So
is buttermilk good or not? I never could reconcile the stories my
grandmother told of churning milk to separate the butter from the buttermilk
with the ghastly-tasting buttermilk available at the grocery. How could
milk go sour just by taking the fat out of it? L.V. Anderson explains
with the history of buttermilk, or rather, the different things that
have been called buttermilk.
