SCIENCE
Obesity and Bacteria
By Dr. Rizwana Rahim
Chicago, IL
We could easily
be the least physically active generation ever.
Being more productive today than ever before in
history is little more than an acknowledgment of
numerous labor-saving, time-consuming devices developed
over the years.
If it wasn’t the TV ‘remote control’
that turned us into a nation of couch-potatoes,
it must be the calorie-dense, low-cost fast-food
and the ‘junk food’, besides the very
stress of being competitively more productive, that
added a few pounds we find so difficult to lose
on the treadmill in our basement or in a growing
number of inspirational, 24-hour health and fitness
clubs in our neighborhoods.
The latest statistics indicate about 64% of the
adult Americans (i.e., close to 130 million, and
roughly similar number in both genders) are overweight
to obese. Over the past 40-plus years, the upward
trend has been unmistakably clear. Obesity is now
indeed an epidemic, a testimony to ‘la dolce
vita’.
What is considered overweight and obese is not,
thank heavens, defined by professional models. One
simple way is to use Body-Mass-Index (BMI), as follows:
Body weight (in lbs), divided by the square of height
(in inches), and that multiplied by 704.5.
American Obesity Association (AOA) considers a BMI
of 30 or more as ‘obese’, and between
25 to 29.9 as ‘overweight’. Both AOA
and Centers for Disease Control and Prevention consider
the 85th percentile of BMI (25) as ‘overweight’
; AOA takes the 95th percentile of BMI (30) as ‘obese’.
Available statistics for the young children are
appalling, to say the least. From 1971 to 2000,
among different age-groups under 20, there has been
a 2-4 fold increase in obesity in both sexes (to
roughly 15% of their current population). Among
black and Hispanic teenagers, roughly 20+% are considered
obese, which is about 2x higher than in Whites (non-Hispanic),
and about 36-44% overweight among older Black and
Hispanic teenagers, as opposed to about 26% in the
same age-group non-Hispanic Whites.
Based on BMI, about 62% women and 67% men would
be overweight. If a person is highly muscular, or
pregnant or lactating, these BMI figures would need
some adjustment. Being obese is not just morbidly
overweight, but it (obesity) is a chronic disease
with a familial component and, according to AOA,
obesity is the second cause of unnecessary deaths
(adding about 300,00 excess deaths in the US).
Obesity contributes to the risk of having high blood
pressure, Type 2 (adult-onset) diabetes, cardiovascular
disease, stroke, and cancer of the breast, prostate
and colon. A 10% reduction in weight would have
significant health benefits, as most physicians
would advise us. Unfortunately however, US National
Institutes of Health, the premier health research
organization of the world, spends less than 1% of
its annual budget on obesity-related research.
Lack of physical activity, the amount and quality
of consumed food and the stress of our daily life
are, individually and in combination, significant
contributing factors to obesity. In addition and
surprisingly, some bacterial population (micro-flora,
micro-biota) in our gastro-intestinal (GI) tract
may also have a major role in obesity, according
to some ground-breaking research by researchers
in Washington University School of Medicine (St.
Louis, MO) led by Jeffrey I. Gordon (also the Director
of its Human Genome Sciences Center) published in
the British journal, ‘Nature’. This
research, along with commentaries on it, came out
(Nature: 444, pages 1009, 1022, 1027, Dec. 21, 2006),
coincidentally, in the midst of the Holiday season.
NOT all bacteria are necessarily harmful or pathogenic.
Both pathogenic and benign (not harmful) exist in
our body. For instance, our gastrointestinal tract
(GI) is home to trillions of bacteria (~ 10x more
than the cells in the human body), some of these
species help us digest the food that would otherwise
have been difficult to process.
Two groups (phyla) of beneficial bacteria –
the Bacteroidetes and the Firmicutes – are
dominant in our GI microflora. Firmicutes, the largest
bacterial phylum (with 250 genera), have considerable
variety and include both that require absolutely
anoxic conditions, i.e., obligate anaerobes, like
Clostridium sp., and others (e.g., Bacilus
sp., and Streptococcus pyogenes that
causes ‘Strep throat’) that need aerobic
conditions. Bacteroidetes -- obligate anaerobes,
mostly benign (but could be ‘opportunistic
pathogens’ under some circumstances) -- have
about 20 genera, and are found in the GI system
of many warm-blooded organisms, including human
GI system where B. thetaiotaomicron is
the most abundant microbe of this group. While human
GI contains fewer than 100 carbohydrate-metabolizing/digesting
enzymes, B. thetaiotaomicron has two-and-a-half
times more (about 240) such enzymes, derived from
550 different bacterial species residing in the
human GI.
This research was first conducted on mice. In the
genetically obese mice (ob/ob), they found that
the Bacteroidetes population was about half of what's
present in the lean mice (+/+), and correspondingly
more Firmicutes in the obese than in their lean
siblings.
Their earlier research showed that mice with injections
of Betathetaiotaomicron (B. theta) were
able to digest food better than mice with no such
bacterial injections, and that mice inoculated with
a combination of B. theta and an archaean
bacteria, Methanobrevibacter smithii (M. smithii),
extracted much more calories from the same amount
of food, and this additional energy was stored as
excess fat.
The microbes in the obese mice seem to be able to
extract calories during digestion more effectively
than those in the lean (+/+) mice. When the GI micro-culture
from the obese mice was transferred to a germ-free
strain of mice, the latter which had remained thin
no matter what they ate, now grew fat. Mice with
GI bacteria ate less (29%) but had more body fat
(42%). However, when the germ-free mice were given
GI bacteria, they got fat within two weeks, reaching
the same weight as the other mice.
This research in mice was followed up in human-volunteers
(12 obese people) for one year. They were randomly
assigned to either (i) a fat-restricted (Fat-R)
or (ii) a carbohydrate-restricted (Carb-R) low-calorie
group. Their GI microbial ecology was monitored
during the course of the experiment, along with
sequencing 16s ribosomal (r) RNA genes for their
stool samples. An increase in Bacteroidetes correlated
well with the % loss in bodyweight, but not with
changes in diet calories over time. As volunteers
lost weight, the number of GI Firmicutes decreased,
with an increase in the Bacteroidetes population.
This correlation was held best after a person had
lost at least 6% of his bodyweight on the Fat-R
diet, and at least 2% on the Carb-R diet.
These researchers had earlier isolated a gene (‘obese
gene’) that produced a hormone, leptin. Mice
that have this gene are obese, and those that lack
it are lean. Both in mice and humans, leptin deficiency
leads to unrestrained caloric intake with a low
expenditure of it, resulting in weight gain. Even
a slight excess of caloric intake (say 1%) over
its expenditure would lead to fat and weight accumulation
over a period of time.
The health store market already has some pre-biotic
items that increase the relative abundance of certain
microbes and probiotics like yogurts that have live
bacteria.
If this research on human GI microbial ecology is
confirmed, it may also present new therapeutic opportunities
for obesity: by adjusting or manipulating, with
the help of diet or medication (antibiotics), a
favorable microflora composition in the GI.
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