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Thursday, December 26, 2013

The FAT GENE-IS OUR ABILITY TO FIGHT FAT, AND KEEP IT OFF, ENCODED IN OUR GENES?

Are you one of those people who has tried every diet
and exercise plan under the sun, without any success?

Have you tried every weight loss pill and product in the
hope of achieving the body you’ve always dreamed of, but nothing
seems to work? Well, there may be a scientific explanation to your
dilemma – the fat gene.
WHILE IT MAY BE OF LITTLE COMFORT TO LEARN THAT
YOUR INABILITY TO LOSE FAT
, and weight, is not from a lack
of trying, but rather your body’s inherent inability to effectively
mobilise fat stores or respond to exercise effectively, you can rest
assured that there are ways and means to win the battle against fat.

Since the international scientific
community decoded the
sequence of the human genome,
through the Human Genome
Project, we have been able to
glean important insights into
how our genetics influences
our predisposition to various
diseases, and the impact that
diet and exercise can have on our
bodies. One of the more recent
areas of interest has been on the
link between our genes and our
ability to lose weight – specifically
fat.
Tests are available today that
can determine our propensity to
gain weight easily, the ease with
which we are able to lose weight,
our response to specific types of
diets, and our body’s ability to
respond to exercise.
“The ability to lose weight
differs significantly between individuals, which is governed by
your genetic make-up,” explains
Helen de Beer, a registered dietician
at DNAlysis Biotechnology.
“For instance, research has clearly
shown that individuals respond
differently to diets. For some,
reducing carbohydrate intake improves
weight loss and prevents
weight gain, while others respond
differently to the quantity
and quality of
the fat in their
diet. Your
genes may also
influence how
you absorb fat,
as well as your
ability to burn
fat for fuel.”
These are important factors
as they have a material impact
on how we should approach our
fat-loss efforts. “Some individuals
need to engage in more intense
exercise for instance, or spend a
greater amount of time exercising
to effectively mobilise fat
stores. Others might get better
results by focusing more on their
diet, while an exercise superresponder
would benefit from a
more targeted and structured exercise
programme,” she explains.
According to De Beer, some
300 genes or chromosomal
regions that are linked to bodyfat
variability have already been
identified – which means it is
not just one gene that governs
our ability to lose fat. However,
it is impossible to implement an
intervention to manipulate the
impact that all of these genes
have on our ability to lose fat –
and keep it off.
“At DNAlysis we therefore
focus on 13 specific genes
that can have an intervention
applied, be it diet or exercise
related,” she continues. “Certain
changes in our DNA code, known
as single-nucleotide
polymorphisms (SNP
– pronounced snip or
snips in the plural form),
have been studied in
detail, and evidence has
emerged that correlates
these polymorphisms
with an individual’s
weight management, and
response to diet and exercise
interventions. Having identified
the presence or absence of these
polymorphisms we are able,
qualitatively, to assess particular
areas of intervention for
improved weight management
related to the specific genes.”
The most (in)famous gene in
question is probably the “fatso”
gene, which today is more
commonly referred to as the
FTO gene. After unravelling the
human genome scientists discovered
that people with two
copies of the gene were 60%
more likely to be obese than
those without it. These people
were also more prone to the
lifestyle diseases associated
with obesity, such as type-II
diabetes. Those with only one
copy of the gene weighed
more too.
A study, published in The
Journal of Clinical Investigation
in August 2013, also showed
that the FTO gene made fatty
foods more tempting to those
with this polymorphism, and
altered levels of ghrelin, the
hormone related to hunger
regulation. The study noted
that: ”(p)olymorphisms in
the fat mass and obesityassociated
gene (FTO) are
associated with human obesity
and obesity-prone behaviors,
including increased food
intake and a preference for
energy-dense foods.”
However, the study also
noted that “the mechanisms
by which FTO predisposes
humans to obesity remain unclear”,
which is why Yael Joffe RD,
Director of Nutrition at DNAlysis,
suggests that it is better to focus
on the genes we have a better
understanding of.
“We have no idea what FTO
does.We know that it is important
though, and that those with
this gene tend to be obese as
they gain weight more easily,
and lose weight more slowly.
We also know that it is closely
linked with snacking behaviour,
especially in kids, but we don’t
understand the physiology behind
it. It is only through various
intervention trials that we now
know what works best for those
with this gene.”
According to Joffe, as our
knowledge and understanding
of the genes linked to obesity
and fat loss has progressed
other, more relevant genes,
have come to the fore. “These
include the ADRB2 and ADRB3
genes,” she explains. “The most
important gene is ADRB2.We
specifically focus on two of the
ADRB2 SNPs, namely Arg16Gly
and Gln27Glu
G ALLELE –
THE FAT GENE




ADRB2 Arg16Gly is a receptor
protein involved in the mobilisation
of fat from fat cells for
energy in response to catecholamines,
and modulates lipolysis
during exercise. The G allele has
been associated with obesity,
and G allele carriers are more
likely to gain and regain weight,
and lose weight more slowly.
These carriers are also less able to
mobilise fat stores in response to
exercise.
The presence of a G allele in
the ADRB2 Gln27Glu gene has
also been associated with an
increased body mass index (BMI)
and fat mass. “Subjects with
these genotypes are less able to
mobilise fat stores for energy,
and have been shown to have
a greater risk of obesity and
elevated insulin levels when
carbohydrate intake is greater
than 49%., explains Joffe.
“This basically means that
carriers of the G alleles in these
genes are exercise, and diet resistant,”
she continues. To highlight
these effects, Joffe cites
a study done on overweight
Japanese men over a period of
24 months. They were all placed
on an exercise programme and
a calorie-controlled diet for
the duration of the study. The
results showed that 37 subjects
maintained weight loss during
24 months, whereas 36 subjects
had rebound weight gain.
“What was most interesting
though was the fact that researchers
identified four groups
– those who lost weight, those
who lost weight slowly but got
there in the end, those who lost

than those who ate fewer carbs,
given the same calorie-intake.
“What these studies clearly
show us is that everyone responds
differently to diet and exercise
based on their genetic make-up.
As such there is no one-size-fitsall
approach to fat loss. There
are people who do better on
low-carb diets, while some will
lose weight on moderate-carb
intakes. There are also those who
will get a better result from dietary
interventions than exercise,
and vice versa,” says Joffe. “For
instance, we now know that those
with the ADRB2 Arg16Gly SNP
should emphasise diet for weight
management, as exercise may
be less effective. For those with
the ADRB2 Gln27Glu polymorphism,
decreasing your intake of
carbohydrates is more beneficial
for weight managemen.

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