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April 8th, 2012 
FAKE NEWS for the Zionist agenda SUNDAY, April 8 (HealthDay News) — For the first time,
scientists have isolated mutations at two gene locations that seem to
predispose children to becoming obese.
“We see a clear genetic signature to childhood obesity, showing that
there is more than just an environmental component to this disease,”
Struan Grant, senior author of the research, said at an April 5 press
conference.
Although known genes have been linked to adult obesity and also to
extreme forms of childhood obesity, the newly identified genes confer only
a modest risk of developing common childhood obesity. But they are “very
common in the population,” Grant added in a telephone interview.
Grant is associate director of the Center for Applied Genomics at the
Children’s Hospital of Philadelphia Research Institute. His research was
published online April 8 in Nature Genetics.
Obesity has become a public health crisis of global proportions,
affecting not only adults but also, increasingly, children.
“In the U.S., the prevalence of childhood obesity has tripled in recent
decades and related health care costs have quadrupled,” said Dr. Karen
Winer, a program officer in the endocrinology, nutrition and growth branch
of the Eunice Kennedy Shriver U.S. National Institute of Child Health and
Human Development, which funded the study.
Clear environmental factors such as changing nutrition and reduced
physical exercise have played a role in the childhood obesity crisis, but
no genes had, until now, been identified.
The authors of this study pooled results from 14 genome-wide
association studies conducted in the United States, Canada, Australia and
Europe, involving a total of 5,530 children who were obese and 8,318
non-obese kids (“controls”), all of European descent.
This is the largest collection of DNA related to childhood obesity in
the world, Winer said.
Obesity was defined as being above the 95th percentile in body mass
index (a measurement that takes into account height and weight) while the
healthy controls were all in the leaner half of the population.
When data was combined, two genes stood out: OLFM4 and HOXB5. The genes
also showed signals in groups of extremely obese children.
And the genes were identifiable but weaker in adults, indicating that
“these variants are conferring their risk early on in life and are really
impactful in the first years of life,” Grant said at the press conference.
Scientific literature to date indicates that the genes may be operating
in the gut.
“We would look probably in that tissue area to see how it was
conferring risk,” Grant said at the press conference.
It’s possible, for instance, that the genes may interact with food, he
said.
Eric Schadt, chairman of the department of genetics and genomic
sciences at Mount Sinai School of Medicine in New York City, said:
“Absolutely, this is a disease that has genetic components and very strong
environmental components and likely very strong genetic-by-environmental
components. It’s very, very complicated. We’re only scratching the surface
of genetic determinations of childhood obesity.”
Once scientists learn more about the genes and how they work, they may
lead to new treatments, added Schadt, who was not involved with the study.
More information
The U.S. Centers for Disease Control and Prevention has more on childhood obesity.
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