Morbid Obesity in Children and Missing DNA
January 6th, 2010 | No Comments | Source: Medical News Today, NatureThe obesity epidemic has become a major public health concern. The phenomenon is typically attributed to changes in diet and lifestyle, and socioeconomic factors like poverty and poor education.
Genetic factors have been known play a role as well, but a recent study by UK-based scientists suggests they play much more prominent role, at least in a subset of people who become morbidly obese at a young age.
In the study, Sadaf Farooqi of the University of Cambridge and colleagues showed that many such kids are missing a large chunk of DNA, known as SH2B1, from chromosome 16.
The missing genetic code had been known to play a role in regulating weight and blood sugar levels. Kids with the chromosomal abnormality tended to overeat on a massive scale, and gain weight easily.
To reach these conclusions, the scientists scanned the genomes of 300 morbidly obese kids in search of copy number variants (CNVs), which are lengthy strands of DNA that are either duplicated or missing.
The scientists compared their findings with information from healthy controls.
In their write-up, which appears in Nature, the scientists wrote, “we identified several rare copy number variants that were recurrent in patients but absent or at much lower prevalence in controls.”
“Part of chromosome 16 can be deleted in some families. People with this deletion have severe obesity from a young age,” Farooqi told Medical News Today: “One particular gene on chromosome 16 called SH2B1 plays a key role.”
The finding may have broad social implications, since it is common to blame parents or guardians for morbid obesity in kids. The scientists noted for example, that some kids in the study had been handed over to Social Services because their parents were assumed to have been deliberately overfeeding them.




The results imply that the genetic basis of the 2 common psychoses are more complex than had been thought, and that the conditions can develop not just from a rare, devastating genetic variant, but from dozens or hundreds of common ones.
Since the heralded announcement in 2003, geneticists have undertaken hundreds of genomewide association studies designed to compare the DNA of healthy people with those of patients having specific diseases.
Plavix-popping patients in posession of a particular gene that prevents its proper metabolism were at twice the risk of sustaining cardiovascular events, and the risk could not be mitigated by high doses of the stuff,
Six of these 7 patients were CYP2C19*2 positive.
Philip Bernard, Joel Parker, Matthew Ellis and many others published the heartening findings in the
Conversely, basal-like breast cancer, which carries an ominous prognosis, turned out to be “the most sensitive to chemotherapy. By identifying (the cancer types correctly) we can ensure they are treated adequately,” Ellis said.
According to the theory, the cellular defense against the culprits-which are enzymes known as superoxide dismutases-gets overwhelmed by the accumulating bad guys and the next thing you know, cells are looking like Methuselah.
Come to think of it, the evidence supporting the oxidative stress theory is circumstantial, Hekimi told BurrillReport.
Such antibodies “could provide broad protection against all seasonal and pandemic influenza A viruses,” according to Wayne Marasco of Harvard Medical School and colleagues.
In fact Brown’s recently born baby boy was conceived the old fashioned way.
Compared with those having neither variant, “the risk associated with these variants was almost six-fold, which is quite extraordinary,” Erich Sturgis, a head and neck surgeon at Houston’s MD Anderson Cancer 









