Suppose you had two groups of 70 year olds, one whose parents had lived to be 100 years old and the other whose parents died at a younger age. Which group would you expect to live longer?

This isn’t a trick question and the answer is no surprise but the question is why. Why do the offspring of centenarian parents live longer?

Dellara F. Terry and colleagues from Boston University make a persuasive case that the benefit is conferred through reductions in cardiovascular risk.

They report in the Journal of the American Geriatrics Society that septuagenarian children of centenarian parents were 81% less likely to die during a 3.5-year follow-up than age-matched controls, and same group was 78% less likely to have a heart attack, 83% less likely to have a stroke, and 86% less likely to develop diabetes.

And yet the children of centenarians were just as likely as the second group to develop cancer, depression, glaucoma, bone fractures, thyroid disease, hypertension, macular degeneration and dementia.

“The most dramatic difference we’ve seen among centenarian offspring, one that’s been consistent throughout the period we’ve been following them, is the decreased prevalence of heart disease and its risk factors,” Dr. Terry told the New York Times.

OK so is it nature or nurture?

“Just because something is familial doesn’t mean it’s all genetic,” Terry explained to the Times. “It could be there are health-related behaviors they have learned from their parents. It’s also possible it’s genes, or the absence of bad genes, they inherited from their parents.”

Which is another way of saying we don’t know right now but if we can figure it out we’ll let you know.

Scientists in St. Louis have decoded the entire genome of a woman who died of leukemia and in the process, they identified several mutations that probably caused the disease, accelerated its progression or rendered it resistant to chemotherapeutic agents.

The researchers sequenced DNA from the woman’s leukemia cells and her non-cancerous skin cells, and then compared them side-by-side. The comparison revealed 10 mutations that were present only in the cancer cells.

“This is the first of many of these whole cancer genomes to be sequenced,” Richard K. Wilson told the New York Times. Wilson is Director of the Genome Sequencing Center at Washington University and a senior author on the paper published in Nature. “They’ll give us a whole bunch of clues about what’s going on in the DNA when cancer starts to bloom,” he added.

The scientists’ strategy to sequence the entire genome of a human cancer cell represents a break from previous approaches that had focused on a few hundred “likely suspect” genes. The strategy has been enabled by recent advances that make it far cheaper and quicker to sequence large amounts of DNA. The advantage of the new strategy is that it eliminates the possibility that the genes actually associated with cancer are not among the “likely suspects.”

Indeed Wilson’s group found that 8 of the 10 mutations in their study were not considered likely suspect genes.

The woman’s sequenced DNA will be made available for other research projects. Before her donation, the only fully sequenced human genomes had come from Craig Venter, the founder of the Institute for Genomic Research, and Nobel Prize winning molecular biologist James Watson.