In the public health field, there is an ongoing debate as to whether improvement in the overall health of the population is linked to increases or decreases in social inequities in health, that is, the inequities between higher-income and lower-income groups. In the most comprehensive study to date addressing this debate, researchers at the Harvard School of Public Health (HSPH) found that, as overall health improved (as measured by a decline in mortality rates), inequities in health both shrank and widened between 1960 and 2002. The study demonstrates that the recent trend of growing U.S. disparities in health status is not inevitable.

“Our paper refutes the argument, currently gaining ground, that as overall population health improves, it is inevitable that socioeconomic disparities in health will increase, allegedly because the better-off more quickly take advantage of health-promoting resources,” said Nancy Krieger, professor of society, human development, and health at HSPH and the study’s lead author. “Instead, we clearly show that this argument is flawed because, in the period from 1966 to 1980, socioeconomic disparities declined in tandem with a decline in mortality rates.”

The study was published in the Feb. 26 issue of the open-access journal PLoS Medicine:


Researchers at Dana-Farber Cancer Institute have found a previously unknown molecular pathway in mice that spurs the growth of new blood vessels when body parts are jeopardized by poor circulation.

At present, their observation adds to the understanding of blood vessel formation. In the future, though, the researchers suggest it is possible that the pathway could be manipulated as a means of treating heart and blood vessel diseases and cancer. The paper appears in the Feb. 21 issue of the journal Nature.

Bruce Spiegelman and his colleagues at Dana-Farber discovered that PGC-1alpha — a key metabolic regulatory molecule — senses a dangerously low level of oxygen and nutrients when circulation is cut off and then triggers the formation of new blood vessels to resupply the oxygen-starved area — a process known as angiogenesis.

A similar response to hypoxia, or oxygen deprivation, has been observed before. The response is regulated by a group of proteins known as hypoxia-inducible factors (HIF) that detect hypoxia and activate the production of VEGF (vascular endothelial growth factor). VEGF, in turn, stimulates angiogenesis.

The newly discovered pathway provides “an independent way of getting there,” says Spiegelman, who is also a professor of cell biology at Harvard Medical School. Along with lead author Zoltan Arany and colleagues, Spiegelman found that HIF was completely left out of the loop when PGC-1alpha accomplished the same feat in single cells and in live mice using a different regulator, known as ERR-alpha (estrogen-related receptor-alpha).

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