Stress Makes Junk Food Worse
Studies of mice and monkeys show that repeated stress — and a high-fat, high-sugar diet — release a hormone, neuropeptide Y, that causes a buildup of abdominal fat.
Manipulating levels of that hormone could melt fat from areas where it is not desired and accumulate it where it is needed.
Stephen Baker said it could also reduce or eliminate the need for extremely expensive fat replacements used in breast and facial reconstruction and in other surgeries.
Zofia Zukowska divided mice into 4 groups: 2 received a conventional diet, and 2 received a diet high in fat and sugar. Then one group from each diet was forced to stand in cold water for an hour every day, “like the Northern European experience of waiting for a bus with wet feet.”
The remaining groups were exposed to an aggressive alpha male for 10 minutes each day, “like having a bad boss.”
For the mice on the normal diet, “it really didn’t matter whether they were stressed or not. They didn’t have much difference in weight. If anything, the stressed ones weighed less.”
But the stressed mice on the “fast food” diet accumulated twice as much belly fat in the first 2 weeks as those that were not stressed. Over 3 months, they became grossly obese.
Biopsies of the fat showed increased levels of neuropeptide Y, or NPY, a hormone discovered nearly 25 years ago. In the brain, NPY stimulates appetite. In the periphery of the body, it is a growth factor that stimulates enlargement of cells and the production of new blood vessels to supply nourishment.
Zukowska and Lydia Kuo found that the hormone not only enlarged fat cells, but stimulated the production of new fat cells and blood vessels to support them.
A buildup of abdominal fat is a prime contributor to “metabolic syndrome,” which affects 60 million Americans, and sharply increases the risk of diabetes, heart disease and stroke.
The researchers attempted to mimic the process of fat formation by implanting NPY in a slow-release tablet under the skin of mice and monkeys. In each the production of new fat was stimulated around the tablet.
Next, they implanted human fat in nude mice, which have an inhibited immune system and are unable to fight off such transplants. Normally, this fat is reabsorbed by the animal within a couple of weeks. But when they implanted NPY along with it, 99% of the fat was retained after three months.
When the researchers implanted a slow-release tablet of a small molecule that blocks the cellular receptor for NPY, the fat buildup did not occur. Implanting the molecule in a fat deposit caused the fat “to just melt away.”
Within two weeks the fat deposit in the mice had shrunk by half.
The hormone and the receptor are nearly identical in mice, monkeys and humans.
There is a Northern European population that, due to a genetic abnormality, secretes excessive amounts of NPY when stressed. That population is unusually susceptible to obesity and diabetes. In contrast, a Swedish population with a genetic mutation that lessens the receptor’s efficacy is resistant to obesity.
NPY has been injected into humans with no apparent side effects, but its long-term effects have not been studied.
“Stress can be fattening, study finds,” by Thomas H. Maugh II