Finally, an answer to the question ‘How to live a long life?’ has been found. At least, that’s what it seems from a recent research.

There’s a multi-billion-dollar industry devoted to products that fight signs of ageing, but moisturizers only go skin deep. Ageing occurs deeper, at a cellular level, and scientists have found that eating less can slow this cellular process.

Recent research published in Molecular and Cellular Proteomics offers a glimpse into how cutting calories impacts ageing inside a cell. The researchers found that when ribosomes, the cell’s protein makers, slow down, the ageing process slows too. The decreased speed lowers production but gives ribosomes extra time to repair themselves.

“The ribosome is a very complex machine, sort of like your car, and it periodically needs maintenance to replace the parts that wear out the fastest,” said Brigham Young University biochemistry professor and senior author John Price. “When tyres wear out, you don’t throw the whole car away and buy new ones. It’s cheaper to replace the tyres.”

So what causes ribosome production to slow down in the first place? At least for mice: reduced calorie consumption.

Price and his fellow researchers observed two groups of mice. One group had unlimited access to food while the other was restricted to consume 35 percent fewer calories, though still receiving all the necessary nutrients for survival.

“When you restrict calorie consumption, there’s almost a linear increase in lifespan,” Price said. “We inferred that the restriction caused real biochemical changes that slowed down the rate of ageing.”

Price’s team isn’t the first to make the connection between cut calories and lifespan, but they were the first to show that general protein synthesis slows down and to recognize the ribosome’s role in facilitating those youth-extending biochemical changes.

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Exercise may be an efficient way for obese pregnant women to lower their risk of diabetes, dangerously high blood pressure and other complications, research suggests.

“The study suggests that a prenatal exercise-based intervention leads to both decreased costs and improved outcomes in obese women,” said Leah Savitsky, a medical student at Oregon Health and Science University in Portland who led the study.

As reported at the 37th annual meeting of the Society for Maternal-Fetal Medicine in San Diego, California, Savitsky and her team analyzed previously published research on the effect of exercise on pregnant women with a body mass index (BMI) of at least 30.

The normal range for BMI – a ratio of weight to height – is 18.5 to 24.9; a BMI of 30 or more indicates obesity. (A BMI calculator is here, on the website of the U.S. Centers for Disease Control and Prevention. Based on their analyses of those earlier studies, the researchers estimated the benefit of exercise for women who are obese at the start of their pregnancy.

They calculated that for every one million such women, there would be 38,176 cases of a dangerous pregnancy-related blood pressure problem known as preeclampsia among those who exercised, compared to 113,000 cases among those who didn’t exercise.

Exercise would also be linked to a decrease in so-called gestational diabetes, with a rate of 195,520 per million among exercisers compared to 305,500 among non- exercisers, according to their calculations.

Likewise, they estimated, for every million obese pregnant women the preterm birth rate would drop from 105,059 to 90,923 with exercise, the maternal death rate would fall from 90 to 70 and the neonatal death rate would drop from 1,932 to 1,795.

Based on a cost-effectiveness threshold of$100,000 per quality-adjusted life year, an exercise intervention could save money as long as expenses are held to just under$3,000. The effects of exercise may be even more beneficial than the study suggests, Savitsky said. “This study did not consider additional downstream benefits on control of weight beyond pregnancy as well as the downstream potential benefits on hypertension and diabetes,” she told Reuters Health by email.

Women who are not obese may benefit as well. The researchers applied their model to women with a normal BMI of 18.5 – 24.9 and found similar improvements in outcomes among those who exercise, although the cost-effectiveness thresholds were lower.

“With the obesity epidemic looming in our society, perhaps we should be turning our attention to prevention of disease. It does not seem to be too late even for obese pregnant women to engage in lifestyle change that may substantially reduce health care costs,” Mottola told Reuters Health by email.

The current study was not designed to develop specific exercise guidelines for obese pregnant women; these women should consult their obstetricians for guidance. In the meantime, the American College of Obstetricians and Gynecologists advises obese pregnant women to “start with low-intensity, short periods of exercise and gradually increase as able.”

Alert! Your memories are in danger of being lost if you are sleep derived, suggests a study. Studying mice, scientists at Johns Hopkins have fortified evidence that a key purpose of sleep is to recalibrate the brain cells responsible for learning and memory so the animals can “solidify” lessons learned and use them when they awaken — in the case of nocturnal mice, the next evening.

A summary of their study appears online in the journal Science.

The researchers, all of the Johns Hopkins University School of Medicine, also report they have discovered several important molecules that govern the recalibration process, as well as evidence that sleep deprivation, sleep disorders and sleeping pills can interfere with the process. “Our findings solidly advance the idea that the mouse and presumably the human brain can only store so much information before it needs to recalibrate,” says Graham Diering, Ph.D., the postdoctoral fellow who led the study. “Without sleep and the recalibration that goes on during sleep, memories are in danger of being lost.”

Diering explains that current scientific understanding of learning suggests that information is “contained” in synapses, the connections among neurons through which they communicate.

On the “sending side” of a synapse, signaling molecules called neurotransmitters are released by a brain cell as it “fires”; on the “receiving side,” those molecules are captured by receptor proteins, which pass the “message” along. If a cell receives enough input through its synapses, it fires off its own neurotransmitters. More specifically, experiments in animals have shown that the synapses on the receiving neuron can be toggled by adding or removing receptor proteins, thereby strengthening or weakening them and allowing the receiving neuron to receive more or less input from nearby signaling neurons.

Scientists believe memories are encoded through these synaptic changes. But there’s a hitch in this thinking, Diering says, because while mice and other mammals are awake, the synapses throughout its brain tend to be strengthened, not weakened, pushing the system toward its maximum load. When neurons are “maxed out” and constantly firing, they lose their capacity to convey information, stymying learning and memory. One possible reason that neurons don’t usually max out in a process that has been well-studied in lab-grown neurons but not in living animals, asleep or awake. Known as homeostatic scaling down, it is a process that uniformly weakens synapses in a neural network by a small percentage, leaving their relative strengths intact and allowing learning and memory formation to continue.