Eating less may help reduce body aging

To improve the immune system, reduce inflammation levels throughout the body, delay the onset of age-related diseases and live longer, you have to eat less food, according to a new study by scientists from the United States and China that provides the most detailed report to date of the cellular effects of a calorie restricted diet in rats.

While the benefits of calorie restriction have long been known, the new results show how this restriction can protect against aging in the cellular pathways, as published in the journal ‘Cell’.

While calorie restriction was already known to increase shelf life, the truth is that all the changes that occur at the single cell level to cause that have now been shown. Thus, it gives objectives with which we can eventually act with medicines to treat aging in humans. Aging is the highest risk factor for many human diseases, such as cancer, dementia, diabetes, and metabolic syndrome.

Caloric restriction in animal models has been shown to be one of the most effective interventions against these age-related diseases. And while the researchers know that individual cells undergo many changes as the body ages, they haven’t known how caloric restriction could influence these changes.

In the new document, Izpisúa and his collaborators, including three alumni from their Salk lab who are now professors running their own research programs in China, compared rats that ate 30 percent less calories with rats on normal diets.

In the new paper, the researchers compared rats that ate 30 percent fewer calories than rats on normal diets.

Both at the beginning and end of the diet, the team isolated and analyzed a total of 168,703 cells from 40 cell types in the 56 rats. The cells came from fatty tissues, liver, kidney, aorta, skin, bone marrow, brain and muscle.

In each isolated cell, the researchers used single-cell genetic sequencing technology to measure activity levels of the genes. They also looked at the general composition of cell types within any given tissue. Then, they compared old and young mice on each diet.
Many of the changes that occurred when rats in the normal diet aged did not occur in rats on a restricted diet. Even in old age, many of the animals’ tissues and cells in the diet closely resembled those of young rats.

Overall, 57 percent of the age-related changes in cell composition observed in the tissues of rats on a normal diet were not present in rats on the calorie-restricted diet.

This approach not only told us the effect of calorie restriction on these cell types, but also provided the most comprehensive and detailed study of what happens at the single cell level during aging.

Some of the cells and genes most affected by diet are related to immunity, inflammation and lipid metabolism. The number of immune cells in almost all of the tissues studied increased dramatically as control rats aged, but was unaffected by age in calorie-restricted rats.

In brown adipose tissue, a type of adipose tissue, a calorie-restricted diet reversed the expression levels of many anti-inflammatory genes to those seen in young animals.

The main finding in the current study is that the increased inflammatory response during aging could be systematically suppressed by calorie restriction.

When the researchers focused on transcription factors, essentially master switches that can vastly alter the activity of many other genes, which were altered by caloric restriction, one stood out. The diet altered the levels of transcription factor Ybx1 in 23 different cell types.

Scientists believe that Ybx1 may be an age-related transcription factor, and they are planning more research into its effects. People say that ‘you are what you eat’, and we are discovering that this is true in many ways. The state of your cells as you age clearly depends on your interactions with your environment, which includes what and how much you eat.

The team is now trying to use this information in an effort to discover aging drug goals and implement strategies to increase life and health.

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