Tricking cells into thinking they ate less food can slow the aging process

You may have heard the age-old adage “you are what you eat,” but what if your cells believe you’re overindulging, even when you’re not? A recent study reveals a fascinating connection between how our cells perceive nutrient levels and the acceleration of aging.

Tricking the cellular messenger

Led by Alejo Efeyan, head of the Metabolism and Cell Signalling Group at the National Cancer Research Centre (CNIO), the research team embarked on an ambitious endeavor to understand the intricate relationship between nutrient intake and aging.

Their focus was on a protein complex called mTOR, a key player in cellular metabolism and energy utilization.

The researchers cleverly devised a way to manipulate mTOR’s activity by tricking the protein responsible for signaling nutrient availability.

This genetic modification led the cells to believe they were receiving an excess of nutrients, even when the animals were on a normal diet.

Inflammation and accelerated cell aging

The consequences of this cellular deception were dramatic. As the animals reached maturity, their cells began to malfunction, leading to a cascade of events that accelerated aging. The skin thinned, and vital organs like the pancreas, liver, and kidneys showed signs of damage.

“The immune system cells come to repair them but are overwhelmed by the amount of damage. They accumulate and, instead of repairing, trigger inflammation that further increases problems in those organs,” explains Ana Ortega-Molina, the first author of the study and head of the Metabolism in Cancer and Ageing Laboratory at the Severo Ochoa Molecular Biology Centre (CBM).

This vicious cycle of damage and inflammation shortened the lifespan of the genetically modified animals by a staggering 20%, the equivalent of about 16 years in humans.

The study also found that blocking the inflammatory response could partially reverse the damage, offering a potential therapeutic avenue for mitigating age-related decline.

Glimpse into our aging cells

The researchers drew parallels between the cellular changes observed in the genetically modified animals and those seen in natural aging.

They compared their model to naturally aging mice colonies and found striking similarities, such as reduced activity of lysosomes, the cellular “recycling centers” responsible for removing waste.

“When there is an excess of nutrients, it makes sense that the cell shuts down the recycling activity of lysosomes, because this recycling operates especially when there are no nutrients,” Efeyan notes.

This decrease in lysosomal activity also occurs in human aging, as confirmed by analyzing blood samples from young people and septuagenarians.

Mysteries of cell aging

Efeyan is optimistic about the potential of this new animal model to unlock the secrets of aging. “It’s a tool that many more people can use,” he says, envisioning future studies that could delve into how nutrient signaling affects specific organs and contributes to neurodegenerative diseases.

This research provides valuable insights into the connection between obesity, aging, and potential interventions for promoting longevity. 

The findings suggest that individuals with a higher body mass index (BMI), often associated with excess nutrient intake, may experience accelerated aging due to similar mechanisms observed in the genetically modified animals.

Furthermore, the study sheds light on the positive effects of calorie restriction, a dietary approach known to extend lifespan in various organisms. 

The research suggests that limiting nutrient intake could activate genes that interact with the mTOR pathway, potentially mitigating the negative impact of excess nutrients on cellular function and aging.

Study significance

The study sheds light on the complex relationship between nutrient perception and aging. By manipulating the mTOR protein complex, researchers have demonstrated how overeating signals can accelerate aging in animal models.

This remarkable research opens up new avenues for exploring therapeutic interventions and understanding the intricate mechanisms behind aging in humans.

It is a testament to the power of scientific inquiry and the potential for future discoveries to improve our health and well-being as we age.

Other benefits of eating less

Limited nutrient intake, commonly known as calorie restriction, offers several benefits beyond promoting longevity. One significant advantage is improved metabolic health.

Calorie restriction enhances insulin sensitivity, reducing the risk of type 2 diabetes. It also lowers blood pressure and cholesterol levels, contributing to cardiovascular health.

Another benefit is the reduction in oxidative stress. Calorie restriction decreases the production of reactive oxygen species, which can damage cells and contribute to aging and various diseases.

This reduction in oxidative stress helps protect against age-related conditions such as Alzheimer’s and Parkinson’s diseases.

Autophagy and calorie restriction for aging cells

Moreover, limited nutrient intake boosts autophagy, a cellular process that removes damaged components and recycles them.

Enhanced autophagy helps maintain cellular health and function, preventing the accumulation of cellular debris that can lead to diseases.

Calorie restriction also strengthens the immune system. Studies have shown that it can increase the production of infection-fighting cells, improving the body’s ability to fend off illnesses.

Additionally, limited nutrient intake can improve mental health. Research indicates that it enhances mood and cognitive function, possibly by increasing brain-derived neurotrophic factor (BDNF), a protein that supports neuron growth and survival.

The study is published in the journal Nature Aging.

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