2019-02-03 10:17:20
Recent research has revealed that humans and animals have developed mechanisms to combat premature aging, allowing them to reach reproductive age wanting to reproduce, thank goodness. One of these mechanisms receives the paradoxical name of cellular senescence.
Senescence is a state that prevents cells from reproducing. This state is reached in response to damage that the cell may have received throughout its life. These damages include oxidative stress or metabolic dysfunctions, as a result of which cells cannot generate enough energy to adequately carry out the vital processes of a healthy cell, including cell division.
Senescent cells are a nuisance to the rest of the cells in an organ, since if too many accumulate, the organ cannot properly perform its function. For this reason, throughout evolution, those organisms that have acquired genes that allow them to better get rid of their senescent cells have been the ones that have most frequently transmitted their genes to the following generations.
Senescent cells require their own collaboration. Senescent cells produce a series of proteins that signal their presence to the immune system. In particular, these proteins attract macrophages to them, phagocytic cells capable of “eating” senescent cells. The senescent cells thus removed make room in the organ for new cells, derived from healthy stem cells, to repopulate it. Thus, the organ maintains its functionality for much longer than if it were impossible to destroy the senescent cells. Elimination of senescent cells also prevents them from becoming tumorous. It has been proven that if the mechanisms of elimination of senescent cells fail, tumors are more likely to develop.
However, everything ends up getting old, including the mechanisms for eliminating senescent cells. When these mechanisms are not as effective as when the organism was younger, senescent cells accumulate in the organs and prevent them from carrying out their function properly. Not only that, but senescent cells, by continuing to attract macrophages to organs, generate a chronic inflammatory state that ends up damaging even neighboring healthy cells, helping to accelerate organ degeneration.
Indeed, an increase in senescent cells in different organs has been observed with age, which is related to degenerative diseases typical of aging. In addition, certain neurodegenerative diseases, such as Parkinson’s disease, are also associated with accumulation of senescent cells. In laboratory mice with these types of diseases, it has been proven that treatments capable of reducing this accumulation improve the state of their disease.
What does this have to do with obesity and anxiety?
Recent studies have shown that obesity is one of the main factors in the development of mental illnesses such as depression and anxiety. This has been observed both in laboratory mice genetically prone to becoming obese, or fed a high-fat diet that induces obesity, and in obese people. Why and how obesity could induce or promote this type of disease was unknown.
However, another relatively recent discovery is that obesity also leads to the generation of excess senescent cells. In this sense, obese people seem to age faster than thin people. Since senescent cells in the brain are related to neurodegenerative diseases, it could be that, in the initial stages of accumulation of senescent cells in the brain, they cause initially less serious diseases, such as depression and anxiety.
A group of researchers is studying this possibility in genetically modified laboratory mice so that they can be effectively treated to eliminate their accumulated senescent cells in the brain. The scientists find that by feeding these mice a diet rich in fat and thus inducing obesity, the animals develop behaviors typical of a state of anxiety whose intensity can be evaluated with concrete tests. Analysis of the brains of these animals revealed that senescent cells with a high fat content accumulated in a region of this organ called the lateral ventricle. This region is characterized by having the capacity to generate new neurons, but in these conditions of accumulation of senescent cells, induced by obesity, new neurons could not be generated.
The scientists then treat the mice to remove their excess senescent cells. After this treatment, they found that, despite being just as obese as before, the mice decreased behaviors related to anxiety and also found that the lateral ventricle can generate new neurons. This is strong evidence that obesity-induced senescence is the cause of anxiety in these animals.
The fact that obese people also develop anxiety problems is an important indication that something similar may be going on in their brains. One more reason to take this diet and exercise seriously, which will surely make us feel younger and stronger, whatever our age.
Referencia: Ogrodnik et al., Obesity-Induced Cellular Senescence Drives Anxiety and Impairs Neurogenesis, Cell Metabolism (2018),
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