Health

Association between stress, weight, and social anxiety in early adolescence


While previous studies have shown this link, there is little way of determining a biological link between the increase in adipose tissue during puberty and the decline in social functioning.

Research published in Scientific advance.

“We know that stress can cause mental illness, including depression,” says Sandi. “Some of the typical behavioral changes that you see in depression are changes in personal sociability, which means that some depressed people tend to be more withdrawn, a little out of society; Some may even develop social anxiety.”

Stress, sociability and rats

In the study, Sandi’s team discovered two insights in this area: first, perinatal stress leads to an increase in adipose tissue and a concomitant decrease in sociability. Second, how the two phenomena are biologically related.

“We investigated whether stress-induced changes in fat composition early in life could induce changes in the brain that would eventually cause changes in brain health,” said Sandi. protracted social behavior”.

To study perinatal stress, researchers needed a model. They turned to mice, during the perinatal period of puberty, and subjected them to chronic, unpredictable stress. A study of their body composition showed an overall increase in fat mass and larger fat cells.

Upon reaching adulthood, the rats were tested for social tasks. The male mice showed a decrease in sociability throughout life as their adipose tissue increased, but interestingly the female mice had no such effect. But whether there are gender-dependent differences in other psychobiological adaptations is something Sandi’s team will investigate in the future.

“What we’re focusing on here is the reduction in sociability that you see when you’re depressed,” says Sandi. “We also know from epidemiological studies in humans, that it may be related to early life stress – perinatal stress, which can make people less sociable.”

Connect NAD +

Then researchers began to identify the underlying biology. A series of tests have shown that a specific enzyme called adipokine nicotinamide phosphoribosyltransferase, (NAMPT), is known to be involved in some of the pathological metabolic problems caused by obesity.

In the body, NAMPT exists in two forms: an intracellular form, which regulates the production of nicotinamide adenin dinucleotide (NAD+), a molecule important for energy generation in cells. In the extracellular form, (eNAMPT), the enzyme is present in the blood.

Stress in the brain

The researchers found that the pre-stressed rats showed decreased amounts of NAMPT in adipocytes and, therefore, of eNAMPT in their blood in adulthood compared with mice that were not stressed. .

Looking at the nucleus accumbens – a brain region that regulates motor behaviors – of both socially impaired and healthy, “control” mice, the researchers identified low levels of NAD+ and problems with the enzyme Sirtuin-1, an enzyme that depends on NAD+ to regulate the expression of genes involved in helping cells self-regulate in response to stressors.

“Since the free-stressed mice had lower NAD+, we assessed whether the effects we saw in sociability were related to the actions of Sirtuin-1 or not,” said Sandi. are not”. “Using a variety of approaches, we have demonstrated that this is indeed the case, meaning that perinatal stress leads to long-lasting changes at multiple levels linking fat to brain function and behavior. .”

NAD+ boosters: A solution?

“Stress before sleep leads to decreased levels of NAMPT in adipose tissue and biological activity in the blood,” says Sandi. “The second factor involved the reduction of NAD+ in nuclear accumulators, where we found a decreased NAD-dependent activity of Sirtuin-1.” The team found that this impairment affects the function of median spiny neurons from the nucleus accumbens and, ultimately, promotes reduced sociability.

After implicating the NAD+/Sirtuin-1 pathway in nuclei, the team tried to see if they could help protect against the effects of perinatal stress in mice. They did this in two ways: bringing eNAMPT blood levels back to normal, or feeding mice nicotinamide mononucleotide (NMN), a NAD+ enhancer. Two approaches worked, preventing both the decline in sociability and also the changes in cumulative nuclear excitability.

But is the NAD+ booster, which is popular in the US and EU, but not in the Swiss market, the solution to treating the social impact of stress increasingly observed in young people? now? “We have to be careful because we applied the nutritional treatments in our study into adulthood,” Sandi cautions. “We are not saying that stressed children or adolescents should take NMN; it is important to first analyze whether they reduce plasma concentrations of NMN or eNAMPT and to conduct targeted studies. to see how effective this approach would be in younger populations.So it makes sense to restore a low metabolic rate, not to treat everyone the same way if there’s no biological reason. .”

Source: Eurekalert



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