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Many of us have experienced the uphill struggle to control our weight as we get older. We cannot eat whatever we like and stay slim like when we were younger, our holiday indulgences refusing to go away. The battle of the bulge gets harder the older we get, and there was little we could do about it, but now science has come to the rescue and is starting to unravel the mystery of why we find it harder to lose weight as we get older.

A new study led by Professor Vishwa Deep Dixit at Yale University shows how both the nervous system and the immune system talk to each other and, in doing so, control metabolism and inflammation in the body[1]. This study sheds light on why older adults often find it difficult to burn stored belly fat, increasing the risk of a number of metabolic disorders.

Perhaps more intriguingly, the study also shows some potential approaches to targeting the problem, thus helping older adults to improve their metabolism, improve weight control and reduce the risk of metabolic disorders.

Stored fat becomes locked in limbo

Regardless of their weight, older adults all have an increased ratio of belly fat compared to younger people. Unfortunately, when they expend energy, they do not burn the energy stored in that belly fat as well as younger people do. This leads to the buildup of increasing amounts of belly fat over time, which increases the risk of age-related diseases. The reason why older adults do not burn belly fat as well had been unknown until now.

The research team investigated the role of macrophages and how they relate to the fat-burning process. Typically, macrophages perform a variety of functions in the body, from mediating tissue repair to fighting infections and clearing up metabolic garbage.

During their study, the researchers discovered a totally new type of macrophage that resides on the nerves present in the stored belly fat. These nerve-associated macrophages get increasingly inflamed as we grow older due to a variety of age-related damages causing inflammation to rise system-wide. The more inflamed the nerve-associated macrophages become, the more they prevent the neurotransmitters, which are chemical messengers, from functioning properly.

The research team isolated the immune cells from the fat tissue of young and old mice, and they sequenced and computationally modeled the genome to better understand what was going on. They discovered that the aged nerve-associated macrophages can cause the breakdown of neurotransmitters known as catecholamines, thus preventing the fat cells from using their stored energy when the body needs it; in effect, the fat is locked into the body in limbo and is not used.

So how might science fix this problem?

The team discovered that when they reduced inflammation via a specific receptor that controls inflammation, the NLRP3 inflammasome, in the aged nerve-associated macrophages, the catecholamines were able to work efficiently again like they do in young mice. This shows clearly that the immune cells are communicating with the nervous system to control metabolism.

The research team then followed up by inhibiting an enzyme that increases in aged macrophages, thereby restoring fat metabolism in aged mice. The team observed that the enzyme, monoamine oxidase-A, or MAOA, is blocked by existing drugs for the treatment of depression. Therefore, MAOA-inhibiting drugs could potentially be used to improve metabolism in older adults, though more research is needed in order to specifically target the nerve-associated macrophages and to ensure the approach is safe. 

The next step for the research team will be to further investigate the immune cells and how they interact with nerves and how crosstalk between the immune cells and nervous system relates to disease progression. The hope is that if controlling inflammation in aging nerve-associated macrophages can improve metabolism, it may have a wider positive effect on the nervous system or even on aging itself.

Conclusion

The reduction of inflammation is a key player in the aging process, and this is why research like this holds great potential for not only helping combat metabolic disorders but also for aging research. Also, the use of senolytics that remove senescent cells, a major source of systemic inflammation in aging, is possibly even more exciting; could reducing systemic inflammation improve these nerve-associated macrophages too?

It really should not need saying, but we do not suggest you take MAOA-inhibiting drugs to lose weight or slow aging as this is extremely dangerous. The researchers in this study have stressed that more research is needed to ascertain safety, so this is absolutely not something you should try at home, you have been warned. 

Literature

[1] Camell, C. D., Sander, J., Spadaro, O., Lee, A., Nguyen, K. Y., Wing, A., … & Rodeheffer, M. S. (2017). Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during aging. Nature.

About the author
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Steve Hill

As a scientific writer and a devoted advocate of healthy longevity technologies Steve has provided the community with multiple educational articles, interviews and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity reporter, Psychology Today and Singularity Weblog. He is a co-author of the book “Aging Prevention for All” – a guide for the general public exploring evidence-based means to extend healthy life (in press).
  1. October 3, 2017

    Saw this recent article on research into converting white fat into brown fat:

    http://www.genengnews.com/gen-news-highlights/love-handles-get-dissolved-by-new-skin-patch/81254933

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