As the saying goes, getting old is no fun. Our appearance changes, our bodies tend to get weaker, and we end up becoming prone to a variety of health troubles. Infections happen more frequently - and take longer to resolve -- and the chances for chronic diseases such as obesity, diabetes, cardiovascular troubles and mental health disorders increase.
Figuring out how aging contributes to this wide spectrum of illness is no easy task. Quite simply, there is no one answer. Yet, researchers have been gaining clues to figuring out how we can delay or prevent the onset of troubles as we get older.
Over the last few weeks, researchers have discovered a natural yet nasty phenomenon leading to troubles in the elderly. The reports focus on two very different parts of our bodies, the immune system and the microbial population in our guts. Though both studies were conducted in mice, the results unveil an inconvenient reality we may all face as we get older.
The first step down this troublesome path involves a change in the immune system. Our natural defense force becomes less capable of holding off enemy invasions leading to more infections. But this isn't the only problem. An unbalanced immunity may also attack our own cells leading to unexpected damage.
This reversal of fortune usually is called chronic low-grade inflammation. In reality, this is a cold war inside the body in which the defense forces are continually awaiting an invasion that may never come. As this happens, some immune soldiers, known as effector T-cells, may go rogue and start attacking perfectly normal cellular citizens. Normally, they are calmed by superior officers known as regulatory T-cells. But in the elderly, the orders are not always obeyed.
While we may know of the problem, how it happens has been a mystery. This is where the first study from a group of Israeli researchers comes into play. They examined the immune system of young and old mice hoping to identify any suspect changes in the immune system.
What they found was rather remarkable. Instead of a massive change to the system, they found one particular alteration capable of causing all the troubles. The effector cells had not defied their regulatory superiors. They had simply become deaf to them.
At the molecular level, cells interact through contact. A particular protein, known as L-selectin, helps this process along. When the protein is present, effector cells can communicate with their regulatory counterparts. However, the researchers discovered the rogue cells had lost this protein. They could no longer communicate with the regulatory cells and as such, continued their attacks.
While this situation is bad, it is also usually rare. A surge in effector cells is only needed when there is a potential risk. If the body is balanced, then they are not needed in large numbers. The chances for going rogue are minimized.
Enter the second study and what can only be described as a biological one-two punch to elderly health.
The report, performed by a group of Canadian researchers, examined the effect of gut microbes on the aging immune system. In this case, the team looked at the difference between mice allowed to develop their own gut microbes and those not possessing any microbes. The hope was to see some difference in the way the immune system reacted.
The results couldn't be more conclusive. The normal mice developed inflammation as they aged while those without any microbial flora did not. As to why this difference occurred, the answer was relatively simple. The affected mice had an imbalance in their gut microbial diversity, also known as dysbiosis.
One of the hallmarks consequences of dysbiosis is the development of inflammation. It's because many of the microbes found in these situations produce a variety of chemicals known to aggravate the immune system. They include toxins, waste products, and cell debris.
In younger animals, these molecules are kept away from the immune forces thanks to a strong intestinal wall. But as the body ages, the chemicals have an easier time getting through the barrier. The end result is a rise in chronic low-level inflammation both in the localized area as well as the rest of the body. This then increases the chances for a rogue effector T-cell and the potential for disease.
Taken together, these studies highlight how the normal aging process can end up causing significant health problems later in life. However, the news is not entirely glum. Both groups have suggestions to ameliorate the situation although one is far easier than the other to incorporate.
The Israeli group discovered a possible means to restore normal communications between the defense forces. It's a molecule known as interleukin 2 and it acts as a regulator of the immune system. In this case, the protein helped to reduce the emergence of rogue staff. The authors suggest one day this chemical may help relieve the issues associated with chronic low-level inflammation. Unfortunately, this type of treatment need to undergo proper clinical testing to prove it can be useful in humans.
As for the Canadian study, the best way forward appears to be balancing the microbial population. This may be helped though a change in diet from the Standard American Diet to one that is higher in fibre, polyunsaturated fatty acids, and vegetables. Although it may not resolve dysbiosis completely, there is evidence to suggest this behaviour change may have a secondary benefit. In a dietary study conducted in mice, a poor diet also led to the loss of L-selectin on immune defenders.
In essence, switching to a healthier eating regimen not only may balance the gut microbial population, but also reduce the numbers of rogue immune soldiers. This course of action undoubtedly will require testing in humans to prove its worth in the context of this double-shot to elderly health. But since the recommended diet is beneficial in many other regards, it may be worth looking into now rather than later.
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