Inflammation-Good and Bad for Health ?

Leslie Nemo, Discover magazine, discusses what inflammation is and why it can sometimes be bad for health. September 2020.

Your immune system is built to help you. And usually, it does. When an injury or infection damages cells in your body, immune cells and proteins rush to the site to draw attention to the problem and improve your condition. This is the process of inflammation. 

Ideally, the surge of inflammatory cell activity tapers off when cellular repair begins. “That’s if everything goes according to plan,” says Keenan Walker, a neurologist at Johns Hopkins University School of Medicine. When inflammation doesn’t go as planned — like when it continues at low levels for a long time — that can cause more harm than good. 

The potential for inflammation to be a healthy, normal reaction or a counterproductive force can make learning about it confusing. And the line between the good and the bad gets even muddier with particular health conditions. In some cases, researchers still don’t know what to make of the inflammation they see — is it a symptom or source of the problem?

Sometimes You Feel It, Sometimes You Don’t

We all know the classic sensations that go along with inflammation. If you twist your ankle, for example, it will swell up — thanks to immune cells making the blood vessels more permeable to let other immune system agents in, Walker says. Some of the arriving proteins give off the sensation of heat or pain. These sensations dissipate when this short burst of what’s called acute inflammation dies down. 

During chronic inflammation, lower levels of those same immune system agents circulate through the body all the time. Older individuals might be prone to this scenario. As immune systems age, they have a harder time winding down once started, Walker says. In other cases, physical changes in our bodies trigger inflammation. For example, chronic high blood pressure injures blood vessel walls. An inflammatory response will dispatch to take care of the damage — but the damage is always going, perpetuating immune system activity. If fat cells around the abdomen grow, they issue signals calling for inflammatory responses, too. 

In these cases, the constant immune activity interferes with other biological processes. Inflammation proteins disrupt how cells interact with insulin, for example. Too much obstruction can decrease insulin sensitivity, which can progress to diabetes. In the brain, some immune system agents might cut connections, or synapses, between cells. This is often a helpful activity, “but it can become out of control,” Walker says, “and essentially make it harder to learn and form memories because the synapses are pruned faster than they should be.”

Is It the Solution or the Problem?

The way the immune system interacts with the brain is Walker’s speciality, and it’s also one area of chronic inflammation research that researchers are still figuring out. When it comes to obesity, high blood pressure, inflammation and diabetes, those associations are better understood. Researchers know that some of those conditions can exacerbate each other. But what’s happening with neurological conditions — like in Alzheimer’s disease, for example — are less clear. 

Genes that put people at risk of the neurodegenerative disorder also regulate immune responses, and there is strong scientific consensus that the conditions are wrapped up in one another somehow, Walker says. Even dissections of brains affected by Alzheimer’s show inflammatory proteins are present during the neural decline, trying to break up problematic clumps of proteins associated with the condition. But researchers still don’t know if the inflammation appears in Alzheimer’s as a reaction to another problem in the immune system, or if chronic inflammation drives the disease itself.

If the latter were true, reducing chronic inflammation should also reduce the likelihood of someone developing Alzheimer’s. In studies where people were given ibuprofen or aspirin — two medications that reduce inflammation — their risk for developing Alzheimer’s stayed unchanged, however. “When it’s human studies, that’s the only way to know without a doubt causality,” Walker says. “To turn this one thing down and reduce the appearance of a disease, that’s the holy grail.”

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