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Inflammation - temporary and chronic
(extract from a National Geographic article).
Inflammation gets a bad rap. Consider the various anti-inflammatory diets, supplements, medications, and lifestyle tips aimed at providing some degree of relief from uncomfortable symptoms like redness, pain, heat, or swelling from an injury or infection.

“People definitely associate [inflammation] with something that’s negative,” says Wolfgang Marx, a senior research fellow and expert in nutritional psychiatry at Deakin University in Melbourne, Australia.

But the truth is far more complicated—and potentially beneficial. After centuries of debate and research, scientists now know that inflammation is as much a hero as it is an enemy. Ideally, the physiological process conquers infections, prevents cancer from taking hold, allows injuries to heal, turns vaccines into long-lasting disease protection, and more. In fact, we could not survive without the many roles that inflammation plays in the daily functioning of our bodies.

“Every facet of human health impinges on inflammation,” says Bali Pulendran, an immunologist at Stanford University. “Without the appropriate type and level of inflammation, the immune system would not be capable of launching effective immunity against pathogens.”

As with many biological reactions, though, the danger lies in how much. When inflammation persists at chronically elevated levels after an initial infection or injury has passed, it can shift functions, leading to long-term illnesses such as heart disease, cancer, type 2 diabetes, depression, and Alzheimer’s. Many of these conditions become more common with aging, which is also linked to rising levels of inflammation. The immune system is capable of attacking the body’s own tissues, resulting in autoimmune conditions such as rheumatoid arthritis, multiple sclerosis, and Crohn’s disease. Some researchers are also exploring whether there’s a connection between excessive inflammation and long COVID.

Over the past two decades, such major yet often contradictory health impacts have galvanized scientists to dig deeper into understanding this process. When geriatrician and epidemiologist Luigi Ferrucci started looking into the links between inflammation and aging in 1999, there were five or six known molecules, called markers or mediators, that were used as measures of inflammation in the body. Today there are thousands.

“Now we can measure 10,000 proteins in a drop of blood, and so we start understanding that there are many subsets of inflammation, and those are driven by different inflammatory mediators,” says Ferrucci, who is scientific director of the National Institute on Aging. “By studying how they are organized and connected, we understand more about the inflammatory response than we did before.”

This deepened knowledge suggests that “inflammation,” as a single word, is relatively meaningless, because it has so many expressions. Rheumatologists, immunologists, orthopedic surgeons, vaccinologists: For each type of specialist, the word describes a distinct but often overlapping set of molecules, molecular interactions, symptoms, and outcomes. “The word ‘inflammation’ is a word of convenience. It’s something that we all bandy about haphazardly, but it clouds clarity, and it clouds thinking,” Pulendran says.

As researchers learn more about the inflammatory process, they are getting better at tinkering with it to harness the good that it can do. On the horizon are new medications and more refined diet and lifestyle recommendations to address the many forms of inflammation and help prevent and treat more diseases. Figuring out how to make these innovations accessible and affordable to everyone is an urgent task.

The emerging consensus among scientists is that inflammation isn’t inherently bad or good; we need just the right amount of it depending on the situation. It is not something we want to eliminate. It is something we want to learn how to control.

A BRIEF HISTORY OF INFLAMMATION
The condition has been under investigation for thousands of years. The better we understand it, the more we see just how much there is to learn.

In the beginning, there was swelling, pain, heat, and redness. These cardinal signs of inflammation were described by Aulus Cornelius Celsus, a Roman encyclopedist, more than 2,000 years ago. Eventually, a fifth major sign emerged: loss of function.
Today the reaction Celsus described is called the acute inflammatory response, and it is known to involve hundreds of molecules and pathways that lead to healing when things go right and to infection or disease when they don’t. Scientists working in increments and leaps over centuries pieced together a detailed story of what inflammation is and how it works on the level of cells, proteins, and other molecules.

It all started in earnest with the microscope, which gave scientists their first window into this response at a molecular level, says Klaus Ley, an immunologist at the Medical College of Georgia at Augusta University. In 1839 German scientists first described seeing leukocytes, or white blood cells, respond to an injury in experiments with frogs. In 1882 Russian scientist Ilya Mechnikov described the way leukocytes consumed bacteria and dead cells, a discovery that earned him a Nobel Prize in 1908.
Scientists now know there are many types of leukocytes, but the key observation at the time was that these cells migrated out of blood vessels into tissues, where they did the work of cleaning up messes. “Their understanding was essentially, OK, there are these components of blood, the white blood cells, that do the repair,” Ley says, “and we can see them in this state of what we consider inflammation.”

Incremental advances came over the next few decades. In 1927, for one, Welsh cardiovascular specialist Sir Thomas Lewis discovered that chemicals called histamines played an important role in the response of blood vessels during bodily harm. It took nearly 60 more years until this basic understanding exploded into something infinitely more intricate: the discovery of the first cytokine, an inflammatory marker called interleukin-1. There are now about 200 known cytokines—small proteins released by cells that tell the immune system to do its job. Some are better understood than others.

As research has progressed, so too have treatment strategies, moving on from the dried myrtle the ancient Chinese used for rheumatic pain and the opium poppies used by the Greeks. One modern breakthrough came with the discovery in 1928 of penicillin, which could kill the bacteria that caused life-threatening inflammation. And the cytokine revolution has provided yet another window into which treatments actually work.

Today there are numerous anti-inflammatory medications, but in some cases it may not make sense to use them, says Karim Khan, a sports medicine specialist at the University of British Columbia. “I’ve got hip arthritis, and I’m not taking anti-inflammatory drugs,” Khan says. “I don’t want to damage and block the other processes I want.”
After nearly two millennia, we know that sometimes getting in the way of inflammation can be a bad idea.

COLD DUNKS, PLASMA INJECTIONS, AND SAUNAS ARE POPULAR WAYS TO BATTLE INFLAMMATION. BUT DO THEY WORK?
AN ATHLETIC teenager in Ireland, Joseph Costello often followed hard Gaelic football sessions with ice baths. By the time he was a graduate student, he had found a more extreme method to chill the sore muscles and joints that come with exercise-induced inflammation: standing in a chamber cooled to minus 110°C (-166°F) for a few minutes at a time.
The experience was equal parts excruciating and invigorating, says Costello, now an exercise and environmental physiologist at the University of Portsmouth in the United Kingdom. “It was literally out of this world,” he says. “The coldest temperature ever recorded on Earth was about 20 degrees Celsius warmer than this.”

Ice plunges and cold showers are trendier than ever as strategies for battling inflammation, but they are not the only ways people are trying to hack their health. The options range from a set of specialized injections that require assistance from a health-care provider to heat-exposure sessions that essentially fight fire with fire.

But do any of these techniques accelerate healing? Evidence is both promising and murky, with some studies showing benefits, some showing no effects, and others showing that inflammation-control tactics can backfire.

A color-enhanced x-ray shows a knee replacement for degenerative joint disease in a 79-year-old woman. Inflammation may contribute to joint pain, especially in older people, but this bodily response is also part of the healing process.

MOST OF US ARE DESTINED for some very specific aches and pains. As we get older, our odds of developing a musculoskeletal injury increase, and our body heals more slowly. By the age of 55, an estimated 80 percent of people suffer from osteoarthritis (the degeneration of cartilage around the joints), leading to more stiffness and soreness. Inflammation is a major driver of these types of pain, according to some studies. But preventing or controlling the discomfort is tricky, in part because inflammation is an essential process that our bodies need to repair damage.
Here’s how it works: When someone strains or tears a ligament or tendon, the injury triggers the release of inflammatory molecules and cytokines, starting a sequence of events known as acute inflammation. Immediately blood vessels dilate to allow more fluid to flow into the injured area. Swelling and clotting ensue while more inflammatory cells arrive to clear out the damage and mobilize other cells to rebuild tissue.

The idea of tinkering with inflammation is tantalizing because, in some ways, you could augment this process. For those less excited about full-body refrigeration, the most direct way to do that right now is with a simple shot.

This increasingly popular medical approach, called platelet-rich plasma (PRP), is aimed at treating more chronic types of pain from tendinitis, arthritis, and other problems. Injections of PRP are made from a person’s own blood, which is first spun rapidly to filter out red blood cells and isolate platelets, essential for clotting and full of anti-inflammatory growth factors.

PRP shots can contain various concentrations of white blood cells and other ingredients that dial inflammation up or down as needed, says Dean Wang, an orthopedic surgeon and chief of the sports medicine division at the University of California, Irvine. For his arthritis patients, he uses an anti-inflammatory PRP. For people with chronic tendon injuries such as tennis elbow, he makes pro-inflammatory formulations.

Evaluating the effectiveness of PRP remains a work in progress, in part because it’s being used in many ways. In a 2021 analysis of existing research, Wang and colleagues reviewed 132 studies on the use of PRP for 28 conditions in eight specialties, including musculoskeletal issues, cosmetic uses, and neurology. Overall, 61 percent of the studies supported the use of PRP, though only a third detailed their formulas. Different studies varied in how they measured outcomes, making them hard to compare.
“The practice of it is far outpacing the science,” Wang says. “But our science is good enough to show that there’s some promise with these treatments.”

A mast cell, a type of immune cell, can be activated by allergens, infection, or injury, causing inflammation. In this colorized transmission electron micrograph, the orange oval is the cell’s nucleus.

FOR PEOPLE WILLING to endure extremes, the sort of cold exposure that Costello embraced has become a leading contender, attracting devotees who rave about its ability to ward off pain, anxiety, depression, and more. But scientists are still working on making that direct connection.

While many studies show that cold helps with pain—probably by lowering skin temperature, which reduces how fast nerves can deliver pain messages—Costello says that trying to assess the effects of cold exposure on both acute and chronic inflammation has been a challenge. For instance, scientists in Japan and Germany have found that infusing cold saline can reduce inflammation in rats, but the effects of animal studies are not directly comparable to humans. In one 2013 study of 20 men who ran downhill at a 10 percent grade for 40 minutes, a team of New Hampshire-based researchers tracked a slight reduction in inflammatory molecules among the 10 participants who sat in a 4°C (40°F) ice bath for 20 minutes afterward. Still, those results aren’t statistically significant, and the ice bath made no difference in muscle soreness.

Researchers have also learned that cold therapy may counteract the muscle gains that come with exercise, possibly by interfering with the inflammatory process. In some cases, cold interventions might even increase inflammation, Costello says.
“There’s more evidence coming out on an annual basis,” he says. “But there are still only a handful of research studies that are supporting the effectiveness of cold therapy for reducing the inflammatory response.”

PERHAPS THE MOST SURPRISING recent finding is that heat therapy could be another way to address inflammation and improve health. Regular sauna users have a lower risk of cardiovascular disease, according to research on more than 1,600 men in Finland. And physician-supervised procedures using tools such as targeted lasers, ultrasounds, fluid infusions, or heat chambers to raise body temperature have shown promise for treating depression and cancer.

In a 2021 review of research on repeated sauna and hot tub use, University of Oregon environmental physiologist Chris Minson and colleagues found evidence that heat can suppress pro-inflammatory pathways and enhance anti-inflammatory ones in both animals and people.

Minson recently put a sauna in his backyard. Most days, he spends about half an hour in it, punctuated by a cold shower. His research has convinced him that by adhering to a new regimen against inflammation, he’s making a healthy choice. All evidence aside, he can feel it. “When I take care of my body by doing these kinds of things, I sleep better,” he says. “I’m happier. I feel healthier.” To Minson, that feels like a pain-free step in the right direction.

AS WE GET OLDER, MORE INFLAMMATION DRIVES ACHES AND PAINS. BUT EXPERTS SAY IT DOESN’T HAVE TO, AND SOLUTIONS ARE ON THE WAY.
IT HAPPENS to everyone. With age come achy joints and a rising risk for cancer, heart disease, dementia, arthritis, and other illnesses. Those changes follow an uptick in inflammatory molecules over the course of a lifetime so common it has a scientific name: inflammaging.

Now researchers are racing to unravel how the inflammatory process changes over our lifespan, what instigates the shift, and how it might be possible to interfere with it.

As people age, increasing amounts of pro-inflammatory cytokines and other inflammation-related molecules circulate in the blood. When the shift occurs depends on the person, says Ron DePinho, a cancer biology and aging researcher at the University of Texas MD Anderson Cancer Center in Houston. But 50 is generally when inflammation starts to increase, with a dramatic shift after 60.

The uptick tracks closely with disease trends. Starting at 65, the number of people with Alzheimer’s doubles every five years. In the United States, 80 percent of adults over 65 also have at least one chronic condition. By 85, a third of people may have Alzheimer’s, while a third of men and a quarter of women have had cancer.

ON THE MOST BASIC LEVEL, anti-inflammatory medications and healthy habits like exercise can slow some aspects of the inflammaging process, says DePinho. But to find more targeted solutions, researchers are working to understand the problem better.

A dozen biological changes corresponding with age have been identified so far. All those hallmarks of aging are associated with inflammation, says Ferrucci of the National Institute on Aging. As people age, their immune cells lose their protective functions and stop fighting off invaders, turning into what scientists call senescent cells. Other kinds of cells can also become senescent in response to stress. They cease replicating, stop working, and start secreting powerful inflammatory molecules that cause yet more cells to become senescent.

Meanwhile, DNA damage inside cells accumulates over time, especially at the tips of chromosomes in protective regions called telomeres, which are long stretches of bunched-up DNA. Each time a cell divides, its telomeres become shorter until they reach a critical length that is perceived by the cell as DNA damage or instability, which may spark deterioration.

As telomeres become damaged, they initiate a signaling process through proteins that turn certain genes on and off. Some of those genes support the function of mitochondria (the cell components that produce energy). As a result of the gene disruption, mitochondria become defective and leak their DNA into cells, causing inflammation.

Scientists used to consider telomere shortening, mitochondrial damage, inflammation, and other processes separate theories of aging that could contribute to diseases like cancer, DePinho says. Now it is clear that all these changes are connected and that inflammation acts as a co-conspirator in the aging process.
As chronic inflammation sets in, it becomes harder for the immune system to perform routine tasks such as detecting and eliminating cancer cells and pathogens, which could make diseases more likely. But this burgeoning understanding of inflammaging as a relentless circuit of steps that all exacerbate inflammation is revealing new ways to break the cycle.

DEVELOPING ANTIAGING interventions that target inflammation remains a challenge because they need to be specific enough to avoid causing more harm than good, Ferrucci says. Trying to tackle chronic inflammation with general anti-inflammatory drugs, for example, could make us more susceptible to disease by impairing the inflammation we need to stay healthy.
“When you have an infection, if you don’t have inflammation, you’re going to die,” Ferrucci says. “Shutting down inflammation with a bomb like a corticosteroid or some monoclonal antibodies works. It’s also quite dangerous.”

One of the most promising new strategies for dealing with inflammaging is attacking senescent cells. In mice, a low-dose combination of two substances, dasatinib (a drug) and quercetin (a plant pigment), appears to be particularly effective at getting rid of deadbeat cells in the intestines. Clinical trials are now under way to see if these so-called senolytics work in people.
This is a magnified cross section of a blueberry, which has antioxidant and anti-inflammatory properties that may help brain function.

Scientists are hopeful that they’ll soon understand which interventions will help most. “Tissues retain a remarkable capacity to renew themselves if you remove the underlying instigators of the aging process,” DePinho says.
For now, exercise really is one of the best medicines, enhancing DNA repair and improving mitochondrial function. Studies show it can reduce the risk of serious disease. As little as 15 minutes a day can make a difference, DePinho says.

Dietary choices too can improve inflammaging, according to a raft of international studies that support eating a Mediterranean-style diet with an emphasis on whole grains, fresh produce, nuts, and fish. Consuming a wide variety of vegetables may also support the gut microbiome.

When Ferrucci shops, he buys 10 kinds of vegetables. “That is something that has been suggested in the literature,” he says. “And I think that’s a simple way of following that advice.”

CAN YOU EAT TO COMBAT INFLAMMATION?
The global obesity epidemic has been fueled by a diet that’s high in calories, fat, and sugar, all of which can lead to weight gain and have an inflammatory effect on the immune system. But plenty of cultures eat for longevity instead.

In 2021 researchers from the University of Valencia and the German Institute of Human Nutrition compared several well-known healthy diets—the Nordic, Mediterranean, Washoku, and Jiangnan—to find the most common foods associated with anti-inflammatory effects.

This sample menu includes recommendations from the study, emphasizing unprocessed foods, nuts, fruits, and vegetables for a more filling, healthier meal plan.

•
BREAKFAST
Start with two slices of whole wheat bread with mashed avocado and a fresh fruit salad. Sip on some soy milk.
•
SNACK
Grab a handful of almonds, and pour a glass of pomegranate juice.
•
LUNCH
Mix a green salad with carrots, olives, cucumbers, shallots, sweet potatoes, white beans, tomatoes, and chicken. Add olive oil and a squeeze of lemon.
•
SNACK
Blend together kale, avocado, pineapple, blueberries, and banana to make a smoothie.
•
DINNER
Grill salmon with olive oil, eggplant, artichoke, and rosemary. Serve with brown rice or lentils.

Linking Depression and Inflammation
INFLAMMATION IN THE BODY CAN AFFECT THE BRAIN AND ALTER MOOD, FINDINGS THAT COULD LEAD TO NEW SOLUTIONS FOR HARD-TO-TREAT ISSUES.
SUFFERING FROM a chronic illness can obviously alter your mental health. Not surprisingly, depression affects over 40 percent of cancer and rheumatoid arthritis patients, and nearly 30 percent of those with diabetes, according to the Centers for Disease Control and Prevention. But there is another factor that these and other severe diseases have in common: inflammation.
Scientists now believe that in many cases, inflammation may exacerbate mental health conditions. Their work is leading to new medications and insights for treatment. “All along the pathway of that clinical course of depression, inflammation seems to play at least some sort of role,” says Marx of Deakin University.

For a long time, researchers considered depression to be a simple story of neurotransmitters gone wrong, Marx says. Serotonin and dopamine are two particularly important neurotransmitters, messenger molecules in the brain that help regulate mood, motivation, and emotion. When those molecules got out of whack, the thinking went, mental health problems followed.

In the past few decades, however, multiple lines of evidence have converged to suggest that while neurotransmitters matter, the immune system is linked to mental health, and inflammation can alter mood. As knowledge of the number of molecules involved in the inflammatory process has exploded, so too have studies linking a variety of inflammatory cytokines with major depressive disorder, as well as bipolar disorder and schizophrenia.
Some of the strongest evidence that inflammation can wreak havoc in the brain comes from research on a drug called interferon alpha. An inflammatory cytokine secreted by infected cells, interferon alpha works as a powerful antiviral. Synthetic versions are used to treat hepatitis C, malignant melanomas, and other conditions. But side effects include psychosis and depression: A quarter of people who take interferon alpha for hepatitis C develop major depression.

There could be several ways inflammation might damage mental health. Among them, Marx says, chronic inflammation may impair the production of serotonin and other neurotransmitters, inhibit the creation of new brain cells, or damage brain cells’ ability to form new connections. The hippocampus, responsible for memory, emotional regulation, and mood, seems to take the biggest hit.

ON A GRANULAR LEVEL, specific molecules involved in inflammation are under study, as are ways they might alter brain processes. For example, certain kinds of T cells and cytokines cross the blood-brain barrier and affect microglia, the central nervous system’s resident immune cells. Normally, microglia repair damage and eliminate injured cells, but when stimulated by excessive inflammation, they appear to damage neurons instead, essentially eating up parts required for neuronal functioning, says Eléonore Beurel, a biochemist at the University of Miami Miller School of Medicine. “We are still trying to put the puzzle together,” she says.

To understand how inflammation-related depression develops, some researchers are looking to key risk factors in the earliest stages of life. Scientists have known for decades that trauma in childhood raises the risk for adult depression, the treatment-resistant type in particular. Inflammation could explain the association and might help mitigate it, says Andrea Danese, a child and adolescent psychiatrist at King’s College London.
Danese has found that kids under 10 who experience abuse and neglect show elevated levels of several in¬flammatory molecules by the time they are in their early 30s, putting them at heightened risk for cardiovascular disease, type 2 diabetes, and other physical health conditions.

“Individuals who have a history of childhood maltreatment tend to have more chronic and more persistent types of depression, and they also tend to respond more poorly to conventional treatment,” he says. “Inflammation may be one of the biological reasons for why this happens.”

A colorized, microscopic close-up depicts gut microbes, the health of which is shaped by our dietary choices. Anti-inflammatory foods are key to overall wellness.
 

AS SCIENTISTS DISCOVER more about inflammation’s role in mental health, they hope to find more ways to combat depression. The opportunity appears most promising for the estimated 30 percent of people who don’t respond to standard treatments like antidepressants. This group, studies show, tends to have the most inflammation.

Many mood stabilizers and other mental health drugs already have anti-inflammatory effects. And a wide variety of anti-inflammatory medications also appear to ease depression, according to a 2019 analysis by Chinese scientists of existing research, which included 26 studies that involved more than 1,600 people. Compared with people who took a placebo, the analysis found, those who took anti-inflammatory medications or supplements—including NSAIDs, statins, omega-3 fatty acids, and antibiotics—reported reduced depressive symptoms, especially when they combined the anti-inflammatories with antidepressants.

Working with a doctor to try multiple interventions at once is important, Marx says, because mental health issues are complex. Your risk for depression may be tied to genetics, environmental factors, and life experience—and your mood is also influenced by many processes. Traditional medications aren’t always necessary either; solutions that have worked to curb other kinds of inflammation may have an impact here too.

Mediterranean-style eating in particular has been linked to a reduction in depression symptoms, Marx and his colleagues found in a 2020 review of related research. That may be because the diet’s key ingredients¬—produce, legumes, fish rich in omega-3, raw nuts, and whole grains¬—all have anti-inflammatory properties.

Evidence also supports sufficient sleep, time outside, and meditation as ways to lower inflammation and, in turn, boost mood.

This holistic approach shows promise. “By exercising, by engaging with nature, by eating healthily, we can actually make a pretty substantial difference,” Marx says. “Not only in physical outcomes but also our mental health.”

HAPPY GUT, HAPPY BRAIN?
Science is increasingly finding a relationship between gut health and mental health. In 2017 U.S. researchers discovered that a healthy gut microbiome is extremely important for people suffering from depression and anxiety. Diet is just one component that influences the microbiome, but because our digestive process takes about a day, changing the foods we eat can affect our brain and mental health within 24 hours.

One increasingly popular way of eating—the Mediterranean diet—may cut the risk of depression by a third. This approach focuses on plants, moderate amounts of animal protein, and less saturated fat. It also incorporates fiber, which keeps gut microbiomes in balance.
Nutritionists recommend eating about 30 grams of fiber a day.