Traditionally, we have sorted diseases into categories, separating contagious from noncontagious illnesses; acute events like strokes from chronic conditions like asthma; diseases of cell proliferation, like cancer, from diseases of cell death, like Alzheimer’s; and those that affect one organ or bodily system from those that impact another. Our medical disciplines reflect this logic, too. But we have lately realized how interconnected the body’s systems really are. More and more, researchers are starting to see things the way that Peter Libby, a professor at Harvard Medical School and a cardiologist at Mass General Brigham, put it to me: “We all study the same disease” — inflammation is involved with everything.

That new understanding has inspired countless researchers to look deeper for links between inflammation and the conditions they study. At the same time, the more connections they find, the more their advances fuel a booming wellness industry that profits by marketing anti-inflammatory products and advice.

Mainstream media headlines tell us how to “fight” inflammation by eating these six fruits and following those nine healthy habits. Articles question whether treating inflammation can prevent dementia or reduce depression. Longevity influencers dive into the ills of chronic inflammation on their podcasts. On platforms like TikTok and Reddit, users eagerly seek and dispense advice on how to eliminate their chronic inflammation by any means necessary: by fasting or humming or taking ice baths or injecting themselves with copper peptides. They urge one another to avoid ultraprocessed foods, plastics, pollution, pesticides, tick bites, loneliness — these are a just a few of the suggestions.

Kernels of truth can be found in much of this advice. There is evidence that, at the population level, the stressors and contaminants of modern life are contributing to chronic inflammation and that these insults accumulate over time, eventually increasing the risk of disorders related to aging like cancer and cardiovascular and neurodegenerative disease.

Last year, a study published in Nature Aging tested people with very different lifestyles — Indigenous populations in nonindustrialized regions of Bolivia and Malaysia and residents in Italy and Singapore — for inflammatory markers thought to increase with age and lead to chronic illness. The markers behaved as expected in the developed countries. But while the Indigenous groups had the same markers at high levels, they remained steady over life spans and did not result in disease.

These findings suggest that mutable factors — including inactivity and poor diet, air pollution and other toxins, lack of sleep and stress — might have an even more significant interaction with chronic inflammation than previously realized.

It’s quite difficult to tell if any individual has chronic inflammation, however. It’s not true that you can observe inflammation in the faces and “body movements” of American children, as Secretary of Health and Human Services Robert F. Kennedy Jr. claimed at a bill-signing event in Texas last year. (The administration often refers nonspecifically to the potential for inflammation to lead to illness.) You can’t see or feel it. There’s no agreed-upon way to measure what your inflammation levels are and how they’re changing.

Without that information, it’s easy to feel perpetually anxious about what inflammation might be doing to you and to see it as a threat you should try to eliminate. “We tend to think of this chronic low-grade inflammation as a bad thing that we should suppress with drugs,” Alan A. Cohen, a professor of environmental health science and researcher on aging at the Mailman School of Public Health at Columbia University and the senior author of the Nature Aging paper, told me.

The problem is that inflammation isn’t a single entity — a virus or cell we can target with a particular drug or therapy. Instead, it’s the product of an incredibly complex regulatory network that we’re just beginning to understand. As Cohen put it to me: “Inflammation is basically a set of systems that says something’s going wrong.” Turning it off without knowing exactly why it’s present, then, risks doing more harm than good.

Once the immune system has destroyed a pathogen or helped heal a wound, the macrophages direct the body to return to a baseline level of functioning. If all goes well, inflammation disappears. Taking steps to reduce the acute inflammatory symptoms we’re all familiar with is rather straightforward: ice the swelling, take an aspirin. You can see and feel the results almost immediately.

But if any step in the process doesn’t work right, some inflammation lingers, though the initial threat appears to be gone. This is low-level, chronic inflammation, and why it sticks around is a big question that researchers are getting closer to answering.

Hundreds of proteins, in different combinations, can be involved in chronic inflammation, which is why it can be so hard to detect. And there isn’t a way for most people to track those proteins over time to figure out what a healthy or unhealthy state looks like for them.

Dvorak’s insight didn’t explain what enabled cancer cells to evade the immune system in the first place. But cancer risk increases sharply with age, as do a range of metabolic, neurological and cardiovascular diseases. In 2000, Claudio Franceschi, a researcher at the Italian National Research Center on Aging, and his colleagues coined the term “inflammaging” to describe what they believed might be an underlying cause. Over the course of a person’s lifetime, they noted, macrophages encounter all sorts of stressors: not just bacteria and viruses but also chemicals, heat, radiation. Even physical activity and food, while necessary for survival, can add strain.

The older we get, the greater the toll of these cumulative impacts on macrophages. These cells gradually become less efficient at removing and repairing the damage, meaning they’re active all the time. Inflammaging appears to be inevitable but not always detrimental. Because healthy centenarians have similarly elevated levels of chronic inflammation to those of their counterparts with age-related illness and disability, the researchers reasoned that inflammaging is most likely a necessary precondition before some second factor — a genetic predisposition, perhaps — kick-starts the onset of disease.

These and other studies were part of the growing body of evidence that emerged in the early 2000s correlating chronic inflammation with both aging and serious health problems. But the studies didn’t prove that inflammation caused the problems. To do that would require a randomized controlled trial with thousands of participants.

That opportunity came in 2011, when the pharmaceutical giant Novartis funded a clinical trial of a new anti-inflammatory drug intended to reduce the risk of complications from atherosclerosis, a buildup of fatty plaques on the inner walls of the arteries that is a serious risk factor for heart disease (another condition that becomes more common with age). Doctors knew that high cholesterol could cause atherosclerosis, but puzzlingly, lots of people who developed the condition had cholesterol levels that were considered healthy. Researchers wondered if inflammation could explain the discrepancy.

Over four years, the trial found that the drug decreased the risk of heart attack or stroke by about 15 percent. This was a notable result, proving that inflammation by itself could cause those events related to atherosclerosis. Surprisingly, the study participants who got the drug also experienced significantly fewer cancer deaths than the participants who were given the placebo. But the cohort receiving the drug also had a small but significant increase in fatalities from infections and sepsis, presumably because reducing inflammation also reduced the immune system’s ability to defend against pathogens. Ultimately, the drug was only approved for limited uses, highlighting the paradox that often makes treating chronic inflammation so difficult: It can be vital and harmful at the same time.

The results of the study, published in The New England Journal of Medicine in 2017, captured the attention of scientists across disciplines. A commentary on the trial in the journal Circulation Research called the results “groundbreaking” and “a widely heralded milestone” that implied that treating chronic inflammation could have immediate health benefits.

The problem was how to separate those possible benefits from the immediate risk — weakening the body’s ability to fight disease. “The whole name of the game is picking out people where benefit is going to outweigh the risks,” Peter Libby, one of the physicians who led the Novartis trial, told me.

Jonathan Kipnis, a neuroscientist and immunologist at Washington University, St. Louis, who studies the impact of inflammation on cognition and neurodegenerative disease, suggests picturing chronic inflammation as a road crew that shows up on your street to fix a broken pipe. As they go about their important repair work, they inevitably create additional problems: noise, dust, traffic snarls. Depending on how long the workers stick around, those new problems may become as troublesome as — or even worse than — the broken pipe itself. In which case, you’re forced to choose between two potentially bad outcomes. Treat the inflammation — send the crew home — and let the pipe continue to leak. Or let them stay and try to mitigate the mess that their presence creates.

“It’s not simple good or bad, it’s good that comes at a cost,” Kipnis told me, adding: “I think we are all looking for simple answers. There will be answers. They will not be simple.”

The widespread use of GLP-1s like Ozempic and Zepbound has upended ideas about what those answers might be and how soon we might have them. These drugs appear to modestly reduce chronic inflammation throughout the body without impeding the immune system’s ability to fight infection. People taking GLP-1s to treat diabetes and spur weight loss have found that some of their chronic conditions seem to get better, too.

Daniel Drucker, an endocrinologist at the University of Toronto’s Mount Sinai Hospital, gave me some examples of what patients are experiencing: “They’re emailing me and calling me and saying: ‘My arthritis is better. My Crohn’s disease is better. My post-Covid lung fatigue syndrome’s better. My concussion symptoms are better. My endometriosis is gone away. My chronic pain and headaches are gone away.’”

At first, researchers chalked up these results to weight loss: Excess fat tissue itself releases chemical messengers that initiate inflammation, so losing fat can reduce it. Earlier this year, though, a large clinical trial showed that the drug Wegovy lowered the risk of death from cardiovascular disease, including heart attack and stroke, by 20 percent — and weight loss accounted for only a third of that reduced risk. GLP-1s have also succeeded in treating metabolic liver disease, diabetic kidney disease and sleep apnea.

It seems that GLP-1s are directly influencing pathways throughout the body that cause inflammation, though how exactly they do so is not fully understood. “We have struggled as a field for more than 20 years to accurately detect where the GLP-1 receptor is,” Drucker says. His lab has shown that the drugs act directly on immune cells in the gut and on some T cells. GLP-1s also appear to interact with neurons in the brain that mediate certain types of bodily inflammation.

Still, scientists are only in the early stages of figuring out how these relationships work. Here’s an example of where our understanding comes up short. Given the successes GLP-1s have shown with other conditions, it seemed plausible to researchers that they might treat Alzheimer’s and Parkinson’s disease, because neural inflammation accompanies both of them. But randomized controlled trials have so far shown that they do not consistently improve symptoms.

GLP-1s aren’t the only drugs already in use that interact in important ways with chronic inflammation. Nucleoside reverse transcriptase inhibitors, or N.R.T.I.s, which prevent H.I.V. from replicating, have been shown to also reduce the risk of Alzheimer’s and macular degeneration by blocking a group of inflammatory proteins from combining at the point at which they can cause disease.

Most major pharmaceutical companies now have drug-development projects based on this concept; one of them, Inflammasome Therapeutics, has two such drugs in clinical trials, one for a type of macular degeneration and another for A.L.S. Jayakrishna Ambati, the company’s co-founder and the director for the Center for Advanced Vision Science at the University of Virginia School of Medicine, says they have shown very promising results. “This is something that could reach patients literally in the next 18 to 24 months,” he told me.

Advances in our ability to measure chronic inflammation in people are accelerating, too. Typically, to detect chronic inflammation, doctors and scientists test for a single protein released by the liver into the bloodstream when there is any immune activation in the body. The test can’t say anything about where the inflammation is or why, and it requires an office visit and a blood draw. Next year, researchers at Northwestern plan to begin piloting inflammation monitors akin to those used by diabetics to track their glucose levels. These devices will measure, in real time, four or five proteins that are involved in inflammation.

Shana Kelley, a professor of chemistry and biomedical engineering at Northwestern University whose lab developed the inflammation-monitoring devices, gave me examples of the sorts of questions their extensive use could help answer: “How does our diet affect levels of inflammation in the body? How does our environment affect us? When does inflammation start in the brain for somebody who’s on a trajectory to end up with neurodegenerative disease? How does inflammation affect cognition and behavior and mental illness?”

Ideally, this wealth of real-time data will enable us one day soon to check our inflammatory proteins as simply as we now do our cholesterol or blood pressure. If they are out of balance, we can adjust our habits or take medication to restore an equilibrium so that they don’t increase our risk of more serious health problems. “It’ll be routine,” says Eric Topol, the founder and director of the Scripps Research Translational Institute, whose book “Super Agers” explores advances in longevity science. “This is all part of the story about prevention, preventing age-related diseases,” he told me. “When your immune system is losing its integrity, that’s when your age-related diseases crop up.”

Miriam Merad, an immunologist and the director of the Lipschultz Precision Immunology Institute at Mount Sinai in New York, thinks that one reason our macrophages are less effective as we get older is because our metabolism changes and deprives them of nutrients. She envisions primary care physicians testing patients’ macrophage levels and prescribing supplements that provide these cells with the additional energy they need to function optimally, offsetting any age-related decline.

In a 2024 paper in Science, she and her colleagues described an experiment that illustrated how this process might unfold: First they demonstrated that aging immune cells could catalyze the growth of lung cancer tumors; then they delayed that process by infusing old mice with immune cells taken from young mice.

Historically, though, drug companies have prioritized investing in treatments over preventive therapies, which are less profitable. Merad told me the anti-inflammatory supplements on the market now are “super under-dosed.” She’s pushing the pharmaceutical industry to pursue more potent medications that can treat chronic inflammation before it becomes cancer.

One impediment is logistical: It’s incredibly difficult to observe what’s happening in the brains of living people. Another obstacle, until recently, was a longstanding belief that the immune systems of the brain and body were separate. Anatomically speaking, there didn’t appear to be any lymph vessels in the brain to allow communication with the immune system.

Then, in 2015, Jonathan Kipnis and his colleagues found a network of tubes hidden in the meninges, the layers of membranes that surround the brain and spinal cord, linking them to the lymph nodes in the neck. The presence of these tubes overturned the assumption that the brain had its own self-contained immune system.

“There’s a lot of cross talk that’s going on between the whole body and the brain,” Beth Stevens, a neuroscientist who directs labs at Boston Children’s Hospital and the Broad Institute of M.I.T. and Harvard, told me. “I think with aging it becomes even more apparent, because when the body’s immune system is starting to become more inflammatory, that can affect the brain and maybe even vice versa.”

A little over a decade ago, Stevens made a discovery that changed what we know about immune-cell activity in the brain. She saw that macrophages exclusive to the central nervous system called microglia do more than clear away waste and damage; they also prune nerve cells that other immune proteins tag for removal during brain development so that synaptic connections are as efficient as possible. This synapse sculpting, which continues throughout our lives, raises the possibility that the immune system — if it malfunctions and trims the wrong cells — could be a driver of neurological disorders like schizophrenia as well as degenerative diseases like Alzheimer’s and Parkinson’s.

Stevens and her colleagues are trying to find ways to detect how the behavior of microglia and other immune cells changes when a healthy brain first begins to decline. That could give them a way to detect those diseases before a person develops symptoms by testing their blood or spinal fluid. “I don’t think it’s so crazy to think we might have that in the next few years,” Stevens says. That would in turn offer more options for developing ways to prevent and treat cognitive decline.

All of this means that it’s quite likely that our ability to measure and track our individual inflammation will initially outstrip our ability to understand what to do about those numbers. As tempting as it may be to experiment with off-label drugs or supplements, the wisest course of action according to most researchers is still a holistic one: Eat a balanced diet, exercise, sleep. The person whose advice you should follow remains your doctor.

But advances in inflammation monitoring will also offer ways for individuals to interact with the scientific process, experimenting with how our behavior and environment affect our inflammation readouts and contributing to the wealth of new data that scientists are gathering. Already, Daniel Drucker told me, hearing the experiences of patients taking GLP-1s is influencing his research: “I listen to everybody, and sometimes I go, ‘Oh, my gosh.’ I go right into the lab and say: ‘We have to start a new project. How does this work?’”

The challenge then will be whether researchers across specialties can put all that information together to create a coherent picture of how chronic inflammation engages with the body’s other systems. “That’s the key,” Stevens says. “It can’t be done in a vacuum. It has to be done together.”

Traditionally, we have sorted diseases into categories, separating contagious from noncontagious illnesses; acute events like strokes from chronic conditions like asthma; diseases of cell proliferation, like cancer, from diseases of cell death, like Alzheimer’s; and those that affect one organ or bodily system from those that impact another. Our medical disciplines reflect this logic, too. But we have lately realized how interconnected the body’s systems really are. More and more, researchers are starting to see things the way that Peter Libby, a professor at Harvard Medical School and a cardiologist at Mass General Brigham, put it to me: “We all study the same disease” — inflammation is involved with everything.

That new understanding has inspired countless researchers to look deeper for links between inflammation and the conditions they study. At the same time, the more connections they find, the more their advances fuel a booming wellness industry that profits by marketing anti-inflammatory products and advice.

Mainstream media headlines tell us how to “fight” inflammation by eating these six fruits and following those nine healthy habits. Articles question whether treating inflammation can prevent dementia or reduce depression. Longevity influencers dive into the ills of chronic inflammation on their podcasts. On platforms like TikTok and Reddit, users eagerly seek and dispense advice on how to eliminate their chronic inflammation by any means necessary: by fasting or humming or taking ice baths or injecting themselves with copper peptides. They urge one another to avoid ultraprocessed foods, plastics, pollution, pesticides, tick bites, loneliness — these are a just a few of the suggestions.

Kernels of truth can be found in much of this advice. There is evidence that, at the population level, the stressors and contaminants of modern life are contributing to chronic inflammation and that these insults accumulate over time, eventually increasing the risk of disorders related to aging like cancer and cardiovascular and neurodegenerative disease.

Last year, a study published in Nature Aging tested people with very different lifestyles — Indigenous populations in nonindustrialized regions of Bolivia and Malaysia and residents in Italy and Singapore — for inflammatory markers thought to increase with age and lead to chronic illness. The markers behaved as expected in the developed countries. But while the Indigenous groups had the same markers at high levels, they remained steady over life spans and did not result in disease.

These findings suggest that mutable factors — including inactivity and poor diet, air pollution and other toxins, lack of sleep and stress — might have an even more significant interaction with chronic inflammation than previously realized.

It’s quite difficult to tell if any individual has chronic inflammation, however. It’s not true that you can observe inflammation in the faces and “body movements” of American children, as Secretary of Health and Human Services Robert F. Kennedy Jr. claimed at a bill-signing event in Texas last year. (The administration often refers nonspecifically to the potential for inflammation to lead to illness.) You can’t see or feel it. There’s no agreed-upon way to measure what your inflammation levels are and how they’re changing.

Without that information, it’s easy to feel perpetually anxious about what inflammation might be doing to you and to see it as a threat you should try to eliminate. “We tend to think of this chronic low-grade inflammation as a bad thing that we should suppress with drugs,” Alan A. Cohen, a professor of environmental health science and researcher on aging at the Mailman School of Public Health at Columbia University and the senior author of the Nature Aging paper, told me.

The problem is that inflammation isn’t a single entity — a virus or cell we can target with a particular drug or therapy. Instead, it’s the product of an incredibly complex regulatory network that we’re just beginning to understand. As Cohen put it to me: “Inflammation is basically a set of systems that says something’s going wrong.” Turning it off without knowing exactly why it’s present, then, risks doing more harm than good.

Once the immune system has destroyed a pathogen or helped heal a wound, the macrophages direct the body to return to a baseline level of functioning. If all goes well, inflammation disappears. Taking steps to reduce the acute inflammatory symptoms we’re all familiar with is rather straightforward: ice the swelling, take an aspirin. You can see and feel the results almost immediately.

But if any step in the process doesn’t work right, some inflammation lingers, though the initial threat appears to be gone. This is low-level, chronic inflammation, and why it sticks around is a big question that researchers are getting closer to answering.

Hundreds of proteins, in different combinations, can be involved in chronic inflammation, which is why it can be so hard to detect. And there isn’t a way for most people to track those proteins over time to figure out what a healthy or unhealthy state looks like for them.

Dvorak’s insight didn’t explain what enabled cancer cells to evade the immune system in the first place. But cancer risk increases sharply with age, as do a range of metabolic, neurological and cardiovascular diseases. In 2000, Claudio Franceschi, a researcher at the Italian National Research Center on Aging, and his colleagues coined the term “inflammaging” to describe what they believed might be an underlying cause. Over the course of a person’s lifetime, they noted, macrophages encounter all sorts of stressors: not just bacteria and viruses but also chemicals, heat, radiation. Even physical activity and food, while necessary for survival, can add strain.

The older we get, the greater the toll of these cumulative impacts on macrophages. These cells gradually become less efficient at removing and repairing the damage, meaning they’re active all the time. Inflammaging appears to be inevitable but not always detrimental. Because healthy centenarians have similarly elevated levels of chronic inflammation to those of their counterparts with age-related illness and disability, the researchers reasoned that inflammaging is most likely a necessary precondition before some second factor — a genetic predisposition, perhaps — kick-starts the onset of disease.

These and other studies were part of the growing body of evidence that emerged in the early 2000s correlating chronic inflammation with both aging and serious health problems. But the studies didn’t prove that inflammation caused the problems. To do that would require a randomized controlled trial with thousands of participants.

That opportunity came in 2011, when the pharmaceutical giant Novartis funded a clinical trial of a new anti-inflammatory drug intended to reduce the risk of complications from atherosclerosis, a buildup of fatty plaques on the inner walls of the arteries that is a serious risk factor for heart disease (another condition that becomes more common with age). Doctors knew that high cholesterol could cause atherosclerosis, but puzzlingly, lots of people who developed the condition had cholesterol levels that were considered healthy. Researchers wondered if inflammation could explain the discrepancy.

Over four years, the trial found that the drug decreased the risk of heart attack or stroke by about 15 percent. This was a notable result, proving that inflammation by itself could cause those events related to atherosclerosis. Surprisingly, the study participants who got the drug also experienced significantly fewer cancer deaths than the participants who were given the placebo. But the cohort receiving the drug also had a small but significant increase in fatalities from infections and sepsis, presumably because reducing inflammation also reduced the immune system’s ability to defend against pathogens. Ultimately, the drug was only approved for limited uses, highlighting the paradox that often makes treating chronic inflammation so difficult: It can be vital and harmful at the same time.

The results of the study, published in The New England Journal of Medicine in 2017, captured the attention of scientists across disciplines. A commentary on the trial in the journal Circulation Research called the results “groundbreaking” and “a widely heralded milestone” that implied that treating chronic inflammation could have immediate health benefits.

The problem was how to separate those possible benefits from the immediate risk — weakening the body’s ability to fight disease. “The whole name of the game is picking out people where benefit is going to outweigh the risks,” Peter Libby, one of the physicians who led the Novartis trial, told me.

Jonathan Kipnis, a neuroscientist and immunologist at Washington University, St. Louis, who studies the impact of inflammation on cognition and neurodegenerative disease, suggests picturing chronic inflammation as a road crew that shows up on your street to fix a broken pipe. As they go about their important repair work, they inevitably create additional problems: noise, dust, traffic snarls. Depending on how long the workers stick around, those new problems may become as troublesome as — or even worse than — the broken pipe itself. In which case, you’re forced to choose between two potentially bad outcomes. Treat the inflammation — send the crew home — and let the pipe continue to leak. Or let them stay and try to mitigate the mess that their presence creates.

“It’s not simple good or bad, it’s good that comes at a cost,” Kipnis told me, adding: “I think we are all looking for simple answers. There will be answers. They will not be simple.”

The widespread use of GLP-1s like Ozempic and Zepbound has upended ideas about what those answers might be and how soon we might have them. These drugs appear to modestly reduce chronic inflammation throughout the body without impeding the immune system’s ability to fight infection. People taking GLP-1s to treat diabetes and spur weight loss have found that some of their chronic conditions seem to get better, too.

Daniel Drucker, an endocrinologist at the University of Toronto’s Mount Sinai Hospital, gave me some examples of what patients are experiencing: “They’re emailing me and calling me and saying: ‘My arthritis is better. My Crohn’s disease is better. My post-Covid lung fatigue syndrome’s better. My concussion symptoms are better. My endometriosis is gone away. My chronic pain and headaches are gone away.’”

At first, researchers chalked up these results to weight loss: Excess fat tissue itself releases chemical messengers that initiate inflammation, so losing fat can reduce it. Earlier this year, though, a large clinical trial showed that the drug Wegovy lowered the risk of death from cardiovascular disease, including heart attack and stroke, by 20 percent — and weight loss accounted for only a third of that reduced risk. GLP-1s have also succeeded in treating metabolic liver disease, diabetic kidney disease and sleep apnea.

It seems that GLP-1s are directly influencing pathways throughout the body that cause inflammation, though how exactly they do so is not fully understood. “We have struggled as a field for more than 20 years to accurately detect where the GLP-1 receptor is,” Drucker says. His lab has shown that the drugs act directly on immune cells in the gut and on some T cells. GLP-1s also appear to interact with neurons in the brain that mediate certain types of bodily inflammation.

Still, scientists are only in the early stages of figuring out how these relationships work. Here’s an example of where our understanding comes up short. Given the successes GLP-1s have shown with other conditions, it seemed plausible to researchers that they might treat Alzheimer’s and Parkinson’s disease, because neural inflammation accompanies both of them. But randomized controlled trials have so far shown that they do not consistently improve symptoms.

GLP-1s aren’t the only drugs already in use that interact in important ways with chronic inflammation. Nucleoside reverse transcriptase inhibitors, or N.R.T.I.s, which prevent H.I.V. from replicating, have been shown to also reduce the risk of Alzheimer’s and macular degeneration by blocking a group of inflammatory proteins from combining at the point at which they can cause disease.

Most major pharmaceutical companies now have drug-development projects based on this concept; one of them, Inflammasome Therapeutics, has two such drugs in clinical trials, one for a type of macular degeneration and another for A.L.S. Jayakrishna Ambati, the company’s co-founder and the director for the Center for Advanced Vision Science at the University of Virginia School of Medicine, says they have shown very promising results. “This is something that could reach patients literally in the next 18 to 24 months,” he told me.

Advances in our ability to measure chronic inflammation in people are accelerating, too. Typically, to detect chronic inflammation, doctors and scientists test for a single protein released by the liver into the bloodstream when there is any immune activation in the body. The test can’t say anything about where the inflammation is or why, and it requires an office visit and a blood draw. Next year, researchers at Northwestern plan to begin piloting inflammation monitors akin to those used by diabetics to track their glucose levels. These devices will measure, in real time, four or five proteins that are involved in inflammation.

Shana Kelley, a professor of chemistry and biomedical engineering at Northwestern University whose lab developed the inflammation-monitoring devices, gave me examples of the sorts of questions their extensive use could help answer: “How does our diet affect levels of inflammation in the body? How does our environment affect us? When does inflammation start in the brain for somebody who’s on a trajectory to end up with neurodegenerative disease? How does inflammation affect cognition and behavior and mental illness?”

Ideally, this wealth of real-time data will enable us one day soon to check our inflammatory proteins as simply as we now do our cholesterol or blood pressure. If they are out of balance, we can adjust our habits or take medication to restore an equilibrium so that they don’t increase our risk of more serious health problems. “It’ll be routine,” says Eric Topol, the founder and director of the Scripps Research Translational Institute, whose book “Super Agers” explores advances in longevity science. “This is all part of the story about prevention, preventing age-related diseases,” he told me. “When your immune system is losing its integrity, that’s when your age-related diseases crop up.”

Miriam Merad, an immunologist and the director of the Lipschultz Precision Immunology Institute at Mount Sinai in New York, thinks that one reason our macrophages are less effective as we get older is because our metabolism changes and deprives them of nutrients. She envisions primary care physicians testing patients’ macrophage levels and prescribing supplements that provide these cells with the additional energy they need to function optimally, offsetting any age-related decline.

In a 2024 paper in Science, she and her colleagues described an experiment that illustrated how this process might unfold: First they demonstrated that aging immune cells could catalyze the growth of lung cancer tumors; then they delayed that process by infusing old mice with immune cells taken from young mice.

Historically, though, drug companies have prioritized investing in treatments over preventive therapies, which are less profitable. Merad told me the anti-inflammatory supplements on the market now are “super under-dosed.” She’s pushing the pharmaceutical industry to pursue more potent medications that can treat chronic inflammation before it becomes cancer.

One impediment is logistical: It’s incredibly difficult to observe what’s happening in the brains of living people. Another obstacle, until recently, was a longstanding belief that the immune systems of the brain and body were separate. Anatomically speaking, there didn’t appear to be any lymph vessels in the brain to allow communication with the immune system.

Then, in 2015, Jonathan Kipnis and his colleagues found a network of tubes hidden in the meninges, the layers of membranes that surround the brain and spinal cord, linking them to the lymph nodes in the neck. The presence of these tubes overturned the assumption that the brain had its own self-contained immune system.

“There’s a lot of cross talk that’s going on between the whole body and the brain,” Beth Stevens, a neuroscientist who directs labs at Boston Children’s Hospital and the Broad Institute of M.I.T. and Harvard, told me. “I think with aging it becomes even more apparent, because when the body’s immune system is starting to become more inflammatory, that can affect the brain and maybe even vice versa.”

A little over a decade ago, Stevens made a discovery that changed what we know about immune-cell activity in the brain. She saw that macrophages exclusive to the central nervous system called microglia do more than clear away waste and damage; they also prune nerve cells that other immune proteins tag for removal during brain development so that synaptic connections are as efficient as possible. This synapse sculpting, which continues throughout our lives, raises the possibility that the immune system — if it malfunctions and trims the wrong cells — could be a driver of neurological disorders like schizophrenia as well as degenerative diseases like Alzheimer’s and Parkinson’s.

Stevens and her colleagues are trying to find ways to detect how the behavior of microglia and other immune cells changes when a healthy brain first begins to decline. That could give them a way to detect those diseases before a person develops symptoms by testing their blood or spinal fluid. “I don’t think it’s so crazy to think we might have that in the next few years,” Stevens says. That would in turn offer more options for developing ways to prevent and treat cognitive decline.

All of this means that it’s quite likely that our ability to measure and track our individual inflammation will initially outstrip our ability to understand what to do about those numbers. As tempting as it may be to experiment with off-label drugs or supplements, the wisest course of action according to most researchers is still a holistic one: Eat a balanced diet, exercise, sleep. The person whose advice you should follow remains your doctor.

But advances in inflammation monitoring will also offer ways for individuals to interact with the scientific process, experimenting with how our behavior and environment affect our inflammation readouts and contributing to the wealth of new data that scientists are gathering. Already, Daniel Drucker told me, hearing the experiences of patients taking GLP-1s is influencing his research: “I listen to everybody, and sometimes I go, ‘Oh, my gosh.’ I go right into the lab and say: ‘We have to start a new project. How does this work?’”

The challenge then will be whether researchers across specialties can put all that information together to create a coherent picture of how chronic inflammation engages with the body’s other systems. “That’s the key,” Stevens says. “It can’t be done in a vacuum. It has to be done together.”