<\/p>\n
Traditionally, we have sorted diseases<\/strong> 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\u2019s; 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\u2019s 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: \u201cWe all study the same disease\u201d \u2014 inflammation is involved with everything.<\/p>\n <\/p>\n 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.<\/p>\n <\/p>\n Mainstream media headlines tell us how to \u201cfight\u201d inflammation by eating these<\/em> six fruits and following those<\/em> nine healthy habits. Articles question whether treating inflammation can prevent dementia or reduce depression<\/a>. 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 \u2014 these are a just a few of the suggestions.<\/p>\n <\/p>\n Kernels of truth can be found in much of this advice. There is <\/em>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.<\/p>\n <\/p>\n Inflammation is basically a set of systems that says something\u2019s going wrong.<\/span> <\/p>\n<\/div>\n <\/svelte-scroller-background><\/svelte-scroller-background-container> <\/p>\n Last year, a study published in Nature Aging<\/a> tested people with very different lifestyles \u2014 Indigenous populations in nonindustrialized regions of Bolivia and Malaysia and residents in Italy and Singapore \u2014 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.<\/p>\n <\/p>\n These findings<\/a> suggest that mutable factors \u2014 including inactivity and poor diet, air pollution and other toxins, lack of sleep and stress \u2014 might have an even more significant interaction with chronic inflammation than previously realized.<\/p>\n <\/p>\n It\u2019s quite difficult to tell if any individual has chronic inflammation, however. It\u2019s not true that you can observe inflammation in the faces and \u201cbody movements\u201d 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\u2019t see or feel it. There\u2019s no agreed-upon way to measure what your inflammation levels are and how they\u2019re changing.<\/p>\n <\/p>\n Without that information, it\u2019s 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. \u201cWe tend to think of this chronic low-grade inflammation as a bad thing that we should suppress with drugs,\u201d 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 <\/em>Aging <\/em>paper, told me.<\/p>\n <\/p>\n The problem is that inflammation isn\u2019t a single entity \u2014 a virus or cell we can target with a particular drug or therapy. Instead, it\u2019s the product of an incredibly complex regulatory network that we\u2019re just beginning to understand. As Cohen put it to me: \u201cInflammation is basically a set of systems that says something\u2019s going wrong.\u201d Turning it off without knowing exactly why it\u2019s present, then, risks doing more harm than good. <\/p>\n <\/div>\n 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\u2019re all familiar with is rather straightforward: ice the swelling, take an aspirin. You can see and feel the results almost immediately.<\/p>\n <\/p>\n But if any step in the process doesn\u2019t 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.<\/p>\n <\/p>\n 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\u2019t a way for most people to track those proteins over time to figure out what a healthy or unhealthy state looks like for them.<\/p>\n <\/div>\n Dvorak\u2019s insight didn\u2019t 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 \u201cinflammaging\u201d to describe what they believed might be an underlying cause. Over the course of a person\u2019s 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.<\/p>\n <\/p>\n 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\u2019re 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 \u2014 a genetic predisposition, perhaps \u2014 kick-starts the onset of disease.<\/p>\n <\/p>\n 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\u2019t prove that inflammation caused <\/em>the problems. To do that would require a randomized controlled trial with thousands of participants.<\/p>\n <\/p>\n 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.<\/p>\n <\/p>\n 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<\/em> in fatalities from infections and sepsis, presumably because reducing inflammation also reduced the immune system\u2019s 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.<\/p>\n <\/p>\n The results of the study, published in The New England Journal of Medicine in 2017<\/a>, captured the attention of scientists across disciplines. A commentary on the trial in the journal Circulation Research called the results \u201cgroundbreaking\u201d and \u201ca widely heralded milestone\u201d that implied that treating chronic inflammation could have immediate health benefits.<\/p>\n <\/p>\n The problem was how to separate those possible benefits from the immediate risk \u2014 weakening the body\u2019s ability to fight disease. \u201cThe whole name of the game is picking out people where benefit is going to outweigh the risks,\u201d Peter Libby, one of the physicians who led the Novartis trial, told me.<\/p>\n <\/p>\n 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 \u2014 or even worse than \u2014 the broken pipe itself. In which case, you\u2019re forced to choose between two potentially bad outcomes. Treat the inflammation \u2014 send the crew home \u2014 and let the pipe continue to leak. Or let them stay and try to mitigate the mess that their presence creates.<\/p>\n <\/p>\n \u201cIt\u2019s not simple good or bad, it\u2019s good that comes at a cost,\u201d Kipnis told me, adding: \u201cI think we are all looking for simple answers. There will be answers. They will not be simple.\u201d<\/p>\n <\/p>\n Researchers at Northwestern plan to begin piloting inflammation monitors akin to those used by diabetics to track their glucose levels.<\/span> <\/p>\n<\/div>\n <\/svelte-scroller-background><\/svelte-scroller-background-container> <\/p>\n The widespread use of GLP-1s<\/strong> 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\u2019s 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.<\/p>\n <\/p>\n Daniel Drucker, an endocrinologist at the University of Toronto\u2019s Mount Sinai Hospital, gave me some examples of what patients are experiencing: \u201cThey\u2019re emailing me and calling me and saying: \u2018My arthritis is better. My Crohn\u2019s disease is better. My post-Covid lung fatigue syndrome\u2019s better. My concussion symptoms are better. My endometriosis is gone away. My chronic pain and headaches are gone away.\u2019\u201d<\/p>\n <\/p>\n