The reason we haven't heard of it is that this condition acts imperceptibly, usually doesn't raise too many warning signs, and until recently doctors didn't have it on their radar. But we would be surprised if we made a list of all the diseases and conditions that are caused as a consequence of chronic inflammation. For these reasons, in recent years numerous scientists have dedicated themselves to studying this condition and its interrelationships with the main chronic diseases such as diabetes, cancer, depression, Alzheimer's, and obesity, to name a few.
But what do we mean specifically when we talk about chronic inflammation?
In Latin the word inflammatio means “to ignite”, “to make fire”. Our body “inflames,” it “ignites,” it “ignites” as a “response” to aggression. The most common attacks are infections and bacteria. Our body's reaction to this type of attack is quite well known since most of us have at some point suffered an infection or an insect bite. Whatever the case may have been, we have surely experienced some characteristic symptoms of inflammation such as acute pain, swelling, redness, a sensation of “heat” and even loss of functionality in the affected area.
Inflammation of this type acts locally, appears quickly in response to an attack and is extinguished when our body has managed to eradicate the threat and repair the damage.
Since the beginning of time, our body has been exposed to environmental aggression. Since for most of our evolution we did not have access to antibiotics or modern medicines we had to develop our own defense mechanisms. For this reason, our body is already equipped with self-regulated biological processes that act automatically every time we need to repair a wound, cure an infection or fight a bacteria. In these cases, there are specific cells of the immune system that are activated when they detect that our body is being attacked by an external agent (ie viruses, bacteria). From this signal, our body coordinates a synchronized response in which the circulatory and vascular system, our endocrine system and various mediators such as white blood cells (leukocytes), mast cells (which release a chemical called histamine that helps repel action of various pathogens), and macrophages (which release cytokines, a type of pro-inflammatory protein that reinforces the defensive action of the immune system).
So far there are no major problems.
But there is another type of inflammation that is not visible, where the characteristics of acute inflammation are not observed (ie redness, swelling) and where the response of our immune system is not extinguished once the threat has disappeared. When inflammation stops being focused and becomes systemic, our body remains “on” even when it is not being attacked. Under normal conditions, the activation of the immune response and the release of various mediators such as cytokines is beneficial, but when this response remains active and the production of cytokines becomes chronic, they end up causing other problems. And the danger lies in the fact that chronic inflammation continues to do its job and does not become visible until the person suffers an episode. We see an example in people who suddenly suffer a heart attack despite not having previously felt any discomfort or warning signs.
The first to observe the effects of systemic inflammation were precisely cardiologists when they identified the presence of markers associated with chronic inflammation in people with cardiovascular diseases.
But why should we worry?
It turns out that chronic inflammation is a source of oxidative stress. We have already explained how oxidation and the action of free radicals damage our cells (and mitochondria), accelerate the aging process and also how they affect the homeostasis of our brain. And not only that. As we said at the beginning of this section, chronic inflammation is capturing the attention of many researchers since it is present in a set of very common diseases such as cancer, depression, diabetes and Alzheimer's, to name a few.
Take for example the relationship between chronic inflammation and obesity.
In obese people, an “abnormal” increase in systemic concentrations of cytokines is usually observed, especially the types TNF-α (Tumor necrosis factor-alpha), IL-6 (Interleukin-6), and CRP (C-reactive protein). . In these cases, overactivation of the immune system occurs in response to the accumulation of fat, especially adiposity in the abdominal areas. In obese people, excess fat ends up being deposited in areas that were not designed for that purpose. Immune cells mistake fat deposits for intruders or aggressors that must be attacked. The excessive release of cytokines ultimately alters the balance of other chemicals and some hormones that regulate appetite, such as leptin, which regulates the feeling of satiety. This is the beginning of a vicious circle, since when inflammation becomes permanent, obese people end up developing resistance to leptin. From that moment on, the body cannot feel satiated even shortly after eating food. It is known that obese people have a greater predisposition to suffer cardiovascular attacks. As expected, overweight people usually have markers associated with inflammation at levels higher than “normal” values and the amount of cytokines in their body usually doubles and triples the levels observed in people without overweight.
One of the markers used to measure the degree of systemic inflammation are the levels of the protein CRP (C-reactive protein), which is produced in the liver as part of the immune response. This blood test uses a variation that is expressed in hs-CRP (high sensitive C-Reactive protein). Low levels of hs-CRP are essential to prevent the appearance of cardiovascular events and the development of Alzheimer's disease. High levels (>3.0) of hs-CRP triple our risk of suffering from coronary and cardiovascular diseases (ie arteriosclerosis) independently of other risk factors.
Let's take yet another example, in this case the relationship between chronic inflammation and depression. For some researchers, it is no coincidence that the characteristic symptoms of depression such as lack of motivation, fatigue and mental lethargy are the same symptoms that a person has when they are “sick.” If sick people and depressed people “feel” and “behave” similarly, there should be some common denominator between them. Apparently this common denominator would be chronic inflammation and the excessive release of cytokines when they are not necessary. Various scientific studies have attempted to validate this relationship and what they found was that there are greater amounts of cytokines during depressive episodes, and vice versa during remissions. In other similar studies where bacteria were injected into healthy people to induce depressive states, it was observed that the immune response and the release of cytokines coincided with the activation of brain areas associated with depression. These findings are reinforced by cases observed in people with rheumatoid arthritis and multiple sclerosis where depression is very common. In cancer patients who are administered “interferon alfa” it is also observed that depression is a fairly common side effect. Speculation is that depression appears due to the pro-inflammatory effects of interferon.
Chronic inflammation is also an underlying characteristic in people with high levels of stress and the reason why prolonged stress inexorably leads to depression. As a result of these findings, many professionals have introduced the use of anti-inflammatory herbs and nutrients such as curcumin and omega 3 essential fatty acids (EPA/DHA) as part of the pharmacological arsenal to treat depression.
The best way to control chronic inflammation and avoid its negative effects is by eliminating the causes that give rise to it. The latter are strongly rooted in our habits and lifestyle, our diet, and our exposure to environmental toxins, so there are many things we can do about.
What does inflammation in the body have to do with the risk of developing Alzheimer's disease, suffering a heart attack or succumbing to colon cancer?
More than you think. As scientists delve deeper into the root causes of these and other diseases, they are beginning to see links to an immune defense mechanism called inflammation - the same biological process that turns the tissue around a wound red and causes swelling in an injured toe. If they are right - and the evidence is starting to become very strong - they could radically change doctors' understanding of what makes us sick. It could also be a boon for pharmaceutical companies looking for new ways to keep us healthy.
Most of the time, inflammation is a lifeline that allows our body to defend itself against various diseases caused by bacteria, viruses and parasites. (Yes, even in the modern world, we are constantly bombarded by pathogens.) The instant any of these potentially deadly microbes slip into the body, inflammation mounts a defensive attack that ravages the invaders and any tissue there. could be affected. Then, just as quickly, the process slows and healing begins.
From time to time, however, all that vehement production doesn't close at the right time. Sometimes the problem is a genetic predisposition, other times actions such as smoking or high blood pressure keep the process going. In either case, the inflammation becomes chronic rather than transient. When that happens, the body turns on itself - like a stubborn child who can't resist touching a wound - with consequences that seem to underlie a wide variety of diseases.
Suddenly, inflammation has become one of the hottest areas of medical research. Not a week goes by without the publication of another study that discovers a new form of chronic inflammation that damages the body. It destabilizes cholesterol deposits in the coronary arteries, leading to heart attacks and potentially even strokes.
Nerve cells are lost in the brains of Alzheimer's victims. It can even encourage the proliferation of abnormal cells and facilitate their transformation into cancer.
In other words, chronic inflammation may be the driving force behind many of the most feared diseases of middle and older age.
This concept is very interesting because it suggests a new and possibly much simpler way to protect yourself from disease. Instead of different treatments for, say, heart disease, Alzheimer's and colon cancer, reducing inflammation could be a single remedy, preventing all three. Chronic inflammation also fascinates scientists because it indicates that our body can, from an evolutionary perspective, become a victim of its own success. "We have evolved as a species because of our ability to fight off microbial invaders," says Dr. Peter Libby, chief of cardiovascular medicine at Brigham and Women's Hospital in Boston. "The strategies that our body uses for survival were important at a time when there were no plants to purify water, when we also did not have sewage systems to protect us."
But now that we're living longer, those inflammatory strategies are more likely to slip out of our control. To make matters worse, it appears that many of the attributes of a Western lifestyle - such as a diet high in sugars and saturated fats, accompanied by little or no exercise - also make it easier for the body to become inflamed.
The new view of inflammation is changing the way some scientists do medical research. "Virtually all of our R&D effort is focusing on inflammation and cancer," says Dr. Robert Tepper, president of research and development at Millennium Pharmaceuticals in Cambridge, Massachusetts.
In medical schools in the US, cardiologists, rheumatologists, oncologists, allergists and neurologists are communicating with each other - and are discovering that they are looking at the same thing. The speed with which researchers are jumping on the inflammation bandwagon is impressive. Just a few years ago, "no one was interested in these things," says Dr. Paul Ridker, a cardiologist at Brigham and Women's Hospital who has done some of the pioneering work in the area. "Now the entire field of inflammation research is about to explode."
Meanwhile, another group of sentinels, called macrophages, begin an immediate counterattack and release more chemicals, called cytokines, signaling more reinforcements. Soon, wave after wave of immune cells flood the site, there is destruction of pathogens and damaged tissues alike - there is no removal of the wounded from the battlefield in this war. (No wonder the ancient Romans compared inflammation to being under fire.) Doctors call this generalized response to virtually any type of attack...innate immunity. Even bodies of animals as primitive as starfish defend themselves in this way.
But higher organisms have also developed a more precision-guided defense system that helps direct and intensify the innate response and creates specialized antibodies, tailored to target certain types of bacteria or viruses. This so-called evolutionary immunity is what allows pharmaceutical companies to develop vaccines against diseases such as smallpox and the flu. Working together, innate and evolutionary immune defenses fight pitched battles until all invading germs are wiped out. In a final burst of activity, a final wave of cytokines is released, the inflammatory process recedes, and healing begins.
The problems begin when, for one reason or another, the inflammatory process persists and becomes chronic, the final effects are varied and depend greatly on which part of the body the uncontrollable reaction takes over.
Among the first to recognize the broader implications were heart doctors who realized that inflammation appears to play a key role in cardiovascular disease.
Is your heart at risk?
Not long ago, most doctors thought of heart attacks primarily as a plumbing problem.
Over the years, fatty deposits gradually build up inside the main coronary arteries until they become so large that they cut off the blood supply to a vital part of the heart. A complex molecule called LDL, the "bad" cholesterol, is always the raw material for these deposits.
It was evident that anyone with high levels of LDL was at greater risk of developing heart disease.
There is only one problem with this explanation: sometimes it is completely wrong. In fact, half of all heart attacks occur in people with normal cholesterol levels. Not only that, with improved imaging techniques, doctors discovered, much to their surprise, that the most dangerous platelets were not necessarily large. Something that had not yet been identified was causing the deposits to burst, causing large clots that cut off the coronary blood supply.
In the 1990s, Ridker became convinced that some kind of inflammatory reaction was responsible for the breakdown of platelets, and he set about trying to prove it. To test his hunch, Ridker needed a simple blood test that could serve as a marker for chronic inflammation. It settled on C-reactive protein (CRP), a molecule produced by the liver in response to an inflammatory signal. During an acute illness, such as a severe bacterial infection, C-reactive protein levels quickly skyrocket from less than 10 mg/L to 1,000 mg/L or more. But Ridker was more interested in the low levels of CRP - less than 10 mg/L - found in healthy people and which indicate only a slightly elevated level of inflammation. In fact, the difference between normal and elevated is so small that it must be measured using a specially designed high-sensitivity PCR test.
In 1997, Ridker and his colleagues at Brigham and Women's showed that healthy middle-aged men with the highest levels of CRP were three times more likely to suffer a heart attack in the next six years than those with the highest levels of CRP. lower CRP levels. Finally, experts determined that inflammation that has a CRP reading of 3.0 mg/L or more can triple the risk of heart disease. The danger seems even greater in women than in men.
In contrast, people with very low levels of C-reactive protein, less than 0.5 mg/L, rarely have heart attacks.
Doctors still don't know for sure how inflammation can cause platelet rupture. But they have a theory. As the level of LDL cholesterol in the blood rises, they speculate, some leak into the walls of the coronary arteries and stay there. Macrophages, alerted to the presence of something that doesn't belong to them, move in and try to clean up the cholesterol. If, for whatever reason, the cytokine signals gradually increase, the inflammatory process will begin instead of going down, the platelet becomes unstable.
"It's not about replacing cholesterol as a risk factor," Ridker says. "Cholesterol deposits, high blood pressure, smoking - contribute to the development of underlying plaques. What inflammation does is contribute to the propensity for plaques to rupture and cause a heart attack If there is only inflammation, but no disease "At this point, cardiologists are still not willing to recommend that the general population be screened for inflammation levels. But there is growing consensus that CRP should be measured in those at moderately elevated risk of developing cardiovascular disease. At the very least, a high CRP level could tip the balance in favor of more aggressive therapy with treatments - such as aspirin and statins - that are already known to work.
A new vision of Diabetes
Before Dr. Frederick Banting and his colleagues at the University of Toronto isolated insulin in the 1920s, doctors treated diabetes with high doses of salicylates, a group of compounds similar to aspirin. (They were desperate and were also treated with morphine and heroin) Indeed, salicylate reduces sugar levels, but at a high price: side effects include constant ringing in the ears, headaches and dizziness. Today, diabetes treatments are much safer and, in general, work by replacing insulin has increased its production or helped the body make more efficient use of the hormone. But researchers in recent years have re-studied the salicylate approach for new clues about how diabetes develops.
What we have discovered is a complex interaction between inflammation, insulin and fat - whether in the diet or in large folds under the skin. (In fact, fat cells behave much like immune cells, expelling inflammatory cytokines, especially as weight is gained.) How does inflammation fit into this scenario – whether as a cause or a effect - not yet clear. But the case for it occupying a central role is getting stronger. Dr. Steve Shoelson, a senior researcher at the Joslin Diabetes Center in Boston, has generated a strain of mice whose fat cells are inflammation factories. The mice become less efficient in using insulin and develop diabetes. "We can reproduce the entire syndrome, just by inciting inflammation," Shoelson says.
This suggests that timely intervention in the inflammatory process can reverse some of the effects of diabetes. Some of the medications already used to treat the disorder, such as metformin, may work because they also impair the inflammatory response. Additionally, preliminary research suggests that high levels of CRP may indicate an increased risk of diabetes. But it's too early to say whether lowering CRP levels can actually keep diabetes at bay.
Cancer: The wound that never heals
Back in 1860, renowned pathologist Rudolf Virchow speculated that cancerous tumors arise at the site of chronic inflammation. A century later, oncologists paid more attention to the role that different genetic mutations play in promoting abnormal growths that eventually become malignant. Researchers are now exploring the possibility that mutation and inflammation mutually reinforce processes that, if left unchecked, can transform normal cells into life-threatening tumors.
How can this happen?
One of the most powerful weapons produced by macrophages and other inflammatory cells are the so-called oxygen free radicals.
These highly reactive molecules destroy almost anything that crosses their path - particularly DNA. An indirect hit that damages but does not destroy a cell could lead to a genetic mutation that allows it to continue growing and dividing.
The abnormal growth is not yet a tumor, says Lisa Coussens, a cancer biologist at the Comprehensive Cancer Center at the University of California, San Francisco. But to the immune system, it looks a lot like a wound that needs to be fixed. "When immune cells are called, they bring growth factors and a lot of proteins that will call on other inflammatory cells," Coussens explains. "Those things come and they're going to heal, heal, heal." But instead of healing, what they do is 'feed, increase, provide.'
Sometimes the reason for the initial inflammatory cycle is obvious - as with chronic heartburn, which continually bathes the lining of the esophagus with stomach acid, predisposing a person to esophageal cancer. Other times, it's less clear. Scientists are exploring the role of an enzyme called cyclo-oxygenase 2 (COX-2) in the development of colon cancer. COX-2 is another protein produced by the body during inflammation.
In recent years, researchers have shown that people who take daily doses of aspirin - which is known to block COX2 - are less likely to develop pre-cancerous tumors called polyps. The problem with aspirin, however, is that it can also cause internal bleeding. Then, in 2000, researchers showed that Celebrex, another COX-2 inhibitor less likely than aspirin to cause bleeding, also reduced the number of polyps in the large intestine. Therefore, should Celebrex be taken to prevent colon cancer? It's still too early to say. It is evident that COX-2 is one of the factors in colon cancer. "But I don't think it's the only answer," says Ray DuBois, director of cancer prevention at the Vanderbilt-Ingram Cancer Center in Nashville, Tennessee. "There are a lot of other components that need to be explored."
Aspirin for Alzheimer's disease?
When doctors treating Alzheimer's patients took a closer look at what appeared to be succumbing to the disease, they discovered a tantalizing clue: those who were already taking anti-inflammatory medications for arthritis or heart disease tend to to develop the disorder later than those who were not taking anti-inflammatories.
Perhaps the immune system mistakenly saw the characteristic neurofibrillary plaques and tangles that accumulate in the brains of Alzheimer's patients as damaged tissue that needed to be cleaned out. If so, the inflammatory reaction that followed was doing more harm than good. Blockade with anti-inflammatories can limit, or at least delay, any damage to cognitive functions.
The most likely culprits this time are glial cells, whose function is to nourish and communicate with neurons.
Researchers have discovered that glial cells can also act much like mast cells in the skin, producing inflammatory cytokines that call other immune cells into action. "Glial cells are trying to return the brain to a normal state," explains Linda Van Eldik, a neurobiologist at Northwestern University's Feinberg School of Medicine in Chicago. "But for some reason, in neurodegenerative diseases like Alzheimer's, the process seems to be out of control. You're looking at chronic glial activation, which leads to an inflammatory state."
It seems that some people are more sensitive to plaques and tangles than others. Maybe they have a genetic predisposition. Or perhaps a long-standing bacterial infection, such as gingivitis or gum disease, that maintains internal activity and tips the balance toward chronic inflammation.
Preliminary research suggests that low-dose aspirin and fish oil capsules - two of which are known to reduce inflammatory cytokines - appear to reduce a person's risk for Alzheimer's disease. Unfortunately, most of these preventive measures must be started long before neurological problems develop. "What we've learned with dementia is that it's very hard to get better for those of us who already have it," says Dr. Ernst Schaefer, professor of medicine and nutrition at Tuft's Friedman School of Nutrition in Boston. "But at least it will be possible to stabilize people and prevent the disease."
When our body attacks itself.
The doctors who have the most experience treating chronic inflammation are those who specialize in rheumatoid arthritis, multiple sclerosis, lupus, and other autoimmune diseases.
For decades, these diseases have provided the clearest example of a body at war with itself. But the spark that fuels your internal destruction doesn't come from excess cholesterol deposits or a persistent bacterial infection. Instead, in a strange twist of fate, the super-sophisticated organism misguides its immune defenses and directs an inflammatory attack against healthy cells in places like joints, nerves and connective tissue.
In recent years, powerful drugs like Remicade and Enbrel, which specifically target inflammatory cytokines, have worked wonders against rheumatoid arthritis and other autoimmune disorders. But as often happens in medicine, drugs have also created some problems. Patients taking REMICADE, for example, are slightly more likely to develop tuberculosis, since the same inflammatory cytokines that attack their joints also protect them against tuberculosis.
Inflammation can be more of a problem in the early stages of autoimmune diseases like multiple sclerosis. So much tissue is eventually destroyed that nerve damage becomes permanent. "The initial goal is to keep the immune response under control, but then you have to ask how damaged tissue regenerates," says Dr. Stephen Reingold, vice president of research programs at the National Multiple Sclerosis Society. The solution could take decades.
Asthma without allergies?
One of the most intriguing questions in immunology today is why not everyone suffers from asthma. After all, the air we breathe is full of germs, viruses, and other irritants.
Since half of the 17 million Americans with asthma are hypersensitive to common substances like cat dander or pollen, it stands to reason that allergic reactions trigger chronic inflammation in their bodies. However, people who develop asthma as adults - one of the fastest-growing segments of the population - often do not have allergies. Doctors still don't know what is driving his illness, but signs of inflammation are present in his lungs.
Many asthma treatments are designed to control inflammation, although they do not yet cure the disease. "It may mean that the inflammatory hypothesis is not entirely correct or the medications we use to treat inflammation are not fully potent," says Dr. Stephen Wasserman, an allergist at the University of California, San Diego. "There are a lot of gaps to fill" Everywhere, in turn, doctors are finding evidence that inflammation plays a bigger role in chronic diseases than previously thought. But that doesn't necessarily mean they know what to do about it. "We're in a dilemma right now," says Dr. Gailen Marshall, an immunologist at the University of Texas Medical School in Houston.
"We're moving forward with the idea of awareness. But I can't really recommend specific treatments yet." That may change soon. Researchers are looking beyond aspirin and other multi-use medications toward experimental drugs that block inflammation more precisely. Any day now, Genentech is awaiting a decision from the FDA on its colon cancer drug, Avastin, which targets one of the growth factors released by the body as inflammation gives way to healing. .
Millennium Pharmaceuticals is testing a different type of drug, called Velcade, which has already been approved for the treatment of multiple myeloma, lung cancer and other malignancies. But there is a sense that much more basic research into the nature of inflammation needs to be done before scientists better understand how to limit the damage of chronic diseases.
In the meantime, there are things we can all do to curb our inflammatory fires. Some of the advice may sound awfully familiar, but we have new reasons to keep going. Losing weight induces fat cells – remember them? - to produce fewer cytokines. The same goes for regular exercise, 30 minutes a day most days of the week. Flossing fights gum disease, another source of chronic inflammation. Fruits, vegetables and fish are full of substances that deactivate free radicals.
So if you want to stop the inflammation, get off the couch, put your head in the green, and try not to stub a toe along the way.
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