Inflammation in the body is associated with many diseases: cancer, heart disease, obesity, autoimmune disorders, diseases of the digestive system, and many others. And if you had any of these diseases, then it is only logical that you feel depressed and possibly suppressed.
But what if depression is not always a logical response to illness or even stress? Edward Bulmore, a professor of psychiatry at the University of Cambridge in the UK, suggests that for some, depression is actually a direct result of inflammation, which helps explain why for some people the typical treatment (medication, talking therapy, even deep brain) stimulation for severe cases of depressive disorder) provides incomplete or fleeting relief. We asked Bulmore about his amazing theory.
It is difficult to overestimate how important and potentially contradictory this theory is. What led you to believe that inflammation and depression are related?
I saw a patient with arthritis in 1989 – arthritis is an inflammation of the joints. She was the first person I had, where it was clear to me that she was both inflamed and depressed. I asked the responsible doctor what he thought. He said: “Depressed? Of course she is. Is not it? "And that was it. Depression was considered a normal emotional reaction to feeling unwell.
Looks like you had a suspicion that the inflammation caused the arthritis and depression separately, and not the inflammation that causes arthritis, leading to depression. How it works?
Inflammation is an established science. After certain diseases, injuries or stress, the body has a natural inflammatory response. But uncontrolled or prolonged inflammation is dangerous. The theory is that immune cells secrete proteins known as cytokines that send an inflammatory signal to the brain. Brain immune cells can produce cytokines themselves, which affect the ability of the brain to use serotonin.
And that is why drugs do not always work.
Yes. If the brain is having problems using serotonin – a chemical that causes a good feeling – antidepressants such as SSRIs that are supposed to increase serotonin levels will not be effective.
It seems to make sense.
Yes, but it is based on new knowledge about the relationship between the immune and nervous systems. In the 1980s, it was believed by medical evidence that the blood-brain barrier protects the brain from inflammatory proteins and immune cells circulating in the blood. Thanks to advances in science and technology, we now know that there are many ways in which inflammatory cellular signals can pass through a barrier.
Does this mean that everyone who is depressed is experiencing some kind of inflammation?
Not. Not everyone who is in inflammation, depressed, and not all who are depressed, in inflammation. We need to move away from the idea that depression is the same for everyone, and there is only one way to treat it. This thinking we are stuck for 40 or 50 years.
How did this affect our understanding of depression?
Well, it certainly influenced the way drugs were developed, and why successful therapeutic innovations stalled.
The drugs worked a little, or people won't continue to use them, right?
It is clear that SSRIs work well on average. The key phrase is "average". What hides the fact that for some people with depression, they work very well. But for others they do not work at all.
How long, until we have new depression drugs that are aimed at inflammation?
I am careful with predictions. The process is long and complicated. There are some clinical trials with people who have arthritis and other inflammatory diseases, and figuring out how levels of fatigue and depression respond to medications aimed at inflammation. For them, we may, in five years, see approved treatment. For a wider group, this will take longer.
What is the ultimate goal?
There should be several approaches to treating depression. There are clear individual differences in how patients respond to treatment. As for inflammation, then, whether it leads to depression in some people, and not in others, may be due to differences in genetic makeup, or possibly due to differences in life experience.
So far, what can we do with this knowledge?
Both patients and physicians should review what “visiting the doctor” looks like. Visiting one physician for mental health and another for physical health, as if these are two completely different things, is a disadvantage for patients dealing with both types of problems. Unfortunately, this is how the system works. The patient must decide whether his physical state and mental state are related.
And if he thinks so?
Look at various things that can lead to inflammation: diet, exercise, and stress. The practice of relieving stress can also have an anti-depressive effect. There is no one way to treat depression, but there are several ways to start.