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The depression epidemic and why the medical profession is failing patients


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The depression epidemic and why the medical profession is failing patients
In a groundbreaking book, British psychiatrist Edward Bullmore claims that what doctors are taught about depression is wrong. By William Leith


Edward Bullmore, 57, professor of psychiatry at the University of CambridgeRobert Wilson
The Times, April 21 2018, 12:01am
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In 1989, a trainee physician called Edward Bullmore treated a woman in her late fifties. Mrs P had swollen joints in her hands and knees. She had an autoimmune disease. Her own immune system had attacked her, flooding her joints with inflammation. This, in turn, had eaten away at Mrs P’s collagen and bone, noted Bullmore, who was 29, and whose real ambition was to become a psychiatrist.

He asked Mrs P some routine questions about her physical symptoms, and made a correct diagnosis of rheumatoid arthritis. Then he asked her a few questions he wasn’t supposed to ask. How was she feeling? How would she describe her mood? Well, said Mrs P, she was feeling very low – she was tired, listless and losing the will to live. She couldn’t sleep.

At this point, Bullmore made another diagnosis. “She’s depressed,” he told his boss at the hospital.

“Depressed?” said the consultant. “Well, you would be, wouldn’t you?”

Both of these doctors understood that Mrs P had an inflammatory disease. They knew that it had wrecked her joints. They understood the basic process that caused the joints to be wrecked. And they also knew that Mrs P was depressed.

But still, there was something about Mrs P’s symptoms that Bullmore and his boss had missed – something they didn’t see. That’s because they had been trained not to see it. As Bullmore puts it, they had a “blind spot”.

This blind spot was, and still is, part of the medical mindset. What Bullmore and his boss couldn’t see concerns inflammation, and the way it is connected to depression. It might even solve the mystery of why a quarter of the population of the developed world gets depressed. Why do hundreds of millions of people who are safer, better fed and richer than humans have ever been in their entire history suddenly lose the will to live?

——————————

Ed Bullmore is now 57, a professor of psychiatry at the University of Cambridge. Sitting in his office at Addenbrooke’s Hospital, he will, over the course of an afternoon, tell me some extraordinary things. He will say that Mrs P was probably depressed because she was inflamed. He will say that he believes inflammation in the body can cause depression in the mind. This is the subject of his new book, The Inflamed Mind. We sit at his round table, with a life-size plastic model of a brain between us, and by the timeI leave his office, I will see human history in a different light.

“Of course!” That’s what I will keep saying to myself over the next few days. Bullmore says that inflammation causes depression. And stress causes inflammation. And the modern world is full of things that make us stressed. We are the product of ancient genes, many of which were designed to help us survive in the African savannah tens or even hundreds of thousands of years ago. In those days, we weren’t stressed by mortgages or PowerPoint presentations. We were stressed by different things – for instance, when we thought we might be wounded in a fight. That’s because, for most of human history, a wound might easily become infected and kill you. When you’re stressed, your body is flooded with inflammation. It’s getting ready to save your life.

And what happens in the modern world? Mostly, the wound never comes. Instead, the PowerPoint presentation comes. The mortgage comes. And the emails. And the texts. And the beeps and buzzes emanating all day from the phone in your pocket.

Stress, I will think, is chronic. So the body is chronically inflamed. The inflammation gets into the brain. The wound never comes. Sometimes the depression does.

So what do you do? You go to a psychiatrist. Because you think your problem is a mental one. It’s not physical, you think. It’s in the mind. And the mind is different, isn’t it?

——————————

Mrs P – she was inflamed. She was depressed. The consultant had said, “You would be, wouldn’t you?” He thought she was depressed because she was thinking about being inflamed. Her physical problems had made her reflect on the future, which looked bleak. So naturally she was depressed. As the consultant said, you would be, wouldn’t you?

“There is quite a lot under the surface of that remark,” Bullmore tells me. “He said it almost without thinking. It was like an automatic response. But it did mean, frankly, as far as we were concerned, as her physicians, if that’s what we thought was the cause of her depression – that she was reflecting on her arthritis, that she was thinking too much about it – that was equivalent to saying, ‘It’s not our problem.’ ”

If Mrs P was depressed, the doctors felt, it was not a medical problem at all. It was a problem for a psychiatrist to solve.

But what would a psychiatrist do?

——————————



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May/12/2018, 1:01 pm Link to this post  
 
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Re: The depression epidemic and why the medical profession is failing patients


Shortly after Bullmore treated Mrs P, he started training as a psychiatrist at the Maudsley Hospital in south London. By now he was 30. One day, in 1990, he treated a patient, Mr Q. “He wasn’t much older than me,” says Bullmore. “He told me he’d got depression.” To look at “you wouldn’t think he had psychiatric problems”. His condition was not immediately visible. Like Mrs P, his mood was low. He was tired, listless, losing the will to live. Nothing gave him pleasure any more.

The mystery is, why does a quarter of the population of the developed world get depressed?
The young Bullmore diagnosed Mr Q with depression. “When I told him he was depressed, he wasn’t very impressed by that,” says Bullmore. “Because, in effect, he’d told me that himself. I’d just written it down and translated some of his ordinary language into some of this neoclassical gobbledegook that doctors tend to talk. Like, he told me he’d lost pleasure in simple things, and I told him, ‘You’ve got anhedonia.’ He told me he was feeling gloomy, and I told him he had major depressive disorder. Although I was putting it in different words, I wasn’t telling him anything he didn’t already know.”

That’s one thing a psychiatrist would do. Bullmore suggested drugs. That’s another. “He asked me how they worked. I told him all about how they changed the serotonin level in the brain, because there was supposedly a serotonin imbalance the drug could correct. He said, ‘How do you know that about me?’ And it was quite a shock, actually.”

This was the world of psychiatry in 1990, and there are several things that might shock you about it. A man tells a doctor he feels extremely low and has lost the ability to feel pleasure. The doctor tells him he’s suffering from depression and anhedonia. He then prescribes an SSRI drug – a selective serotonin reuptake inhibitor such as Prozac or Seroxat – in order to raise the level of a substance called serotonin in the patient’s brain. But he has no idea whether or not the patient’s levels of serotonin are too low. He’s just guessing.

Also, he has no idea whether or not the drug will work. It works, or seems to work, for some patients. Sometimes it works for a while, and then stops working, at which point some patients respond well to increased doses. Others don’t. Sometimes there are side-effects. SSRIs can make patients gain weight or lose interest in sex. Sometimes the patient might find the side-effects another set of reasons to be depressed.

“I realised,” says Bullmore, “that there was quite a lot we didn’t know about why and how we were using these treatments.”

And now he says another shocking thing. “There still isn’t a good answer to that question. The crucial thing is: anybody prescribing SSRIs to anybody for depression or anxiety – nobody knows that that particular patient has a problem with serotonin in the first place. There is no biomarker.”

In medicine, drugs are usually prescribed to respond to biomarkers. For instance, a doctor might diagnose an inflammatory disease by analysing a blood sample, and then decide to prescribe a steroid to treat the inflammation. It was shocking that, in the world of mental illness in 1990, doctors were prescribing drugs that might or might not work, without responding to a biomarker. It’s even more shocking that they’re still doing it now. Nothing much has changed for almost 30 years.

—————————

I’ve never been depressed, although I’ve suffered from anxiety, a disorder that shares some characteristics with depression. But we all know at least one person who has suffered from depression. At any one time, 10 per cent of us are depressed. Sometimes it creeps up; sometimes it happens suddenly. It happens to more women than men, but more men commit suicide as a result of it. Several studies suggest that it happens to people whose status is low – underlings are more depressed than their bosses. It’s been linked to obesity and diabetes. It happens to people with heart disease more than people without heart disease, all else being equal. There is a genetic component – if members of your immediate family have suffered, you are more likely to suffer. People are always depressed for a reason, or several reasons. But often we can’t say what those reasons are. For a long time, depression has seemed to be one very big mystery.

It’s reasonable to ask what, if anything, depression does for us. Why hasn’t it been selected out of our genome? After all, depressed people live shorter lives, are less likely to prosper and have fewer children. Think of all those lost work days, all that time and money spent on recovery. It knocks billions off the national GDP, says Bullmore, if you want to think of it that way. But think of all the broken relationships. Think of all those people who fall, quite suddenly, to depression. Think of the futures they never get to have.


Edward BullmoreRobert Wilson
According to the writer Andrew Solomon, depression is emotional pain beyond sadness. Sadness such as grief, he writes in his brilliant book The Noonday Demon, is like being attacked by rust, which weakens the structure of your mind. Depression is what happens when the structure collapses. Solomon describes his own depression as a living force trying to take him down. “Its tendrils threatened to pulverise my mind and my courage and my stomach, and crack my bones and desiccate my body. It went on glutting itself on me when there seemed nothing left to feed it.”

Solomon says that depression is what happens when things go catastrophically wrong with the mind. He says it’s the price we pay for being creatures who are able to love. Creatures who love must also be primed for loss. To Solomon, “Depression is the flaw in love.”

And Bullmore says something that most of us, until now, hadn’t thought of. Depression can be a product of both the mind and the body. The mind picks up sensory signals that cause stress, the body becomes inflamed, and the inflammation enters the brain, and this in turn affects the mind. It’s a hall of mirrors. It’s not something a doctor would think of; a doctor treats the body. It’s not something a psychiatrist would think of; a psychiatrist treats the mind. It exists in the blind spot.

——————————

About halfway through our afternoon together, Bullmore leaves the room to make us both a cup of coffee. I pick up the life-size plastic brain, which is sitting upside down in a holder. But the brain slips from my hands and falls into lots of different pieces – the left and right hemispheres, the frontal lobe, the reptilian brain, the limbic system. The bit at the base that controls heartbeat and breathing, the bit in the middle that generates emotion, and the bit at the top that enables us to make decisions. That’s the extent of my knowledge.

For years, using magnetic resonance imaging (MRI), Bullmore studied the brains of living people. He interviewed people, many of whom were depressed, while they sat in brain-scanning machines. He watched what happened in their brains as the depressed people used them in different ways. He took pictures.

A doctor prescribing drugs has no idea if a patient’s serotonin is low. He’s just guessing
Bullmore studied these images here at Addenbrooke’s, at a unit funded by the pharmaceutical giant GlaxoSmithKline. He was trying to see what happened in the brains of depressed people because he wanted to find something that would be a more effective treatment for depression than an SSRI. So, of course, did GlaxoSmithKline (GSK), which poured tens of millions into the project.


---
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May/12/2018, 1:01 pm Link to this post  
 
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Re: The depression epidemic and why the medical profession is failing patients


As the technology got better over the years, Bullmore could see, with increasing clarity, what happened when a depressed person looked at pictures of sad faces. The amygdala and cingulate cortex became overactive. This signal was diminished in the brains of people who took SSRIs, but more in some than others. Maybe, if you looked at thousands of brains this way, and experimented with hundreds of drugs, you could engineer better antidepressants. This is what I’m thinking as I try to put the plastic brain back together. It’s like a three-dimensional jigsaw.

Bullmore comes back with our coffee. Then he tells me about the main issue with MRI brain scanning. “The problem is thatthe smallest thing we can see is about 1 cubic millimetre. And that contains about 100,000 neurons.” In other words, if we wantto know what really happens inside the human brain, we’re going to need to wait until we invent a scanner that’s thousands of times more powerful than the ones we have at the moment. “And that won’t happen in my lifetime,” says Bullmore.

We talk about how the brain works. Each brain has about 100 billion neurons, or brain cells. Every thought you have is the effect of tens of thousands of these brain cells making a connection with each other. The more often you have a thought, the stronger the connections become. That’s how we learn. And how do the neurons connect? Electrical currents pass between them, with the aid of proteins called neurotransmitters. We have around 100 different neurotransmitters. Imagine an orchestra with 100 instruments. Some are more important than others. Serotonin is one neurotransmitter out of this hundred. It’s an important one – it’s the violin. But still, it’s only one instrument.

SSRIs prevent the reuptake of serotonin. So they enable neurons to connect – but only in a way that is specific to serotonin. Imagine listening to an orchestra with a very loud violin. It’s better than nothing, and it might suit some people. Others would get sick of it, or their brains might find a way to block it out, which might make them need to turn up the volume even more. I’m speculating here. But that’s all anybody can do, because we don’t have the equipment to get inside that cubic millimetre. We can’t watch neurotransmitters at work while the brain actually thinks.

Around 2010, all the major pharmaceutical companies realised the same thing, more or less at once: that they wouldn’t be able to create a significantly better antidepressant drug by watching people’s brains at work while they were thinking. Not in our lifetime, anyway.

“A number of us were invited to join a conference call,” says Bullmore. “And we were told this decision had been made, and was going to be effective immediately. It was a big shock. So then I thought, OK, GSK has made a decision. I understand that. It’s a simple case of people looking at the productivity of an area and seeing it doesn’t match the level of investment.”

The pharmaceutical industry had wanted to see how SSRIs worked so they could develop new drugs. But it was a dead end. Bullmore reckons the industry as a whole pulled an annual figure of between £5 and £10 billion from their budgets relating to psychiatry and mood disorders.

“The world wasn’t going to keep giving mental health another chance,” he says. The industry view, he says, was essentially, “It’s got to be different next time.”

So he started thinking about immunology. It was an area rich in discoveries. Until quite recently, people visualised the body’s immune response as a sort of firefight between antigens and antibodies – invaders and defence forces. Inflammation in the form of macrophages, the soldiers of the system, lined up to do battle with the bad guys – the bacteria and viruses. Now people realise it’s a bit more complicated. The bad guys sometimes act like spies, finding ways of disguising themselves as good guys. The good guys send signals to each other all over the body.

If you take blood from people who say they are depressed, it shows a higher level of inflammation
Bullmore knew that GlaxoSmithKline had a nearby immunology lab, in Stevenage. He started studying the immune system. He noticed that a few scientists had been making connections between inflammation and depression. “A growing body of knowledge made it seem plausible,” he says. The problem with studying neurotransmitters was that you couldn’t see them at work. But the elements of the immune system – all those tiny soldiers and spies – are much easier to measure. You can find biomarkers. And scientists had recently been looking at the dark side of the immune system. It’s implicated in lots of diseases – multiple sclerosis, heart disease, Alzheimer’s and several types of cancer. Sometimes the good guys turn on us.

Might there be a causal connection between the immune system and depression? He would study it if GlaxoSmithKline would fund it. The Medical Research Council got involved, and the Wellcome Trust. The Wellcome Trust Consortium for the Neuroimmunology of Mood Disorders and Alzheimer’s Disease was formed. Bullmore is the lead scientist in the study of mood disorders.

Now Bullmore collects data about the connection between inflammation and depression. He combs the work of other scientists and conducts his own experiments. Here’s what he’s found. If you take blood from people who say they are depressed, it shows a higher level of inflammation than samples from people who are not depressed. In Copenhagen, 73,131 people were tested. There was a “dose-response” relationship between people who reported low moods and inflammation. Blood with a higher inflammatory profile came from people with blacker moods. A study of English children found that inflamed nine-year-olds were more likely to become depressed eighteen-year-olds nine years later.

But this is correlation – it does not prove that inflammation actually causes depression. To try to do that, you can look at experiments with rats. When you inject rats with cytokines (proteins that signal inflammation), they display “sickness behaviour” – they become listless and anhedonic. They seem to lose the will to live. They behave exactly like people do when they are depressed. But they are rats. What about humans? Well, a significant percentage of people who have been vaccinated – say, for tuberculosis – say they feel low afterwards. First comes the vaccination, which promotes an inflammatory response. Then comes the low mood. And almost everybody who is treated for hepatitis B with interferon, which floods the body with inflammation, reports feeling depressed afterwards. Around a third of these patients feel depressed for weeks. Very recent work on DNA also shows that many genes common to depressed people “turn out to be genes for immune function”. One of the key genes is olfactomedin 4; the mutation of this gene linked to depression causes a strong inflammatory response to certain types of bacteria when they enter the gut.

Does this bring us closer to solving the mystery of why depression evolved? Might it be a response to the stresses of the modern world? Thousands of years ago, being flooded with inflammation would have saved our lives. Infected members of a tribe might have had better survival rates, and avoided infecting others, by slinking away quietly and being on their own. Not wanting to eat and being unable to sleep might have promoted survival in lean and dangerous environments. A bout of depression might have helped you by forcing you to reflect, so you could make changes in your life. But pre-modern people lived lives of short, sharp bouts of stress, not the chronic stress we deal with in the 21st century. They were not usually overweight or very old (adipose tissue, or fat, promotes inflammation, as does ageing). They did not catch buses and trains, or pay mortgages, or get divorced. They dealt with storms and harvests. It’s conceivable that depression was useful to them in ways that are no longer useful to us. But maybe if we look right into our medical blind spot – the fact that the mind and the body can’t be easily separated – we will begin to get the help we need.

“We could be on the cusp of a revolution,” writes Bullmore. “I might be wrong. But I think it has already begun.”

The Inflamed Mind by Edward Bullmore is published by Short Books on May 3 (£[sign in to see URL])

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