The BookBrowse Review

Published January 22, 2020

ISSN: 1930-0018

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The Inflamed Mind
The Inflamed Mind
A Radical New Approach to Depression
by Edward Bullmore

Paperback (31 Dec 2019), 256 pages.
Publisher: Picador
ISBN-13: 9781250318169

Worldwide, depression will be the single biggest cause of disability in the next twenty years. But treatment for it has not changed much in the last three decades. In the world of psychiatry, time has apparently stood still...until now with Edward Bullmore's The Inflamed Mind: A Radical New Approach to Depression.

In this game-changing book, University of Cambridge professor of psychiatry Edward Bullmore reveals the breakthrough new science on the link between depression and inflammation of the body and brain. He explains how and why we now know that mental disorders can have their root cause in the immune system, and outlines a future revolution in which treatments could be specifically targeted to break the vicious cycles of stress, inflammation, and depression.

The Inflamed Mind goes far beyond the clinic and the lab, representing a whole new way of looking at how mind, brain, and body all work together in a sometimes misguided effort to help us survive in a hostile world. It offers insights into how we could start getting to grips with depression and other mental disorders much more effectively in the future.

A Sunday Times (London) Top Ten Bestseller.



We all know depression. It touches every family on the planet. Yet we understand surprisingly little about it.

This dawned on me in an acutely embarrassing way one day in my first few years of training as a psychiatrist, when I was interviewing a man in the outpatient clinic at the Maudsley Hospital in London. In response to my textbook-drilled questioning, he told me that his mood was low, he wasn’t finding any pleasure in life, he was waking up in the small hours and unable to get back to sleep, he wasn’t eating well and had lost a bit of weight, he was guilty about the past and pessimistic about the future. “I think you’re depressed,” I told him. “I already know that,” the patient told me, patiently. “That’s why I asked my GP to refer me to this clinic. What I want to know is why am I depressed and what can you do about it?”

I tried to explain about anti-depressant drugs, like selective serotonin reuptake inhibitors, or SSRIs, and how they worked. I found myself burbling about serotonin and the idea that depression was caused by a lack of it. Imbalance was the word I had heard more experienced psychiatrists deploy with aplomb on these occasions. “Your symptoms are probably caused by an imbalance of serotonin in your brain and the SSRIs will restore the balance to normal,” I said, waving my hands around to show how an imbalanced thing could be rebalanced, how his wonky mood would be restored to equilibrium. “How do you know that?” he asked. I started to repeat all the stuff I had just learnt from the textbooks about the serotonin theory of depression, before he interrupted: “No, I mean how do you know that about me? How do you know that the level of serotonin is imbalanced in my brain?” The truth is that I didn’t.

That was about 25 years ago, and we still don’t have confident or consistent answers to these and many other questions about where depression comes from or what to do about it. Is depression all in the mind? Is my depression “just” the way I am thinking about things? But then why is it so often treated with drugs that work on nerve cells? Is it “really” all in the brain? To our friends and family who are depressed, we may not know what to say. If we are depressed ourselves, we may feel ashamed to say so.

The silence around depression and other mental health disorders is less deafening now than it was. We are getting better at talking about it, which is good, even if we don’t always agree with each other. We can see that depression is very common, it can be really disabling in many ways and it can reduce both the quality of life – depressed people have less experience of pleasure – and the quantity of life – depressed people have reduced life expectancy. We’re not surprised to read that the economic costs of depression and related disorders are so vast that if we could completely cure depression in the UK from the start of the next financial year it would be roughly equivalent to adding 4% to GDP, or tripling the projected annual growth rate of the whole economy from 2% to 6%. If the country somehow became totally un-depressed, we’d boost our national wealth massively.

But despite our growing awareness of how commonly depressive episodes and disorders crop up among people we know, and the massive scale of the public health challenge that depression represents globally, we still have only limited ways of dealing with it. There are some widely available and moderately effective treatments out there; but there have been no breakthrough advances in the last 30 years. What we had for depression in 1990 – serotonin-tweaking drugs, like Prozac, and psychotherapy – is pretty much still all that we’ve got therapeutically. And that’s evidently not good enough: otherwise depression wouldn’t be on track to become the biggest single cause of disability in the world by 2030.

Full Excerpt

Excerpted from The Inflamed Mind by Edward Bullmore. Copyright © 2018 by Edward Bullmore. Excerpted by permission of Picador. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.

Neuroscientist and physician Edward Bullmore outlines the relationship between inflammation, stress and depression, defying outdated notions that the mind and body are distinct systems.

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It is common knowledge that depression diminishes the quality of sufferers' lives, but few people realize its full collective impact. Depression is one of the most significant global health issues today, predicted to be the single most common cause of disability in the world by 2030. It also impacts economic growth; for example, it is estimated that depression reduces Britain's annual gross domestic product by 4% annually. In The Inflamed Mind: A Radical New Approach to Depression, Edward Bullmore declares it shocking that the medical establishment's approach to this condition has not changed since the 1990s, considering the pressing social and personal ramifications. The standard regimen of serotonin-changing drugs and psychotherapy remain the only therapeutic avenues available, despite clear signs that these treatments are not universally effective.

Bullmore was drawn to the threshold between body and mind - what is now called immune-psychiatry or neuro-immunology - in 1989 when he was training to become a physician. He consulted with a patient named Mrs. P who had rheumatoid arthritis, a chronic inflammatory joint disease. Veering from the script of questions doctors are told to ask patients about rheumatoid arthritis, Bullmore inquired about her mood, and Mrs. P reported the classic symptoms of depression, such as lowered energy, reduced pleasure, disrupted sleep, pessimism and guilt. Bullmore was eager to share his diagnosis with the senior physician on staff, hoping to more fully treat Mrs. P and improve her quality of life. However, the attending doctor was unimpressed: "Depressed? Well, you would be, wouldn't you?" Mrs. P is a recurring character throughout the book, a reminder of what immunodeficiency looks like and how it is regarded in the medical community. Patients like Mrs. P have been trapped in what Bullmore calls "medical apartheid," the divide between the treatment of the mind and body. The prevailing point of view in the medical field is that if Mrs. P was depressed because she was ill, it was her responsibility to work through the problem on her own by worrying less about her rheumatoid arthritis. Bullmore wonders: What if Mrs. P was not depressed because she was mentally fixated on her pain, but because of a more tangible and direct correlation between these two conditions? In other words, what if Mrs. P's depression was caused by her body instead of her mind?

To make this argument, Bullmore defies conventional medical wisdom, analyzing the philosophical foundations of modern medicine, most prominently René Descartes' mind-body dualism, which suggests that the mind and body are two separate and unrelated systems (this theory is known as Cartesianism, from Descartes' Latinized name, Cartesius). Bullmore explains the gravity of the Cartesian blind spot, suggesting that medical practitioners are positioned and trained to think that if something is caused by the mind, it is a problem of the mind, so it should be cured in the mind. This has created harsh barriers in the medical field that are detrimental to patients' health.

To prove this theory, Bullmore responds to two primary questions: 1. How exactly do inflammatory changes in the immune system modify the brain to make people depressed, and 2. What initially inflames a patient, and how does the immune system - which is designed to help people avoid disease - cause depression? To answer these questions, he compiles the results of surveys, case studies and labs. One key revelation from this research is that scientists have identified the first biomarker in psychiatry: cytokines. A biomarker is a measurable substance that, when present in certain ranges, indicates that something - whether it is disease, infection or exposure - is present in the body. This means that just as doctors can determine vitamin D deficiency through simple blood tests, they can also determine the likelihood and severity of inflammation-caused depression by looking at the number of cytokines present.

While most mass-market publications in the realm of psychology provide some sort of call to action, The Inflamed Mind lacks potential solutions for individuals. In fact, Bullmore clearly identifies the flaws of the slow-moving, conservative pharmaceutical industry, and walks readers through the disappointing reality of what would happen if you were to ask your doctor to consider the ideas presented in this book. Thus, the book ends in a quagmire: Here is all of this information that can positively affect the way depression, schizophrenia and Alzheimer's are treated, but these findings may never be put into practice. Readers like Mrs. P who have issues with inflammation and mental health may remain unempowered by the medical field, especially since no clear steps are detailed to promote these findings. It is implied that all readers can do is wait and see what happens.

One way that Bullmore could have incorporated patient autonomy is by analyzing branches of medicine that focus on a holistic, well-rounded treatment philosophy. This book analyzes Western medicine only, which is inextricably linked to Cartesian thought. Eastern medicine, and homeopathic and alternative approaches to healing are a sampling of practices that more thoroughly combine body and mind in treatment strategies. In 2012, Harvard researchers found that in the prior year, there was a 15% growth rate in the use of homeopathic remedies as a supplement to conventional Western medicine in the United States (though only 2% of Americans reported using homeopathic remedies). In countries such as Germany and Italy, 10-15% of patients supplement Western medicine with these methods. As a trend, people are opting for health and well-being practitioners who approach the mind and the body together, so a discussion on future areas of research that involve these types of treatments would have been an interesting counterpoint.

In light of the contradictions to Western medical ideology and funding cuts to mental health, Bullmore is hopeful but measured about the potential results of his findings, admitting that this connection between the immune system, stress and mind may not ever seep into standard medical practice. Still, he concludes with an optimistic image of what the future might look like if these revolutionary developments are embraced: new treatments, new medications, new biomarkers, new therapies, new doctors, less stigma, less guesswork and fewer blinders.

Reviewed by Jamie Chornoby

Publishers Weekly
[A] targeted, readable primer... [and] a well-informed and cogently argued brief for funding and more investigation in the field.

Kirkus Reviews
Impressive and valuable... aimed at the general public, [The Inflamed Mind is] highly readable, and more than a little provocative.

Author Blurb John H. Krystal, M.D., Robert L. McNeil, Jr., professor of translational research; Chair, department of psychiatry, Yale University School of Medicine
The Inflamed Mind confronts the reader with the converging revolutions in neuroscience and immunology that give rise to a new perspective about depression and its treatment...In an erudite, enjoyable, and accessible way, Professor Bullmore conveys the profound impact of this new perspective by helping us to appreciate the links between traditional 'medical' and 'psychiatric' syndromes and it identifies new anti-inflammatory treatments that may cross the boundary from general medicine to psychiatry.

Author Blurb Jeremy Vine, BBC
Suddenly an expert who wants to stop and question everything we thought we knew…This is a lesson in the workings of the brain far too important to ignore.

Author Blurb Steven E. Hyman, Harvard University
Ed Bullmore provides a clearly written and compelling argument for the importance of the immune system and inflammation in depression. This lively book explains a major frontier in clinical neuroscience that is not only influencing research on depression, but also on schizophrenia and Alzheimer's disease.

Author Blurb Sir Robert Lechler, president of the Medical Sciences
As one of the first people to brand themselves as animmunopsychiatrist, Professor Bullmore has led us out of the dark ages and shone the light on the crucial link between systemic inflammation and mental illness. This set of insights is creating a paradigm shift in psychiatry which heralds a new field of personalized psychiatry in the same way that we are seeing personalized therapy in cancer.

Author Blurb Tom Insel, MD, cofounder and president of Mindstrong Health
An important book, a hopeful book, for anyone who wants to think about depression in a new way.

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How the Cure for Tuberculosis Led to the Development of Anti-Depressants

Black and white photo of nurses at a library cart at Seaview TB hospital in Staten IslandSometimes inventions are derived by chance. In The Inflamed Mind: A Radical New Approach to Depression, Edward Bullmore notes that the first antibiotic treatment of tuberculosis (TB) led to the creation of the world's most widely used antidepressant drug: Prozac.

Tuberculosis is an infectious bacterial disease that most severely affects the lungs. Globally, just over a million people die from TB per year. While this is a substantial number of fatalities, it is a fraction of the number that died before the advent of the Bacille Calmette-Guerin vaccine. In fact, at the start of the 20th century, it was the leading cause of death in the United States, known as the "white plague." To develop an antibiotic that could treat infected people, pharmaceutical companies sought a molecule that would target and kill the root cause, a germ known as Mycobacterium tuberculosis, without causing fatality.

This process started in test tubes. Which substances could kill the bacteria? Hydrazine - a stockpiled chemical used as fuel in World War II - surfaced as the answer. That one chemical compound was broken down into hundreds of new molecules that were tested on mice that had been infected with TB. One molecule - iproniazid - halted bacterial reproduction of the germ and prolonged the lifespan of the mice. A clinical trial was established to test whether or not iproniazid could cure human patients. The clinical trial took place at Seaview Hospital, a sanatorium in the New York City borough of Staten Island devoted exclusively to TB patients. It served as an isolated facility to quarantine the infected population. Since its opening in 1913, many people viewed the facility as a death sentence, a place where those with TB wasted away. However, the 1952 clinical trial of iproniazid demonstrated that it effectively halted the progression of the disease. For the first time, patients left Seaview Hospital alive. Moreover, patients receiving the treatment became more energized, active, sociable, and hungry.

It was clear that iproniazid had massive positive effects on patients with TB. However, some scientists were intrigued by the euphoria that coincided with use. Some wrote it off as a placebo effect, and noted that the study was neither blind nor controlled. However, reports about dancing in the ward led some to think that there might be unexpected benefits to the medication. Nathan Kline was one such doctor, referring to iproniazid as a "psychic energizer." Mental health treatment at this time was largely confined to Freudian thought and psychoanalysis, so the notion that a medication could have psychological benefits was fringe.

In 1957, 24 depressed, TB-free patients were given iproniazid in a five-week clinical trial. (Though many of these patients would be classified as schizophrenic by today's standards.) The researchers reported that 18 of those patients experienced improvements in their mood and social behavior. The study was flawed; there were no experimental controls or mechanisms to minimize placebo effect. The sample size was minute. The results were far from generalizable. However, despite these limitations, the drug dispersed into wider use for depression. Within one year, a shocking 400,000 depressed people were effectively treated with iproniazid. Kline collaborated with the pharmaceutical company that produced the iproniazid - Roche - to license the drug for the treatment of depression. Within a decade, around ten other anti-depressants were on the market, treating over four million people.

Although these medications offered relief to patients with depression, there was no understanding of the mechanisms - the hows and the whys - behind their results. In fact, they defied prevailing logic that mental problems should have mental cures (such as Freudian analysis). A contemporary of Freud's, Santiago Ramón y Cajal, now known as the founder of neuroscience, believed that nerve cells are distinct, individual entities that allow for communication in the gaps between one another. This idea was confirmed with the invention of the electron microscope. Scientists reflected on how, specifically, iproniazid functions in the brain to create anti-depressant effects, realizing that perhaps the answer was its ability to enhance the signaling across the gaps between nerve cells.

In 1965, Joseph Schildkraut examined the implications of these findings and proposed that anti-depressant drugs worked by boosting the effects of adrenaline and noradrenaline in the brain. Believing that Schildkraut was only partially right, scientists at pharmaceutical company Eli Lily explored serotonin in their research as an anti-depressant target. They tested for molecules that increase serotonin transmission by limiting its absorption into the brain. This was the first clinical trial of an SSRI (selective serotonin reuptake inhibitor), but it was a failure; patients reported no change in their symptoms.

Eventually, a more effective molecule was pushed through a clinical trial, and it was remarkably successful relative to the placebo. In 1987, it was licensed as Prozac, the pioneer in a class of SSRI drugs. Prozac continues to be the most widely used anti-depressant, prescribed to 54 million people worldwide. A growing number of doctors believe that serotonin imbalance is only one of many potential causes for depression, so treatments targeting SSRIs will not help every depressed person. In The Inflamed Mind, Edward Bullmore explores cutting-edge research that suggests inflammation may be one of the other mitigating factors.

Nurses at Seaview Hospital, courtesy of silive

Filed under Medical, Science and Tech

By Jamie Chornoby

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