ONE AFTERNOON IN 1996 a mother and her son arrived in my consulting room for an appointment. The mother looked deeply anxious, the son, Anthony, sat slumped in his chair, silent and looking at the floor.
Anthony had apparently been suffering from severe clinical depression since the age of 14. I could see clearly that he was in a bad way. Now 21, he was a tall, dark-haired young man whose clothes hung loosely on his lean frame, suggesting that he had lost weight. Like many people suffering depression, he found it difficult to make eye contact and spoke hesitantly and quietly.
Depression is a truly disabling disease and, for those who suffer from it, it is a clearly defined condition. Even if the experience of depression sufferers varies in the detail, such as the degree or longevity of their illness, or the precise symptoms they experience, the core feeling of ongoing despair and hopelessness is always the same.
Depression is not just feeling low; depression is to a low mood what flu is to the common cold. Every winter people catch a cold virus, feel rough for a week, and go around telling all their friends that they’ve had flu. But if you have ever experienced real flu, you will know that there is an enormous difference.
The same is true of depression. The trouble with depression is that, if you have never experienced it, it is a very difficult disease to understand. This is true of the relatives and friends of a depressed person, and it is often true also of the medical practitioners faced with a depressed patient.
Anthony and his mother told me that his condition had grown steadily worse over the years, despite different treatments, and that the past two years had been particularly tough for him. Somehow he had continued to go to school and even attended college, but he had found it hard to study or take part in any college activities such as sport or social life. He often spent hours and even days just lying on his bed feeling miserable and low, unable to carry on any semblance of a normal life.
Anthony had several other classic symptoms. His sleep patterns were disrupted. He might go to sleep, but then wake very early in the morning and not be able to get to sleep again. He had lost his appetite and had lost weight, he found it difficult to concentrate and was in danger of dropping out of college and, most crucially, he frequently felt suicidal.
As I listened to this articulate, intelligent young man put forward his arguments for how to kill himself, I felt deeply saddened. I seriously considered whether it might be necessary to admit him to hospital. However, after careful discussion with his mother, she was able to assure me that she would keep a close eye on him and remove all potentially dangerous items that could be used in an attempt to commit suicide.
So how was I to treat him? How could I help a case where all the major textbook treatments for depression had been tried unsuccessfully? In the back of my mind I had an idea – but it hadn’t been tried before on depression, so Anthony would have to agree to be a test case.
The treatment was eicosapentaenoic acid, or EPA, which is a derivative of a naturally occurring essential fatty acid (EFA). The richest source of this omega-3 fatty acid is oily fish, including salmon, tuna (not tinned), mackerel, pilchards and sardines. But what I had in mind was a highly purified form of EPA, which could deliver a higher dose than you would get from eating oily fish.
My belief that EPA might help Anthony was based in part on a large trial of patients with schizophrenia that had recently taken place (prompted by research done more than 25 years ago by Professor David Horrobin). I was one of the doctors running the trial and several of my patients had taken part. Three-quarters of the patients had been given EPA in varying doses, while the others were given a placebo. It was a double-blind trial, meaning that neither the doctor administering the treatment nor the patient receiving it knew who was being given EPA, and who the placebo.
Patients suffering from schizophrenia are often depressed, and one of the most striking things I had noticed in the study was that the symptoms of depression cleared in many of the patients taking EPA. But I had to admit to Anthony and his mother that there were no published studies to date of EPA as a treatment specifically for depression. So Anthony would be the first.
Because EPA is a naturally occurring food substance it has no adverse side-effects. I would give it to Anthony alongside his prescribed antidepressant medication, for although his current treatments were not alleviating his symptoms, it could be dangerous to stop taking the drugs suddenly.
On this basis, Anthony and his mother agreed to go ahead with EPA. I gave him a highly purified form of a particular derivative of EPA, known as ethyl-EPA, and then monitored the results. Anthony also agreed to allow me to run several highly specialised tests, including brain scans, to observe the effects of the EPA.
Nine months later, Anthony and his mother were once again in my consulting room. This time they were both smiling and his mother was declaring that a miracle had taken place.
Anthony was transformed. A confident, self-assured young man, he shook my hand warmly and had no problem looking me in the eye. All the signs of depression had gone. He was eating and sleeping well, and enjoying catching up with his studies and his social life. His suicidal thoughts had completely disappeared and he was excited about his plans for the future.
Anthony and his mother told me that within two to three months of starting the ethyl-EPA all his depressive symptoms had cleared. After seven years of struggle against the tyranny of this unremitting disease, Anthony had at last won back his health and his will to live.
A few days after this visit, I finished analysing Anthony’s brain scans. I compared the brain scan I had taken after the course of EPA with the one taken nine months earlier before treatment began. The results were astonishing.
Because Anthony was already an adult, I would not expect to see any change in the brain structure over a nine-month period. If he had started to develop a brain disease such as dementia, in which he was losing nerve cells and cerebral tissue, then I would expect to see that the two largest brain ventricles, or chambers, had become larger as the brain deteriorated. In fact what I saw was the opposite: Anthony’s brain ventricles had become smaller and parts of his cerebral cortex had become thicker — both changes that pointed to the possibility that regrowth might have taken place in parts of his brain.
It used to be taught as fact in medical schools that the human brain, in an adult, is not capable of further growth. However, recent American research on rats has confirmed that brain cells do regenerate as a result of brain exercise, although we still know little about this process. Anthony’s brain scans led me to believe that EPA can, in some ways, stimulate stem cells in our brains to produce new nerve cells, offering hope for a variety of conditions that adversely affect the brain.
Extracted from The Natural Way to Beat Depression by Dr Basant Puri and Hilary Boyd, to be published by Hodder Mobius on February 2, at £10.99. © Dr. Basant Puri and Hilary Boyd 2004.
To order a copy for £8.79 plus 99p p&p call Times Books First on 0870-160 8080 www.timesonline.co.uk/booksfirstbuy
