Out of the Blue: Six Non-Medication Ways to Relieve Depression (Norton Professional Books) (18 page)

But I don’t want you to think that I recommend this cavalierly. It wasn’t easy for me, not even being depressed, to become active, and it probably won’t be easy for any person who is depressed to get moving. However, I’m convinced that it can be a crucial element in helping your clients recover or at least alleviate their depression.

After reading
The Brain That Changes Itself
, I came across a book called
Spark: The Revolutionary New Science of Exercise and the Brain
by psychiatrist John Ratey (2008). Ratey got on to this topic when one of his new patients said that he had been a runner much of his life, but after a knee injury put an end to his running, he became profoundly depressed. Ratey had heard this story before and, indeed, had noticed that when he himself had stopped running marathons, he’d had to up his dose of attention deficit disorder medicines. He began to investigate the connection between exercise and mood disorders such as depression and anxiety and found that there was a great deal of evidence that depression could be ameliorated by regular aerobic exercise.

After reading Ratey’s
Spark
, I found another book on the subject: Keith Johnsgard’s
Conquering Depression and Anxiety Through Exercise
(2004). Between these three books and other investigations I did subsequently, I discovered many major studies that provide evidence that exercise can be a significant source of help for people who are depressed. I will summarize these ideas below.

While there is scientific evidence behind this last strategy for restarting brain growth, it is very new and not definitive. However, in addition to the evidence, I will describe a new hypothesis explaining how and why may antidepressants work that buttresses the idea that this research may be pointing the way to new understanding and pathways to relief. This new hypothesis will add weight to the evidence and perhaps convince you and your clients that exercise and brain growth can be a powerful pathway to relieving depression. I will spend some time on this evidence, since I know it is a radical departure from contemporary ways of thinking about the causes and cures for depression, and I want you, the therapist, to be convinced enough to encourage your clients to get moving when they’re depressed, which won’t always be an easy sell.

So let’s start with that new hypothesis, since the research will make more sense after you understand what may be going on in the brain with both depression and exercise.

THE NEUROATROPHY/NEUROGENESIS HYPOTHESIS OF DEPRESSION

The quick version of this theory is that the brain is physically affected by stress: Fewer brain cells get made under conditions of stress. And, with chronic stress, the brain can even lose brain cells and function; scars and brain damage have been found in the brains of people who have experienced chronic stress and untreated long-term depression.

Exercise, on the other hand, encourages the growth of new brain cells and can reverse the trend of brain cell death in situation of chronic stress and depression. And exercise can also help forge new connections within the brain. This equals new learning.

Just to create a little suspense, this hypothesis also provides an interpretation of why antidepressants work that is radically different from previous understandings. But we’ll get to that in a little while. First let’s detail the hypothesis and take a look at the evidence.

When I was an undergraduate psychology student, I was taught that the brains of infants and adolescents were changing, developing, and growing, but that growth essentially stopped in the late teen years. After that the brain’s size and function were set. From there we only lost brain cells, a little at a time—or a lot at a time if there was brain trauma and injury or some disease that affected the brain. A high school health instructor went so far as to advise us impressionable students not to ride motorcycles, since the bouncing of the motorcycle on the rough road would kill off a massive number of brain cells that could never be recovered.

In the past several decades, though, this view has been challenged, first by animal experiments that showed that birds who learned new songs grew new brain cells as adults and that the brains of rats who were placed in multicolored, stimuli-rich environments grew bigger. Next came indirect evidence with the development of functional magnetic resonance imaging (fMRI) machines that allowed researchers to see brain activity as it was happening. It was observed that taxi drivers who had memorized the complex labyrinth of London’s streets as adults to become master cabbies had enlarged the parts of their brains that involved visual memories (Keep & Brown, 2007).

Next, dying patients volunteered to allow a dye to be injected into their bloodstreams that bound only to new, dividing cells. In autopsies after their deaths, researchers found that their brains had taken up some of the dye, which meant that new brain cells were being born in adult brains. These were brains of people who were in their fifties, sixties, and seventies, well past infancy and adolescence (Keep & Brown, 2007).

We now know that human brains change all through life, although perhaps a little more slowly as aging occurs, and that new brain cells can be born anytime. This is called neurogenesis.

What kinds of things encourage neurogenesis? For one thing, learning new things that stretch one’s capacities, such as playing music and learning complex musical pieces. Among expert musicians, certain areas of the cortex are up to 5 percent larger than they are in people with little or no musical training, recent research shows. In musicians who started their training in early childhood, the neural bridge that links the brain’s hemispheres, called the corpus callosum, is up to 15 percent larger. A professional musician’s auditory cortex—the part of the brain associated with hearing—contains 130 percent more gray matter than that of nonmusicians (Adams & Janata, 2002).

I mentioned the use of mindfulness meditation earlier as being of help to some with depression. Recent research by Richie Davidson and his colleagues at the University of Wisconsin (Davidson et al., 2003) and Sara Lazar and her colleagues at Harvard University (Hölzel et al., 2010; Lazar et al., 2005) has shown that brain function changes and structural changes happen when people meditate, especially if they develop a long-term habit of meditating. So, not only can brains change by growing new cells, but they can also change when the new brain cells are exposed to new stimuli and the person learns something. Specializing in any motor skill, like skiing, juggling, dancing, and so on, can help grow new brain cells and create new and stronger brain connections.

And so can exercising.

Why exercise? Because strenuous aerobic exercise seems to stimulate the release of certain growth hormones that foster the growth of brain cells directly (usually from the hippocampus, chief among these hormones being brain-derived neurotrophic factor, or BDNF) or that foster the growth of new blood vessels and capillaries to and in the brain (mainly insulin-like growth factor–1, or IGF-1, and vascular endothelial growth factor, or VEGF) (Thakker-Varia et al., 2007).

On the other hand, cortisol, a stress-related hormone, suppresses these growth hormones. Thus, stress, which plays a key role in triggering depression, suppresses neurogenesis in the hippocampus. When the organism is under threat, it doesn’t waste energy growing new brain cells and blood vessels; it hunkers down. Scientists have found evidence that the hippocampus, the source of new brain cells, shrinks in people who have had long-standing depression (Ruso-Neustadt, 2004). This dying off of brain cells and shrinking in parts of the brain or the nervous system is called neuroatrophy.

Because depression is stressful in its own right, even more cortisol is released the longer the depression goes on, which suppresses brain growth further. And, with fewer new brain cells to work with, it becomes more difficult for the depressed person to learn anything new or even take in what information is being offered by treatment personnel, family, or social supporters.

And here is where the new take on antidepressants comes in. The first hypothesis for why antidepressants work had to do with how they alter levels of dopamine, the motivational/reward chemical in the brain; norepinephrine, a hormone/neurotransmitter that helps regulate blood flow, heart rate, attention, and glucose (brain fuel) and suppresses neuroinflammation; and serotonin, a neurotransmitter that regulates and affects mood, appetite, sleep, the gut, blood pressure and clotting, memory, and learning. There was some thought that these chemicals directly caused or alleviated depression.

But the latest thinking is that the main effect these medications have is to help stimulate the growth of new brain cells. That may be why it takes so long for most antidepressants to work to relieve depression. It takes a few weeks to grow new brain cells and then maybe another few weeks for those new brain cells to start functioning fully.

I said earlier in the book that I wasn’t one of those “medication bashers” who think that antidepressants either don’t work (because their main effect is placebo) or that they are a conspiracy by greedy pharmaceutical companies to pathologize our sadness and make us dependent on their magical solutions to life in a pill. It is clear that the placebo effect plays a part in many treatments, but I suspect that antidepressants often do have a positive biological effect beyond that of a placebo. I do think the causes of depression are more complex than merely genetics and biochemistry, as I said in the first chapter, and that exercise has fewer negative side effects and is usually less expensive than medications. But I have seen severely depressed people’s lives saved and changed for the better after they began taking antidepressants.

Why those medications help people may not be because they treat broken brains and misfiring neurotransmitters directly, though. They may work mainly by regulating and encouraging brain cell and blood vessel growth in the brain and the nervous system (Altair, Whitehead, Chen, Wörtwein, & Madsen, 2003). Postmortem studies have shown that depressed patients had decreased hippocampal and cortical BDNF levels, and several studies have shown increased BDNF in people who have been treated with antidepressants for some time (Sen, Duman, & Sanacora, 2008). If an antidepressant is given during a period of chronic stress, it can prevent the decline in neurogenesis that normally occurs (Altair, 1999; Karege, Perret, Bondolfi, Schwald, & Bertschy, 2002).

One thing about depressed people is that they find it hard to sustain positive emotions. It’s not that they never have them; it’s just that they can’t hold on to them. This was demonstrated in a study in which twenty-seven depressed patients and nineteen control participants were presented with visual images intended to evoke either a positive or a negative emotional response (Heller et al., 2009). While viewing these images, participants were instructed to use cognitive strategies to increase, decrease, or maintain their emotional responses to the images by imagining themselves in similar scenarios. Experimenters then used fMRI to measure brain activity in the target areas and examined the extent to which activation to positive pictures was sustained over time in the brain’s reward centers.

The experiment found that depressed patients showed normal levels of sustained activity in the reward centers early on in the experiment. However, toward the end of the experiment, those levels of activity dropped off precipitously. This may be because the brain becomes less effective at creating connections and birthing new brain cells during depression. The scaffolding needed to sustain better feelings is just not there as it is when someone is not depressed.

Another finding that supports this neuroatrophy/neurogenesis hypothesis of depression is that people who have sustained head injuries in early adulthood experience higher rates of depression over their lifetimes (Holsinger et al., 2002).

Perhaps, just as many people have come to believe that medications combined with psychotherapy are more effective for long-lasting effects and prevention of relapse, in the future people will routinely recommend exercise as well as medications and psychotherapy for maximum relief of depression and prevention of relapse.

It doesn’t have to be exercise, of course. Anything that stretches the brain can stimulate neurogenesis and new brain connections. A study done at East Carolina University discovered that playing casual, nonviolent video games (the study used Bejeweled, Peggle, and Bookworm) reduced mild to moderate depressive symptoms in study participants (Russoniello, O’Brien, Zirnov, Fish, & Pougatchev, 2009). The study found that, of the fifty-nine people who participated in the study, the half who spent an average of 40.7 minutes playing the games had a 57-percent reduction in their depression symptoms. There was a 65-percent overall improvement in general mood and anxiety in addition to a reduction in physical symptoms such as tension (49.6 percent), anger (55 percent), confusion (50 percent), and fatigue (58 percent).

Findings from the ACTIVE (Advanced Cognitive Training for Independent and Vital Elderly) study showed that older people who engaged in brain-training exercises on the computer that speeded up their processing speeds were 38 percent less likely than the control group to develop depression, as measured one year out from the study’s end (Wolinsky et al., 2009). The implication is that brain growth can have a preventive effect on depression, especially in the elderly, who are more vulnerable to brain cell loss.

But as I have mentioned, one of the most powerful ways to grow brain cells and stave off or recover from depression seems to be physical exercise. Scientific investigation of this phenomenon has begun only in the past fifteen years, since brain plasticity and the neuroatrophy hypothesis are fairly recent news. One of the most impressive and perhaps surprising studies was a controlled study done by James Blumenthal and his colleagues at Duke University (Blumenthal et al., 2007) that went by the acronym SMILE (Standard Medical Intervention and Long Term Exercise). In this study, 156 adults who had been diagnosed with major depressive disorder were randomly assigned to three different treatment groups: