Toward a new theory of depression

Yesterdays’ New York Times Magazine contains a long article by Siddhartha Mukherjee detailing the history of the serotonin theory of depression, and a newly emerging theory about neuron generation. The whole thing is very much worth the read, and opens a number of fascinating questions and possibilities about what it is that causes what writer Andrew Sullvian called the “flaw in love” that is clinical depression.

Rubenfeld Synergy seeks to approach disturbances in people’s lives – physical ailments, mental distress, emotional pain, spiritual deadness – through an integrative approach, addressing all of a person’s parts, but starting especially with the body. The brain, though, is no less a part of the body than all the other parts, and in many ways, one of the most important. (I say “one of” only because of the enormous over-valuing of the brain that has occurred in recent memory, to the detriment of the heart and the spirit.) While it can be argued that antidepressants have been overprescribed, there is no denying that for some people, they have a profound effect. A combination of drugs and talk therapy is consistently shown as the most effective treatment, and I would never dream of telling a Synergy client that they should stop taking their medications in favor of Synergy alone. There are effects that these drugs can have deep inside the brain that are integral to changing some patients’ outlooks dramatically.

But the mechanism for these drugs, it turns out, might be much different from what we thought, and their effectiveness may depend on the type of depression you have.

One patient Mukherjee mentions fell into a deep depression after being diagnosed with a terminal illness. She knew that it was normal for such a thing to make her grieve, but her symptoms were more disturbing than that, and she asked for help. Prozac improved her more out-of-control symptoms – harming herself, not tending to her appearance – but her emotional state did not improve. Mukherjee notes, “Any sane reader of this case would argue that a serotonin imbalance was not the initiating cause of Dorothy’s depression; it was, quite evidently, the diagnosis of a fatal disease. Should we be searching for a chemical cause and cure when the provocation of grief is so apparent?”

It’s a complicated question, and one that has to do with how we tend to look at mood and affect. “We ‘grow sorrowful,’ says the author, “but we rarely describe ourselves as ‘growing joyful.’ Imprinted in our language is an instinct that suggests that happiness is a state, while grief is a process.” Further studies of the mechanisms of antidepressant drugs suggest that they are involved in a process as well: the process building new neurons in the parts of the brain that control memory and emotion.

This is fascinating news to me, as small parts of our training focused on neuroplasticity, or the brain’s capacity to build new neurons and new synaptic connections – to grow and adapt to circumstances. One study showed that vividly imagining practicing scales on a piano, complete with imagining the movements of your hands, was just as effective practice for a musician as actually performing the scales. If this is the case, what techniques might we have available to us that can strengthen the parts of our brains that can help us feel more vital, more alive, less “flawed in love”? If drugs and therapy together are the best solution, what can we learn about helping people with behavior and patterns of thought from studying the mechanisms of these drugs?

Mukherjee finishes the article with some interesting ruminations on all of this: “How much of mood is behavior anyway? Maybe your brain makes you ‘act’ depressed, and then you ‘feel’ depressed. Or you feel depressed in part because your brain is making you act depressed. Thoughts like these quickly transcend psychiatry and move into more unexpected and unsettling realms.” For me, these thoughts are less unsettling than they are encouraging: if behavior and feeling are interlinked in a way that doesn’t have a definitive direction, then we can begin with one and lead to the other. Remember the smile research? What other possibilities might there be for altering our very brains by altering what we do? Rubenfeld Synergists have known this for a long time, but we haven’t known a lot about the brain’s mechanisms for making the new connections we see our clients make. Knowing that antidepressant drugs may be working on creating new connections in the brain and not just on altering levels of serotonin makes this work I do seem more relevant than ever.

Read the full NYT article here.

Published by Kamela Dolinova

Expressive arts adventuress: writing, performing, healing, loving.

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