Mood-Lifting Drugs of the Future

Last week I tested your patience by playing Mr. Science. This week allow me to introduce you to the real thing—Michael Maes, a flesh-and-blood neuropsychiatrist from Belgium. His method of diagnosing and treating patients with depression may give you and your doctor some innovative options to add to your antidepressant regimen now or down the line.

Maes runs a medical center called Molecular Care for Your Body and Mind Outpatient Clinics. Don’t be put off by its quacky name: Maes has been on the cutting-edge of depression studies for nearly a quarter of a century. His work is cited by many others as science closes in on the true neurochemical causes of this disease (in addition to genetics, lifestyle, and how your mom and dad treated you at age 3).

Maes and just about every other legit expert agrees that Prozac and the dozen or so other antidepressants marketed over the past 20 years work very well for many people. Most were developed to do one thing—raise levels of serotonin in your brain by inhibiting the reuptake of the feel-good chemical by your neurons. (Hence their name: selective serotonin-reuptake inhibitors, or SSRIs.)

Ironically, it was while trying to pinpoint how the drugs performed this task that researchers learned that a lack of serotonin is likely not the only cause of depression, or not the main cause, or possibly not even a cause at all. Few reporters or doctors have caught on to this yet.

Why care about what causes depression? Because progress in treatment and curing disease depends almost entirely on getting closer to understanding the causes. Meanwhile, until new drugs arrive, you may be able to strengthen the effects of antidepressants with other drugs.

Maes believes that depression is an inflammatory disorder caused in large part by an overproduction of so-called pro-inflammatory cytokines, which are key to controlling immune responses, such as the inflammation of rheumatoid arthritis. Explaining how your feelings of hopelessness and helplessness result from these cytokines would only make your eyes glaze over, so suffice it to say that they cause a chemical chain reaction that destroys tryptophan, an essential ingredient in your body’s natural production of serotonin.

It’s long been known that people with type-2 diabetes, heart disease, and other common conditions with an inflammatory component have more cytokines at work in their bodies—and much higher than normal rates of depression.

If you were Maes’s patient, he would treat your depression with an antidepressant, but he might not stop there. He would also diagnose and treat any inflammatory disorder, whether you were conscious of it or not. To do this, he would test for pro-inflammatory cytokines (such as interleukin-1, interleukin-6, and tumor necrosis factor) as well as other markers of inflammation, such as haptoglobin and CRP.

Then he might prescribe Celebrex, a strong anti-inflammatory that inhibits the production of pro-inflammatory cytokines, or the antioxidant curcumin (derived from the spice turmeric, an important ingredient in Indian curry), which takes out the specific enzyme responsible for destroying tryptophan. Other antioxidants with antidepressant capabilities on his shelf include the dietary supplement SAMe and the herb saffron.

If you’re anything like me, the moment anyone compares a heavy-hitting drug like Prozac with something that seems as lightweight as a spice (!), you roll your eyes. But who knows? Google “curcumin” or “saffron,” and you’ll find plenty of scientific experiments and articles investigating their use against depression.

You’ll also notice much excitement about the theory of “neurogenesis”—which posits that growing new brain cells is what heals depression. More about that next week.