Prozac is metallic and bitter. To me, it is the taste of betrayal.
At the end of last year, numbed by both the death of my father and birth of my book, I started my days with the antidepressant (that had been prescribed) and ended them with Xanax (that had not). Subsisting on Tazo organic chai and McVities chocolate-covered digestive biscuits, my diet was smothered in irony. I was a writer urging people to save diversity in food through consumption. ”Savor everything,” I implored. “Scrape the pot, lick the spoon, dig your hands into the messy fruit. Twirl it around on your fork, swallow every drop, find the sweet in the bitter. Smell, taste, touch, hear, feel …” Meanwhile, I had dropped to 87 pounds and stopped eating.
I didn’t forget to eat; I just didn’t care.
As I did outreach for the book, Bread, Wine, Chocolate: The Slow Loss of Foods We Love, I told audiences that the changes we were experiencing in food and agriculture would compromise our ability to eat well in the future. Three-fourths of the world’s food now comes from just 12 plants and five animal species, a trend that makes our our food system not only more vulnerable to challenges such as pests, diseases and climate change, but also less interesting and delicious. We eaters could help solve this problem, I explained, by eating more diverse varieties of what we loved. With that, I’d coach people through tastings—tearing bread from its crust, listening to the snap of a well-tempered chocolate, assessing the lacy structure of beer foam.
Savoring is the route to saving biodiversity, I’d say. But, all the while, I starved my own hungers.
Prozac, known under the generic name fluoxetine, was intended to help me care—about food, about life, about anything other than my father’s absence. When the drug kept me from sleeping and dulled every part of me, I reduced the dosage—snapping pills in half, running my tongue over the rough, acrid edges, thinking about how the desire to please our parents never really leaves us. Thinking about how my father never saw the book I had given myself over to.
A few weeks after the Prozac entered my system, my appetite began to return. In an attempt to wean me off tea and cookies, my mother prepared all the Indian foods I loved: mung bean dal, eggplant bhartha, and saag made with mustard greens and spinach.
I ate. Slowly. But after a week of observing my tentative consumption, she proclaimed, “I think the antidepressant is affecting your taste.” I was confused; I was eating. “Yes,” she said. “But you keep talking about the saag having a metallic taste. My recipe hasn’t changed. It’s what I’ve made for you your entire life.”
I was floored. Food was how I navigated my world, and now my sense of taste and experience of flavor had become unrecognizable. If I was a food writer who could no longer trust my own senses—if I couldn’t properly taste something—how could I know it? And if I smelled and tasted things differently, was I still me? What could I trust as mine—and how could others trust me?
I felt betrayed—by my grief, by my father, my book, my mind, and my palate. And by the bitter pill that was recalibrating my life.
Prozac and other Selective Serotonin Reuptake Inhibitors, or SSRIs, are the Toyotas of antidepressants, widely used because they catch multiple types of depression and anxiety in their net. The drugs—available in generic forms, but also sold under brand names including Prozac, Zoloft, Celexa, and Lexapro—work by preventing the body’s reabsorption of serotonin, one of many chemicals that acts as a neurotransmitter (transmitting messages between nerve cells in our brains).
Serotonin helps regulate a range of physical and mental processes, such as those related to our moods, sexual desire, and appetite. By blocking the reabsorption, or reuptake, of serotonin, SSRIs keep the chemical suspended in tiny gaps between our nerve cells known as synapses. Researchers don’t know exactly how this works (which isn’t uncommon with drugs used in mental health), but they suspect the suspension improves messages between the cells and strengthens the circuits that control our mental state.
Through research for my book, I learned flavor is the culmination of our senses, particularly smell and taste—a commingling that, from an evolutionary perspective, is designed to prevent us from ingesting poison.
The largest family of genes in our body is dedicated to decoding smell. Humans are able to distinguish up to one trillion scents, a process that starts with the airborne molecules in scents that waft into our nose and mouth. These molecules trigger smell receptors in the cells of our nostrils and retronasal passage that are caught by a small patch of tissue known as the olfactory epithelium. From there, messages are sent to multiple parts of the brain where the nerve impulses become what we recognize as a scent.
Our sense of taste, by comparison, is significantly less complex. We can differentiate between five basic qualities: sweet, sour, bitter, salty, and umami (savory), plus the presence of fat. This distinction starts in our mouths, through fleshy bumps that dot our tongue, inner cheeks, and the pathway to the upper esophagus that are often (mistakenly) called taste buds. The bumps are actually taste papillae that contain our taste buds. Each taste bud contains up to 50 taste receptors, the sensory cells which are coded to help our brains recognize basic tastes and fat.
“Foods do not contain flavors,” Napa Valley College professor George Vierra explains. “They contain flavor molecules. The flavors of those molecules are created in our brains.” The brain is where everything we’ve taken in through our senses becomes what we know. It’s also the locus of depression—and the place where grief and flavor (or the loss thereof) collide.
A University of Dresden Medical School study of people who had major depression, and those who didn’t, showed people who were not depressed had greater sensitivity to smells than those who were. By exposing volunteers to increasing concentrations of aromas, researchers determined the portion of the brain responsible for initial processing of smell (the olfactory bulb, tucked under our frontal lobe) was, on average, 15 percent smaller in those suffering from depression, regardless of whether or not they were taking antidepressants.
The changes don’t stop there. Psychologist Bettina Pause and her colleagues strapped 32 electrodes across the scalps of 25 depressed study participants and 25 non-depressed participants. Their goal was to observe brain response to various types of stimuli, ranging from the smell of sweet roses to the stench of rotten butter. While depressed volunteers were able to identify odors—just like their non-depressed counterparts—their brains were less responsive to the smells.
This finding echoed previous studies suggesting that, while depressed individuals don’t have a problem identifying odors, depression does seem to diminish the intensity of the experience. When Pause and her colleagues re-examined 15 of the depressed patients after their recovery, they found that once depressive symptoms were alleviated, the patients’ electrical patterning changed and they responded in the same way as the non-depressed group.
A full return of smell and any lifting of depression is, of course, good news. But it isn’t always guaranteed. Because sometimes the cure for depression is what causes the flavor perversion.
If you study the small print on SSRIs, you’ll find, close to the end of the list of side effects, references to taste disturbances, taste loss, and taste perversion. The official term is dysgeusia (related to ageusia, the complete lack of taste, and hypogeusia, a decrease in taste sensitivity). Adrienne Elizabeth Wasserman of the University of Pennsylvania’s School of Nursing explains. “These changes include sweet, sour, salt or bitter taste changes, decreased taste sensations, and metallic tastes.”
While these shifts are well-known within the medical community, unpleasant taste is what researchers S. M. Miller and Graham J. Naylor describe as a “neglected symptom in depression.” They explain, “Altered taste has been reported in depression and anxiety, but there has been little investigation of the chemosensory deficit, which seems surprising given the potential impact on quality of life.”
I can relate.
This loss isn’t limited to what we experience in the mouth—or to SSRIs. Benzodiazepines (including the Xanax that put me to sleep at night) are thought to enhance sweetness, while tricyclic antidepressants impact perceptions of saltiness. Lithium leaves behind a metallic taste; Zolpidem (Ambien), a bitter one. No matter what the taste, SSRIs and other antidepressants have been shown to distort it—or diminish it.
In a study of 45 non-depressive participants given a placebo or one of two types of antidepressants (an SSRI or a NARI—a drug that works on the reuptake of the neurotransmitter norepinephrine instead of serotonin), volunteers were hooked up to an MRI (Magnetic Resonance Imaging) scanner. They were shown pictures of chocolate and moldy strawberries while being fed liquefied chocolate and an “aversive” strawberry drink through a Teflon tube. When asked to rate the experiences, all subjects rated the strawberry picture and accompanying taste as unpleasant and the chocolate stimuli as pleasant. But the group that had been taking the SSRI showed diminished brain response to the sight and taste of chocolate in areas of the brain related to both pleasure and aversion.
This squares with what anyone who has taken an SSRI experiences: pleasure circuits of all types feel numb. The researchers speculate this “emotional blunting” might explain why overeating is also a side effect of SSRI consumption; it’s a way “to compensate for the reward deficit.”
But these changes aren’t limited to brain function. Researchers from the University of Bristol believe a reduction in serotonin or noradrenaline in our brains and bodies might also impact our taste buds and how they respond to different tastes. Their 2006 paper, “Human Taste Thresholds Are Modulated by Serotonin and Noradrenaline,” not only upended common wisdom that our taste preferences are fixed, but showed these changes occur within the taste receptors themselves. “Taste,” the researchers conclude, would “appear to be an interesting sensory measure with respect to mood.”
I got lucky with Prozac, but, as my late father (a psychiatrist—the irony) often told me mental health diagnoses are wildly imprecise. Many people are locked in years of suffering not only because of their symptoms but because of the cures they are subsequently offered. Taste tests might be a way to help practitioners pinpoint exactly which neurotransmitters are compromised in someone suffering from depression. They might facilitate greater precision—and relief—in both diagnoses and care.
While my story is one of loss due to depression, these changes aren’t limited to those experiencing mental illness. I met project engineer Joshua Loomes during a chocolate-making course in Trinidad we’d both enrolled in to better understand the substance we loved. I, for book research; Joshua, for pleasure. (Okay, both of us for pleasure.)
At some point in our weeklong training, Joshua mentioned he had temporarily lost his taste when undergoing radiation treatment for cancer. I asked if we could discuss it further. A few days later, over bland veggie sandwiches, he explained, “Radiation kills all the fast growing cells. That includes the cancer, along with hair follicles, your taste buds and saliva glands, and your stomach lining. It’s why you puke after treatment. It’s also why, when you start radiation, one of the first people they make you see is a nutritionist.” Recovery, he says, is in many ways, about surviving the treatment itself: “Getting enough nutrition when everything tastes awful—or at least different—is a big part of it.”
I asked if he remembered which taste disappeared first. “I wish I could,” he said. “It was probably sweet, as I remember deciding a tray of coconut ice (an Australian Christmas candy) was off and throwing it away.” To his wife’s chagrin, Joshua threw out about half the foods in the fridge before realizing the off-taste was specific to him. For weeks, his sense of taste was in limbo, he explained, “because taste receptors die and recover at different rates. It was a couple of weeks before I lost my taste completely.” Once it was gone, he subsisted on baby formula he fortified with bananas and raw eggs.
A few weeks after our chocolate course ended, Joshua sent me a follow-up message. “I’m not sure whether this experience led to my current love of foods, but it may have contributed,” he wrote. “To lose my taste (permanently) would take away a big part of the pleasure in life. It’s one of the most basic pleasures we have—that does not rely on somebody else doing something. For me, at least having experienced it briefly, it would be a major loss.”
I didn’t know then, as I read that email, that less than a year later I would experience the same thing. That I, too, would lose—and regain. That a return to flavor would be a return to self.
Flavor, writes novelist Judith Fertig, is how some of us make sense of the world. “We knew that there was a flavor that explained you … A flavor whose truth you recognized when you tasted it. A flavor that answered the question you didn’t know you had.”
Simran Sethi is a journalist, educator and author of the book Bread, Wine, Chocolate: The Slow Loss of Foods We Love, chronicling changes in food and agriculture through bread, wine, coffee, chocolate and beer.