In what year did the first drug to treat depression come out and what was it called
Post-Prozac Nation
Few medicines, in the history of pharmaceuticals, have been greeted with as much crowing every bit a greenish-and-white pill containing 20 milligrams of fluoxetine hydrochloride — the chemical we know as Prozac. In her 1994 volume "Prozac Nation," Elizabeth Wurtzel wrote of a nearly transcendental experience on the drug. Before she began treatment with antidepressants, she was living in "a reckoner plan of total negativity . . . an absence of affect, absenteeism of feeling, absence of response, absence of interest." She floated from one "suicidal reverie" to the next. Nevertheless, merely a few weeks subsequently starting Prozac, her life was transformed. "One morning I woke up and really did want to live. . . . It was as if the miasma of depression had lifted off me, in the aforementioned way that the fog in San Francisco rises as the day wears on. Was it the Prozac? No doubt."
Like Wurtzel, millions of Americans embraced antidepressants. In 1988, a year after the Food and Drug Administration approved Prozac, two,469,000 prescriptions for it were dispensed in America. By 2002, that number had risen to 33,320,000. By 2008, antidepressants were the 3rd-most-mutual prescription drug taken in America.
Fast forward to 2012 and the same antidepressants that inspired such enthusiasm take become the new villains of modern psychopharmacology — overhyped, overprescribed chemicals, symptomatic of a pill-happy civilization searching for quick fixes for complex mental problems. In "The Emperor's New Drugs," the psychologist Irving Kirsch asserted that antidepressants work no amend than sugar pills and that the clinical effectiveness of the drugs is, largely, a myth. If the lodestone book of the 1990s was Peter Kramer's near-ecstatic testimonial, "Listening to Prozac," and then the volume of the 2000s is David Healy's "Let Them Eat Prozac: The Unhealthy Relationship Betwixt the Pharmaceutical Manufacture and Depression."
In fact, the very theory for how these drugs work has been chosen into question. Nerve cells — neurons — talk to one another through chemical signals called neurotransmitters, which come in a variety of forms, similar serotonin, dopamine and norepinephrine. For decades, a central theory in psychiatry has been that antidepressants worked past raising serotonin levels in the brain. In depressed brains, the serotonin signal had somehow been "weakened" considering of a chemical imbalance in neurotransmitters. Prozac and Paxil were thought to increase serotonin levels, thereby strengthening the signals between nerve cells — equally if a megaphone had been inserted in the middle.
But this theory has been widely criticized. In The New York Review of Books, Marcia Angell, a one-time editor of The New England Journal of Medicine, wrote: "Later on decades of trying to prove [the chemical-imbalance theory], researchers have still come up empty-handed." Jonathan Rottenberg, writing in Psychology Today, skewered the idea thus: "As a scientific venture, the theory that depression serotonin causes low appears to be on the verge of plummet. This is as information technology should be; the nature of scientific discipline is ultimately to exist self-correcting. Ideas must yield before evidence."
Is the "serotonin hypothesis" of low really dead? Accept we spent nearly 40 years heading downwardly i path only to find ourselves no closer to answering the question how and why we get depressed? Must we at present starting time from scratch and find a new theory for depression?
Science may be self-correcting, but occasionally information technology overcorrects — discarding theories that instead demand to be rejuvenated. The latest research suggests that serotonin is, in fact, central to the functioning of mood, although its mechanism of activity is vastly more subtle and more than magnificent than we always imagined. Prozac, Paxil and Zoloft may never turn out to be the "wonder drugs" that were in one case advertised. Only they accept drastically improved our agreement of what depression is and how to treat information technology.
Our modern conception of the link between depression and chemicals in the brain was sparked quite by blow in the middle of the terminal century. In the fall of 1951, doctors treating tubercular patients at Sea View Hospital on Staten Island with a new drug —iproniazid — observed sudden transformations in their patients' moods and behaviors. The wards — typically glum and silent, with moribund, lethargic patients — were "vivid terminal week with the happy faces of men and women," a journalist wrote. Patients laughed and joked in the dining hall, as if a night veil of grief had lifted. Free energy flooded dorsum and appetites returned. Many, sick for months, demanded five eggs for breakfast and and then consumed them with gusto. When Life mag sent a lensman to the hospital to investigate, the patients could no longer be found lying numbly in their beds: they were playing cards or dancing in the corridors.
If the men and women at Ocean View were experiencing an awakening, then a few hundred miles due south, others at Knuckles'due south hospital encountered its reverse. In 1954, a 28-year-erstwhile woman was prescribed Raudixin to command her blood pressure. A few months later, she returned to the hospital, complaining of crying spells, dullness and lethargy. She felt futile, guilty and hopeless, she told her doctors. A few months later on, when she returned, the sense of futility had turned into hostility. A 42-year-old woman prescribed Raudixin told her md that "God would cause her to go insane" before she could apologize. The "feeling blueish," equally another patient described it, persisted until the drug was discontinued. At another hospital, ane patient treated with Raudixin attempted suicide. Several people had to exist admitted to psychiatric wards and administered electroconvulsive therapy before the symptoms were alleviated.
Psychiatrists and pharmacologists were quick to notation these baroque case reports. How, they wondered, could unproblematic, seemingly unrelated chemicals like Raudixin or iproniazid produce such profound and opposite furnishings on mood? It was around this aforementioned time that scientists were learning that the encephalon itself was immersed in a soup of chemicals. In the early function of the century, scientists wondered how nervus cells talked to ane some other. By the late 1960s, evidence suggested that signals between neurons were carried by several chemicals, including the neurotransmitter serotonin. Might iproniazid and Raudixin have contradistinct the levels of some neurotransmitters in the brain, thereby changing brain signaling and affecting mood? Strikingly and so, scientists found. Raudixin — the "feeling bluish" drug — drastically lowered the concentration of serotonin and closely related neurotransmitters in the brain. Conversely, drugs known to increase euphoria, like iproniazid, increased those levels.
These early on findings led psychiatrists to suggest a radical new hypothesis about the crusade and treatment of depression. Depression, they argued, was a consequence of a "chemic imbalance" of neurotransmitters in the brain. In the normal brain, serotonin shuttled betwixt mood-maintaining neurons, signaling their advisable function. In the depressed brain, this signal had somehow gone wrong. The writer Andrew Solomon one time evocatively described depression as a "flaw in love" — and certainly, the doctors using Raudixin at Duke had seen that flaw emerge grimly in real time: flaws in cocky-dear (guilt, shame, suicidal thoughts), honey for others (blame, aggression, accusation), even the extinction of a desire for dearest (sluggishness, withdrawal, dullness). But these were merely the outer symptoms of a deeper failure of neurotransmitters. The "flaw in love" was a flaw in chemicals.
Powerful vindication for this theory came from the discovery of new medicines that specifically elevated serotonin concentrations. The first such drug, Zimelidine, was created by a Swedish researcher, Arvid Carlsson. Following Carlsson'south atomic number 82, pharmaceutical chemists threw their efforts and finances into finding serotonin-enhancing drugs, and the new giants of the antidepressant earth were born in rapid succession. Prozac was created in 1974. Paxil appeared in 1975, Zoloft in 1977 (the trade names were introduced years later).
In 2003, in Boston, I began treating a 53-year-old woman with advanced pancreatic cancer. Dorothy had no medical bug until she adult an ominous sign known to every cancer specialist: painless jaundice, the sudden yellowing of peel without any associated pinch of discomfort. Painless jaundice tin take many causes, only the i that oncologists know best, and fear virtually, is pancreatic cancer.
In Dorothy's case, the mass in the pancreas turned out to be large and fist-shaped, with malignant extensions that reached backward to grip blood vessels, and a solitary metastasis in the liver. Surgical removal was impossible, chemotherapy the but option.
The suddenness of the diagnosis struck her like an intravenous anaesthetic, instantly numbing everything. As we started chemotherapy in the hospital, she spent her mornings in bed sleeping or staring out of the window at the river beneath. Most disturbing, I watched equally she lapsed into cocky-neglect. Her previously well-kept hair grew into a matted whorl. The clothes that she had worn to the hospital remained unchanged. At that place were fifty-fifty more troubling signs: tiny abrasions in the skin that were continuously picked at, nutrient left untouched past the bedside table and a gradual withdrawal of middle contact. I morning, I walked into what seemed like a daily emotional flare-up: someone had moved a pillow on the bed, Dorothy had been unable to slumber and information technology was somehow her son's mistake.
This grief, of class, was fully provoked past the somberness of her diagnosis — to not grieve would have been baroque in these circumstances — but she recognized something troubling in her own reaction and begged for help. I contacted a psychiatrist. With her consent, we prescribed Prozac.
Epitome 
In the first weeks, nosotros waited watchfully, and nothing happened. But when I saw her again in the dispensary after a month and a one-half, there were noticeable changes. Her hair was clean and styled. Her cuts had disappeared, and her skin looked good. Yet she however felt deplorable across measure out, she said. She spent her days mostly in bed. The drug certainly affected many of the symptoms of low, even so had not contradistinct the subjective "feeling" of it. It healed the flaws in her skin but not all the flaws in love.
Any sane reader of this example would argue that a serotonin imbalance was not the initiating cause of Dorothy's depression; information technology was, quite evidently, the diagnosis of a fatal disease. Should we be searching for a chemic cause and cure when the provocation of grief is so apparent?
Intermission for a moment, though, to consider the physiology of a centre attack. A heart attack can be fix off by a variety of causes — chronic high blood force per unit area or pathologically high levels of "bad" cholesterol or smoking. Yet aspirin is an effective treatment of a heart attack regardless of its antecedent crusade. Why? Because a eye attack, however it might accept been provoked, progresses through a mutual, final pathway: there must be a clot in a coronary avenue that is blocking the flow of blood to the heart. Aspirin helps to inhibit the formation and growth of the jell in the coronary artery. The medicine is clinically effective regardless of what events led to the clot. "Aspirin," as a professor of mine liked to put information technology, "does not particularly intendance about your medical history."
Might major depression be like a centre attack, with a central mutual pathway and with serotonin as its master regulator? There was certainly precedent in the biological science of the nervous system for such unifying pathways — for complex mental states triggered by unproblematic chemicals. Fear, for example, was institute to involve a mutual hormonal pour, with adrenaline as the main player, fifty-fifty though its initiators (bears, spiders or in-laws) might take little resemblance to one another.
But such a line of research can't tell u.s.a. whether the absenteeism of serotonin causes depression. For that, nosotros need to know if depressed men and women take measurably lower levels of serotonin or serotonin-metabolites (byproducts of serotonin breakdown), in their brains. In 1975, pathologists performed autopsies on depressed patients to measure serotonin levels. The initial findings were suggestive: depressed patients typically tended to have lower levels of brain serotonin compared with controls. But in 1987, when researchers in Scandinavia performed a like experiment with newer tools to measure serotonin more accurately, serotonin levels were found to be higher in depressed patients. Farther experiments but deepened these contradictions. In some trials, depressed patients were institute to have decreased serotonin levels; in others, serotonin was increased; in yet others, there was no difference at all.
What most the antipodal experiment? In 1994, male subjects at McGill University in Montreal were given a chemical mixture that lowered serotonin. Doctors then measured the fluctuations in the mood of the men as serotonin levels dipped in the blood. Though serotonin was depleted, most of them experienced no significant alterations in their mood.
At starting time glance, these studies seem to suggest that there is no link between serotonin and depression. But an of import fact stands out in the McGill experiment: lowering serotonin does non have any effect on healthy volunteers with no history of depression, but serotonin-lowering has a surprisingly brisk effect on people with a family history of low. In these subjects, mood dipped sharply when serotonin levels dropped. An earlier version of this experiment, performed at Yale in 1990, generated even more provocative findings. When depressed patients who were already responding to serotonin-enhancing drugs, similar Prozac, were fed the serotonin-lowering mixture, they became acutely, often profoundly, depressed. Why would serotonin depletion make such a difference in a patient's mood unless mood in these patients was, indeed, being controlled by serotonin?
Other experiments showed that though depressed patients generally didn't have consistently lower levels of serotonin, suicidal patients often did. Might contemplating suicide be the virtually extreme form of depression? Or is it a specific subtype of mood disorder that is distinct from all the other forms? And if so, might depression have multiple subtypes — some inherently responsive to handling with serotonin-enhancing drugs and some inherently resistant?
We may not empathize how serotonin-enhancing antidepressants work, but do we know whether they work at all?
In the late 1980s, studies examined the result of Prozac on depressed subjects. Several of these trials showed Prozac reduced the symptoms of low when compared with a placebo. Depression is usually assessed using a standardized rating scale of dissimilar symptoms. In general, some patients reported clinically meaningful improvements, although the effects were often pocket-size and varied from trial to trial. In existent-world terms, such a alter could exist profound: a transformation in anxiety, the lifting of the anguish of guilt, an end to the desire to commit suicide. But for other patients, the changes were marginal. Peradventure the most important number that emerged from these trials was the nearly subjective: 74 percent of the patients reported feeling "much" or "very much" better on antidepressants.
In 1997, a psychologist, Irving Kirsch, currently at the Harvard Medical School, set out to look at the placebo upshot in relation to low. In part, the placebo effect works because the psyche acutely modifies the perception of affliction or wellness. Kirsch wondered how powerful this effect might exist for drugs that treat depression — where the medical condition itself happens to involve an alteration of the psyche.
To measure this consequence, Kirsch combined 38 trials that included patients who had been given antidepressants, placebos or no treatment and then applied mathematical reasoning to estimate how much the placebos contributed to the improvements in mood. The analysis revealed two surprises. First, when Kirsch computed the strength of the placebo effect by combining the trials, he plant that 75 percent of an antidepressant's consequence could have been obtained only past taking the placebo. When Kirsch and his collaborators combined the published and unpublished studies of antidepressants (they obtained the unpublished information from the F.D.A. via the Freedom of Information Act), the furnishings of the antidepressants were even more than diluted — in some cases, vanishingly so. Now, the placebo issue swelled to 82 percent (i.e., four-fifths of the benefit might have been obtained by swallowing an inert pill lone). Kirsch came to believe that pharmaceutical companies were exaggerating the benefits of antidepressants by selectively publishing positive studies while suppressing negative ones.
Just there are problems in analyzing published and unpublished trials in a "meta-trial." A trial may have been unpublished not just to hide lesser effects but because its quality was poor — because patients were enrolled incorrectly, groups were assigned improperly or the cohort sizes were too pocket-size. Patients who are mildly depressed, for example, might accept been lumped in with severely depressed patients or with obsessive-compulsives and schizophrenics.
In 2010, researchers revisited Kirsch's analysis using six of the almost rigorously conducted studies on antidepressants. The study vindicated Kirsch'south conclusions just only to a bespeak. In patients with moderate or mild low, the benefit of an antidepressant was indeed small, even negligible. But for patients with the most severe forms of low, the benefit of medications over placebo was substantial. Such patients might have plant, as Andrew Solomon did, that they no longer felt "the cocky slipping out" of their hands. The nearly severe dips in mood were gradually blunted. Similar Dorothy, these patients about likely still experienced sorrow, but they experienced it in ways that were less cocky-destructive or paralyzing. As Solomon wrote: "The contrary of depression is not happiness, but vitality, and my life, as I write this, is vital."
These glace, seemingly contradictory studies converge on a surprisingly consistent picture. Start, patients with severe depression tend to reply most meaningfully to antidepressants, while patients with moderate or mild depression do not. Second, in a majority of those who do respond, serotonin very likely plays an important role, because depleting serotonin in depressed patients often causes relapses. And third, the encephalon-as-soup theory — with the depressed brain simply lacking serotonin — was far too naïve.
Equally is oft the case in science, a new theory emerged from a radically different line of inquiry. In the late 1980s, a neuroscientist named Fred Gage became interested in a question that seemed, at first, peripheral to depression: does the adult human being brain produce new nerve cells?
The dogma in neurobiology at the time was that the developed brain was developmentally frozen — no new nerve cells were born. Once the neural circuits of the brain were formed in babyhood, they were fixed and immutable. After all, if new neurons were constantly replacing old ones, wouldn't memories decay in that tide of growth? But Cuff and other scientists revisited old findings and discovered that adult mice, rats and humans did, in fact, experience the birth of new neurons — but only in 2 very specific parts of the brain: in the olfactory bulb, where smells are registered, and in the hippocampus, a coil of tissue that controls memories and is functionally linked to parts of the encephalon that regulate emotion.
Could there be a connexion between emotion and neuronal nascence in the hippocampus? To find out, Cuff and his collaborators began to study stressed mice. When mice are chronically stressed — by sudden changes in their living environments or by the removal of their bedding — they demonstrate behavioral symptoms like anxiety and lethargy and lose their sense of adventurousness, features that mimic aspects of human low. Researchers institute that in these mice, the burst of nervus cells in the hippocampus also macerated.
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The converse turned out to be true too. When mice are housed in an "enriched" environment — typically containing mazes, nesting materials and toys — they get more active and adventurous. They explore more than; they learn faster; they seek pleasure. Enrichment, in short, acts behaviorally like an antidepressant. When Cuff examined the brains of these enriched mice, he institute that more neurons were beingness born in the hippocampus.
At Columbia Academy, another neuroscientist, René Hen, was intrigued past Gage's studies. Hen, working with other researchers, began to investigate the link between Prozac and nerve growth. The birth of neurons in the mice takes well-nigh two or three weeks — about the same fourth dimension it takes for antidepressants to take effect. Might the psychiatric effects of Prozac and Paxil be related to the slow birth of neurons and not serotonin per se?
Hen began to feed his mice Prozac. Over the next few days, their behaviors changed: feet they had exhibited decreased, and the mice became more adventurous. They looked for food in novel environments and were quick to adopt newly learned behaviors. And newborn neurons appeared in the hippocampus in precisely the location that Gage constitute with the environmentally enriched mice. Only when Hen selectively blocked the nascency of neurons in the hippocampus, the adventurousness and the food-exploration instincts of the Prozac-fed mice vanished. Prozac'south positive effects, in other words, depended on the birth of nerve cells in the hippocampi of these mice.
In 2011, Hen and his colleagues repeated these studies with depressed primates. In monkeys, chronic stress produces a syndrome with symptoms remarkably like to some forms of human depression. Even more strikingly than mice, stressed monkeys lose interest in pleasance and become lethargic. When Hen measured neuron nativity in the hippocampi in depressed monkeys, it was low. When he gave the monkeys antidepressants, the depressed symptoms abated and neuron nativity resumed. Blocking the growth of nervus cells made Prozac ineffective.
Hen'south experiments have profound implications for psychiatry and psychology. Antidepressants similar Prozac and Zoloft, Hen suggested, may transiently increase serotonin in the brain, but their outcome is seen just when new neurons are born. Might depression be precipitated by the expiry of neurons in certain parts of the brain? In Alzheimer'south disease, areas of the brain involved in cognition degenerate, resulting in the characteristic dementia. In Parkinson's disease, nerve cells involved in coordinating movement degenerate, resulting in the feature trembling. Might depression also be a degenerative disease — an Alzheimer's of emotion, a dementia of mood? (Even our language begins to fail in this description. Dementia describes a breakup of "mentation" — thinking — but we lack a similar word for a degeneration of mood: is it disaffection?)
And how, exactly, might the death of neurons in the tiny caul of the hippocampus (a office of the brain typically associated with the storage of retentivity) cause this disorder of mood? Traditionally, nosotros think that nerve cells in the brain can form minuscule biological "circuits" that regulate behaviors. One set of nerve cells, for instance, might receive signals to motion the manus and then relay these signals to the muscles that crusade paw movement. It is easy to imagine that dysfunction of this circuit might result in a disorder of move. But how does a circuit of nerves regulate mood? Might such a circuit store, for example, some rules about adapting to stress: what to say or do or recollect when y'all are sick and nauseated and facing expiry and your son has moved a pillow? Did such a degeneration provoke a panic signal in the brain that goaded Wurtzel's deadly reverie: cellular death leading to thoughts of suicide.
And how, and then, does the birth of cells heal this feeling? Are new circuits formed that restore vitality, regenerating behaviors that are adaptive and non subversive? Is this why Prozac or Zoloft takes two or three weeks to commencement working: to become "undepressed," do we have to wait for the slow rebirth of new parts of the brain?
If an reply to these questions exists, it may sally from the work of Helen Mayberg, a neuroscientist at Emory Academy. Mayberg has been mapping anatomical areas of the brain that are either hyperactive or inactive in depressed men and women. Tracing such sites led her to the subcallosal cingulate, a minuscule packet of nerve cells that sit well-nigh the hippocampus and function as a conduit between the parts of the brain that control witting thinking and the parts that control emotion. Recollect of the subcallosal cingulate every bit a potential traffic intersection on the road between our cognitive and emotional selves.
When Mayberg stimulated this area of the brain with tiny bursts of electricity using probes in patients resistant to antidepressant therapy, she institute remarkable response rates: about 75 percent of them experienced powerful changes in their moods during testing. Seconds subsequently stimulation began, many patients, some of them almost catatonic with depression, reported a "sudden calmness" or a "disappearance of the void." The stimulator can be implanted in patients and works like a depression pacemaker: it continues to relieve their symptoms for years. When the bombardment runs low, patients slowly relapse into depression.
At first glance, Mayberg's studies would announced to bypass the serotonin hypothesis. After all, it was electrical, not chemical, stimulation that altered mood. But the response to Mayberg'due south electrical stimulation too seemed to exist linked to serotonin. The subcallosal cingulate is especially rich in nerve cells that are sensitive to serotonin. Researchers establish that if they blocked the serotonin bespeak in the brains of depressed rats, the pacemaker no longer worked.
A remarkable and novel theory for depression emerges from these studies. Mayhap some forms of low occur when a stimulus — genetics, environment or stress — causes the death of nervus cells in the hippocampus. In the nondepressed encephalon, circuits of nervus cells in the hippocampus may transport signals to the subcallosal cingulate to regulate mood. The cingulate then integrates these signals and relays them to the more witting parts of the encephalon, thereby allowing us to register our ain moods or human action on them. In the depressed brain, nerve expiry in the hippocampus disrupts these signals — with some turned off and others turned on — and they are ultimately registered consciously as grief and anxiety. "Depression is emotional pain without context," Mayberg said. In a nondepressed brain, she said, "you demand the hippocampus to aid put a situation with an emotional component into context" — to tell our conscious encephalon, for instance, that the loss of love should be experienced equally sorrow or the loss of a job as feet. But when the hippocampus malfunctions, perhaps emotional pain can be generated and amplified out of context — like Wurtzel's estimator programme of negativity that keeps running without provocation. The "flaw in honey" and so becomes democratic and self-fulfilling.
We "abound sorrowful," simply 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. In a scientific sense as well, the chemical hypothesis of depression has moved from static to dynamic — from "state" to "procedure." An antidepressant like Paxil or Prozac, these new studies propose, is most likely non acting as a passive signal-strengthener. It does not, equally previously suspected, merely increase serotonin or ship more current down a brain's mood-maintaining wire. Rather, it appears to alter the wiring itself. Neurochemicals like serotonin however remain central to this new theory of depression, but they function differently: as dynamic factors that make fretfulness grow, mayhap forming new circuits. The painter Cézanne, against one of Monet'southward landscapes, supposedly exclaimed: "Monet is just an eye, but, God, what an eye." The brain, by the same logic, is still a chemical soup — but, God, what a soup.
At that place are, undeniably, of import gaps in this theory — and by no ways can it claim to be universal. Depression is a circuitous, various illness, with different antecedent causes and manifestations. As the clinical trials show unequivocally, simply a fraction of the most severely depressed patients answer to serotonin-enhancing antidepressants. Practice these patients reply to Prozac because their depression involves cellular decease in the hippocampus? And does the drug fail to work in mild to moderate depression because the cause of that affliction is unlike?
The differences in responses to these drugs could also exist due to variations in biological pathways. In some people, neurotransmitters other than serotonin may be involved; in yet others, at that place may be alterations in the encephalon acquired past biological factors that are not neurotransmitters; in yet others, there may exist no identifiable chemical or biological factors at all. The low associated with Parkinson's affliction, for example, seems to accept piffling to exercise with serotonin. Postpartum low is such a distinct syndrome that it is hard to imagine that neurotransmitters or hippocampal neurogenesis play a principal office in it.
Nor does the theory explain why "talk therapies" work in some patients and not in others, and why the combination of talk and antidepressants seems to piece of work consistently amend than either lone. It is very unlikely that we tin can "talk" our brains into growing cells. Simply perhaps talking alters the way that nerve death is registered by the conscious parts of the brain. Or talking could release other chemicals, opening upwardly parallel pathways of nerve-cell growth.
But the nigh profound implications have to do with how to understand the link between the growth of neurons, the changes in mood and the alteration of behavior. Perhaps antidepressants like Prozac and Paxil primarily alter behavioral circuits in the brain — specially the circuits deep in the hippocampus where memories and learned behaviors are stored and organized — and consequently alter mood. If Prozac helped Dorothy sleep improve and stopped her from assaulting her own skin, might her mood eventually take healed equally a response to her ain alterations of behavior? Might Dorothy, in short, accept created her own placebo outcome? How much of mood is behavior anyway? Maybe your brain makes you "act" depressed, and so you "feel" depressed. Or you feel depressed in role because your brain is making y'all act depressed. Thoughts like these quickly transcend psychiatry and move into more unexpected and unsettling realms. They might brainstorm with mood disorders, but they quickly plow to questions nigh the organizational order of the brain.
John Gribbin, a historian of science, once wrote that seminal scientific discoveries are inevitably preceded by technological inventions. The telescope, which situated the globe and the planets firmly in orbit around the sun, instigated a new management in thinking for astronomy and physics. The microscope, taking optics in a unlike direction, ultimately resulted in the discovery of the cell.
Nosotros possess far fewer devices to look into the unknown cosmos of mood and emotion. We tin only mix chemicals and spark electrical circuits and hope, indirectly, to understand the brain's structure and role through their effects. In time, the insights generated past these new theories of depression will nigh likely lead to new antidepressants: chemicals that directly initiate nerve growth in the hippocampus or stimulate the subcallosal cingulate. These drugs may make Prozac and Paxil obsolete — but any new handling will owe a deep intellectual debt to our thinking most serotonin in the brain. Our current antidepressants are thus best conceived not as medical breakthroughs just as technological breakthroughs. They are chemical tools that have immune us early glimpses into our brains and into the biology of one of the well-nigh mysterious diseases known to humans.
Source: https://www.nytimes.com/2012/04/22/magazine/the-science-and-history-of-treating-depression.html
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