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Are we becoming a nation of depressives? By many estimates depression has become the scourge of Westerners. Already the fourth leading cause of disability in the workforce, it is projected to reach number two by the year 2020 (after respiratory infections).

Psychiatrists have taken the position that the apparent increase in the incidence of depression is just a mirage--that this much depression has always been present in the population; it is simply better diagnosis and the decreased stigma associated with our treatments that are responsible for the escalating numbers of reported depressed people. Some of us remain unconvinced.

Research indicates that in any given year over seventeen million Americans experience major depression. In fact, fifteen percent of the population is diagnosed with depression at some point in their lifetime. The treatment of depression has become an enormous industry in the United States. Sales of antidepressant medications have tripled in just a decade and now total over $13 billion annually. In many parts of the country, people wait for several months or longer for a fifteen-minute appointment with their psychiatrist so that they can continue to receive their antidepressant pills. Family practitioners are dispensing even more of these medications than psychiatrists. Yet the consistent message to the treaters of depression is that only a small portion of the people who are suffering from depression are receiving treatment for it. Countless others are suffering, and it is our responsibility to bring treatment--almost always in the form of expensive new drugs--to the untreated.

This view of depression raises questions in the minds of many observers. Why should this disorder be on the rise despite the treatment efforts of several generations of psychiatrists and the combined resources of multibillion-dollar pharmaceutical companies? Is there something new about depression itself, or does this represent a problem inherent in modern Western society? How did humans manage to get through life before Prozac? Fortunately, some preliminary answers are beginning to emerge. Startling discoveries from basic research in neuroscience have forced us to begin thinking about the problem of depression in new and different ways. Before looking at these new findings, however, a review of how we got to our present state may be worthwhile.

Part of the helping profession's difficulty in dealing with depression is that we have never really understood what would cause one person to be depressed while another in similar circumstances remains symptom-free. A number of theories have had their day: anger turned inward results in depression; depression is a reaction to real or imagined loss; depression represents the gap between our real view of ourselves and our unconscious, idealized version of how our lives should be; depression is a genetically inherited disorder; depression is a result of "chemical imbalances" in neurotransmitter systems that can only be understood by trained psychiatrists. Since each of these models undoubtedly have some truth in them, any new model of depression will have to explain why each of these diverse viewpoints has led to the relief of suffering in at least some individuals.

Clouding our view of depression even further is the fact that bona fide depression can arise from a variety of "physical" causes. Pancreatic cancer, heart attacks, strokes, thyroid problems, side effects of a host of nonpsychiatric medications, even changes in exercise routines have all been clearly linked to the onset of depression in some individuals.

Modern psychiatry has dealt with this uncertainty about the root cause of depression largely by ignoring it. The sequence of Diagnostic and Statistical Manuals released by the American Psychiatric Association have been, by design, heavy on description and devoid of explanatory theories. The most recent manual requires that at least five of nine key symptoms--depressed mood, decreased interest in activities, significant weight loss or gain, disturbed sleep patterns, physical agitation or lethargy, fatigue, feelings of worthlessness or excessive guilt, decreased ability to concentrate or make decisions, and recurrent thoughts of death or suicide--be present for at least two weeks for major depression to be diagnosed. The manual does make the provision that, if these symptoms are "clearly due to a medical condition," the diagnosis of major depression is not given. Otherwise, if you've experienced five of these nine symptoms for at least two weeks you qualify as a depressed person.

The APA's treatment recommendations do acknowledge that some depressions of lesser severity may be treated successfully with either medication or psychotherapy; however, in practice, if you receive a diagnosis of major depression in an American psychiatrist's office, a prescription for an antidepressant medication is almost certain to follow. Today that translates into a prescription for Prozac or one of its chemical cousins (the serotonin specific reuptake inhibitors or SSRI medications like Paxil, Zoloft, Celexa, Luvox, and the like). This new generation of antidepressants has been so much safer and easier to use that it is now rare for psychiatrists to prescribe any of the older, "tricyclic" antidepressants which were the mainstay of treatment until the late 1980s. Millions of Americans take these new medications each day, usually showing some benefit from the treatment. Yet a number of issues make this very common equation of five-of-nine depressive symptoms = treatment with a newer antidepressant rather problematic.

First of all, there is no research to suggest that these newer--and dramatically more expensive--medications are more effective in reducing depressive symptoms than the older ones. In fact, just the opposite seems to be the case. In severe depressions, the tricyclics prove to be a bit more effective than the new drugs. It is the decreased frequency of side effects that have fueled the upsurge in use of the new medications. But that very tolerability has led to them being prescribed for a host of new maladies: mild depression, phobias, obsessions, posttraumatic stress symptoms, anxiety disorders of any kind, eating disorders, excessive shopping, hair pulling, skin picking, religious scrupulosity, sexual disorders, gambling, aggression, environmental sensitivities, and slow eating. It is difficult to imagine a single human problem that American psychiatrists haven't reported as being successfully treated with SSRIs.

This wide-ranging effectiveness raises important questions about whether these drugs could possibly have a specific beneficial action in each of these disorders or whether some other overriding but unrecognized action is at work. The most plausible idea encountered so far is that these medications induce some sort of fundamental shift in the relationships between areas of the brain involved with thought and those involved with emotion. Perhaps SSRIs decrease the emotional response to mental events so that chronic worries, obsessions, sad thoughts, and the like don't result in emotional responses of the usual magnitude. This effect has been likened to turning the brightness knob on your television all the way up. Everything is brighter but there isn't much contrast. Days can feel pretty much the same regardless of their events. Some experience this as a welcome relief from mental anguish; others have described it as "soul robbing."

Compounding matters further is the fact that all sorts of therapies have proven beneficial in reducing depressive symptoms. Psychotherapy looks as good or better at relieving depression, especially at one year followups, as antidepressant drugs. Exercise is a powerful and well-recognized antidepressant. St. John's Wort and other herbal preparations are widely used as antidepressants in some parts of the world. Artificially lengthening the short days of winter with phototherapy lights has dramatic antidepressant effects for some individuals. Some have found that even exposing the back of the knee to such lights can treat depression. Depriving a person of an entire night's sleep is an old but effective antidepressant therapy. While this is just a partial list of effective alternatives to antidepressant medication, it is unlikely that you would hear mention of any of them in a psychiatrist's office these days.

In reality, the newer antidepressant drugs are such a mainstay of treatment for depression that alternatives are rarely considered. The fact that these drugs offer only a 20 percent to 30 percent improvement over treatment with placebos (sugar pills) isn't a common topic of discussion in the office. Nor are patients routinely told that if they don't respond well to antidepressants they might have a great deal of difficulty discontinuing them, even several years down the road.

In some patients, stopping SSRIs may result in a variety of symptoms including depression, insomnia, nightmares, anxiety, headaches, nausea, and even neurological effects such as restlessness and tingling sensations. The Internet abounds with personal tales of people who have been on antidepressants for years and can't get off them no matter what they do. Some also find that they have to increase their dosage over time or add a second antidepressant to maintain the same degree of benefit--"Prozac poop out," as it is known in the trade. By diagnostic criteria used in the third Diagnostic and Statistical Manual, this need for increasing doses (tolerance) and the emergence of significant adverse effects when the medication is stopped (withdrawal) were sufficient to qualify a compound as an addictive drug.

So, a brief and simplistic assessment of modern psychiatry's position on depression would be that we really don't know what causes depression. We don't know why its incidence is increasing in our population. We don't know why depression responds to so many types of treatment. And we don't know how our medications work but we're happy that they do.

It is very difficult to understand depression and its treatment without considering economic factors. Psychiatrists can make an excellent living doing nothing but prescribing SSRIs to people who report having five or more depressive symptoms. If, like a great many prominent American psychiatrists of today, you also receive money directly from the pharmaceutical companies for speaking engagements, research, or "consultation," you can do a whole lot better than merely making a comfortable living. Imagine the outcome if the medical-legal climate dictated that every depressed person had to be offered twice-weekly psychotherapy as an alternative to medication. The financial effects would be catastrophic for all of the major players in the depression industry. The interests of the psychiatric profession, pharmaceutical companies, and health maintenance organizations are so intertwined that it is hard to begin to get an objective view of the questions surrounding depression.

It should come as no surprise that the clearest current look at the issue of depression comes from the hard science researchers. In the late 1990s, several striking findings began to emerge from their laboratories. Perhaps the most unexpected and important finding was that the brain continues to make new brain cells in some key areas all the way through its lifespan. This determination is contrary to the commonly accepted belief that the number of our brain cells was fixed by early adulthood and that a gradual decline in these cells was about the best that could be hoped for. We know that stem cells--the cells capable of transforming themselves into any other kind of cell--operate in the nervous system. And it is looking like the activities of these multipotential cells might be involved in depressive illness.

Two main areas that continue to produce new neurons in the brain have emerged. The olfactory bulb (which is involved with our sense of smell) and the hippocampus. The hippocampus has been the focus of much of the latest depression research. It is a part of the limbic system--an ancient area of the brain that is involved in the generation of emotions in humans and other mammals. Specifically, the hippocampus appears to be primarily involved in the formation of memories. How memory actually works remains quite mysterious. The idea that we can recall specific events from our past as a result of instantaneous electrochemical communications between living nerve cells seems almost farfetched. The idea that forming new nerve cells would be involved does make some intuitive sense. The evolving data suggesting that we add new brain cells in the hippocampus every day raises the intriguing possibility that the nerve cells we make today are somehow connected to the memories we make of today. Perhaps the common experience of having odors trigger powerful, specific memories is related to the fact that each of these brain areas has nerve cells and brain connections that were formed at the same time.

Scientists have also been surprised to discover a connection between the size of the hippocampus and depressive illness. One study suggests that the hippocampus may shrink by an average of 19 percent in depression. Other research has found that SSRI antidepressants and shock treatment, among other factors, restore the hippocampus to more normal volume. This increase in the size of the hippocampus is now considered to be a possible mechanism by which these treatments promote recovery from depressive illness. This puzzling idea would have seemed beyond the realm of possibility a decade ago. Modern psychiatry is in the very early stages of trying to make sense of these findings. How it will impact the treatment of depression in psychiatric practice is anybody's guess.

Psychiatrists have known for decades that there is a powerful connection between depression and memory: memories change when one is depressed. Ask people who are suffering from severe depression about their childhood and a depressing picture may emerge. They had no friends, they had no particular talents, their parents were mean, and nothing good ever happened to them. Ask the same question when they have recovered to a more normal mood and very different, more optimistic stories are recounted.

In some severe depressions a syndrome called pseudodementia is encountered. Basically, the memory functions become so impaired that it can be difficult to determine whether the person is suffering from Alzheimer's disease or some other dementing illness rather than major depression. A number of sophisticated neuropsychological tests have been developed to help make this determination. So the connection between depression and memory is a robust one. But psychiatry hasn't really considered the possibility that memory problems could be anything but a simple result of the depressive process. The idea that causation could somehow be involved is new to us.

Depression involves a good deal more than sad feelings or even memory problems. When we are exposed to any incoming stimuli a predictable sequence of events occurs. The brain processes this raw sensory data through a primary and then a secondary association cortex. Once the information is in usable form it is sent directly down to the limbic system. The brain asks, "What is out there? What is new? What have I seen like this before?" and the new data is compared with existing memories and stored symbols. Once evaluated, we then must decide what to do about it; the appropriate emotions, impulses, and responses are then generated. The most striking feature of many people who suffer from severe memory disorders is that they cannot properly activate themselves in response to the changes in their world. They may seem listless and incapable of motivation or they respond in ways that don't fit their surroundings.

As the link between depression and changes in the hippocampus has become clearer, a search for factors that increase or decrease the growth of these critical cells has ensued. Even more interesting than the emerging list of positive and negative growth factors has been the new picture of brain functioning that has developed within just the past few years. This new model of the brain may ultimately shed some light on the age-old question of what depression really is.

For the past couple of decades psychiatrists have been very concerned with events occurring at the synapse-the area where two nerve cells meet and communicate via the release of neurotransmitters. Antidepressants have been presumed to work by affecting the messages transmitted across these synapses. The introduction of SSRIs is believed to inhibit the reabsorption of serotonin by the cell that released it, extending its time at the synapses and therefore communication by the receiving cells. But why the increase in serotonin should have an antidepressant effect--and why other antidepressant medications like Tianeptine (used in Europe) have exactly the opposite effect--calls into question our assumptions about how SSRIs actually exert their effects.

The new neuroscience has shifted attention from synapses to genes. Messages carried across synapses by neurotransmitters represent just one type of communication that neurons receive. They also receive direct hormonal signals through circulating chemicals like steroids and sex hormones. Even gases such as nitrous oxide are used by neurons to communicate with each other. The ultimate effect of these communications is eventually mediated by turning individual genes on and off.

Several surprising findings have come out of the mapping of the human genome. The actual number of our genes--approximately 35,000--is startlingly low compared to earlier estimates, until one considers the possible variations in arrangement. And the search for factors responsible for influencing genes that are responsible for developing new neurons in the hippocampus--and for fending off depression--has turned up some candidates that psychiatrists may have intuitively expected.

Shock treatment, antidepressant medications, and physical exercise appear to have this effect. And an enriched, stimulating environment promotes new neuronal growth in these key areas involving memory. This might translate into having a decent, safe place to live, some meaningful work, and loving relationships, but there is much room for individual variation.

Novelty--experience that is new or unexpected--is another logical factor that has shown to positively affect the growth of the hippocampus neurons. Why would we spend a lot of our resources supporting areas of the brain involved with making new memories if we weren't having any new experiences to remember? An intriguing outgrowth of this research is the possibility that sameness might ultimately prove to be the worst stressor of all for the human brain.

Mundane jobs, boring routines, and the absence of real struggles for survival may all prove to contribute to depression's increasing place in our society. We cannot discount the possibility that the activities that seem to add diversity to our modern existence don't provide the sort of stimulation that healthy brains thrive on. Perhaps the novelty of images dancing on electronic screens is enough to capture our attention but is insufficient to cause brain changes that depend on real-life experiences.

The role of sleep in the generation of new neurons is an interesting story in itself. Research conducted on rats suggests that a gene called zif-268 is pertinent to the ongoing reorganization of the memory portion of the nervous system. The gene is activated during rapid eye movement (REM) sleep; however, activation only takes place if the rat has been exposed to sufficiently powerful stimuli during the waking hours before sleep. Translated to humans, the implication is that we sleep differently--and do different work reconstructing our brains--if our days are filled with new and interesting experiences. Disturbed sleep or a stimulus-poor life result in a decrease in new neurons.

Circulating hormones are known to affect the hippocampus. Premenstrual mood changes, depression following pregnancy, and depression around menopause may all be mediated by changes in estrogen levels. One researcher suggests that the hippocampus "almost pulsates" in response to estrogens. Testosterone has been implicated in the migration and hook up of undifferentiated neurons throughout the brain. Sex hormones and sexual activity are likely to be recognized as major factors in the emerging model of depression. And the glucocorticoid hormones--released by the adrenal glands in response to stress--may have the most far-reaching implications in terms of why we become depressed.

Scientists have determined that we humans share about 97 percent of our genes with chimpanzees--but that 3 percent difference is very important. Some of the difference is obvious in how our big human frontal lobes are constructed and wired. This enlargement of our frontal lobes is responsible for our ability to manipulate symbols to a far greater extent than all other mammals. We are unparalleled in our ability to construct a different reality in our minds--one that can be entirely separate from the objective external reality with which all animals must interact. The biggest problem with this talent is that we can also attach emotions to these private internal events.

When it comes to the sorts of emotions we attach to our incessant thoughts, we're more similar to chimpanzees than we care to admit. Our big symbol-producing frontal lobes are basically hooked up to limbic, or emotional, systems that aren't too evolved from other primates. As a result we are hard-wired to deal with the same issues and emotional responses as other social primates: who is superior in the troop to whom; who will be an acceptable and willing mate? Eliminate these two basic issues--dominance and mating--and there would be nothing to put on TV. We wouldn't know what to think about anymore. Some have suggested that there wouldn't be as much depression in humans, either.

When humans worry, what is it about? Our place in the hierarchy? What other humans think about us? How the boss will react if we don't land a deal or meet our productivity goals? Are our neighbors superior to us because of their expensive possessions? Do the latest objects of our sexual desires have any inclination to copulate with us? How do we compare today to what we were like when we were at our best? Each of these sorts of mental events can trigger the release of glucocorticoids--the molecular carriers of the stress reaction, which directly impact the genes. No interaction with a synapse is necessary; they result in the inhibition of factors that would lead to continued neural growth in the hippocampus and, perhaps, keep depression at bay. But to what end?

An interesting current theory of depression is that it develops as a way to limit our strivings for dominance in the social hierarchy. Humans aren't generally comfortable with the idea that they are built to compete for status with the social troop--just like apes, chimps, people who drive slowly in the left lane, and other lower primates. One need look no further than the modern equivalent of the Rorschach test--the American freeway--to see these competitive strivings in action.

People buy expensive cars aimed at making themselves look successful and important--in fact, to establish a particular identity. Cut in front of another automobile and rage reactions akin to a gorilla tearing up the shrubbery may result. Drivers compete furiously to get to their destination before others, even though the time saved driving like a NASCAR driver may only be mere minutes compared to traveling at a more moderate speed. Is there really something important that will be accomplished in that extra minute? Or is it about the competition?

If we examine our emotional reactions to the person who is trying to get down the highway faster than us, we may have to admit that some deep-seated and irrational feelings seem to be at work. These same competitive feelings lie behind our culture's preoccupation with accumulating other visible trappings of success. The latest fashions, the biggest homes, the fanciest restaurants all give expression to our desire to set ourselves apart from humans of lesser status. The "silverback male" in our culture is the person with the most zeroes on his or her net-worth statement.

Further proof of our strivings for status is our society's preoccupation with sexuality. Beautiful, young people are used to sell all types of products. Entire industries are devoted to helping people convince themselves they are sexually attractive to other people. The fact that actual copulation with the fantasized partners almost never results doesn't deter us from our preoccupation; our brains simply compel us to attach importance to our sexual status within our groupings.

While such competitive tendencies and sexual preoccupations may hold a great deal of significance for us when we are in our reproductive years, they may ultimately be a burden as we get older. Continue to live life for a sufficient numbers of years as though it were a contest and the brain will be constantly exposed to the stress hormones that result from that world view. If enough stress hormones circulate for a long enough period of time, depression becomes increasingly likely.

If there is one thing that we can absolutely count on it is that our current ideas about how human brains work will seem hopelessly primitive a hundred years from now. We will certainly know more about the causes of depression. Already we are finding out that some of the ways we use to feel good for awhile may cause us to be more depressed in the long run.

Drink too much alcohol and the hippocampus suffers. Depression can result. Opiates? More tablets of Percocet were dispensed in 2000 in the United States than any other prescription drug. There may be a lot of severe pain being treated these days, but one suspects that a little mood elevation is going on as well. Unlike SSRIs, which typically take two to eight weeks to relieve depression, opiate medications like Percocet provide the sort of immediate increase in good feelings that people really want from their antidepressant pills. Unfortunately, opiates have already been shown to decrease the birth of new neurons in the hippocampus. While providing good feelings today, they may carry the cost of increased depression tomorrow. Research finding this to be true of cocaine and methamphetamines is probably just around the corner.

Of course, we'll likely find out that the whole theory of the hippocampus in depression is too simplistic. Maybe it's not just the fact that the hippocampus doesn't grow new nerve cells in depression; it's where that energy goes instead. The amygdala is looking like the next candidate for the root cause of depression. A tiny almond-shaped organ that abuts the hippocampus, the amygdala is involved in producing negative emotions like fear and hostility. It is also involved in "reward pathways." It's activity appears to increase in depression (and addictions) just as the hippocampus declines. A good example may be the stereotype of the powerful businessperson who becomes increasingly argumentative and suspicious after retirement. This might ultimately reflect a shift to using more amygdala as demands on the hippocampus are reduced.

We may never achieve our goal of truly understanding the brain-mind problem. Our idea that one specific area of the brain is involved in one particular action or emotion is hopelessly outdated. Everything seems to happen as a simultaneous network of activities in different brain areas, but our scientific approaches demand that we study one variable at a time. For now the best way to think about depression may be that it is analogous to a warning light glowing on the the dashboard of our car: it tells us that there is something amiss under the hood, but not what the problem is or what should be done about it.

Like a good mechanic, the modern psychiatrist's job should be to figure out what is really wrong with the engine. We should wonder whether someone is depressed because of an unstimulating environment, a lack of satisfying relationships, boring routines, or insufficient physical exercise. The depression might reflect an excessive preoccupation with one self-importance or could be the result of a toxic substance. In some instances, a diet poor in the Omega III fatty acids found in fish oil could be causing depression. In others, the symptoms may be signaling that it is time to reassess one's values and make some basic life changes. Our antidepressant medications are pretty good, but it's a bit unreasonable to think that they or shock treatment would address all of these problems.

An enlightened model of major depression will have to take into account these new research findings about nerve cell growth. It will have to explain why so many diverse treatments may be equally effective in reducing depressive symptoms. The fact that depression is usually self-limited and will eventually go away without treatment must also be considered. The amazing impact of beliefs and expectations that is seen in the placebo response must have a physical correlation but we still know little about the mechanism. The fact that the incidence of depression in our population is increasing suggests that depression may be related to sociological variables that are also poorly understood. The new model cannot come soon enough.

As we become more sophisticated in our understanding of depression, the psychiatric profession will be challenged to help our society grow in new directions. We may eventually be able to provide information about how to raise children in a manner that makes them more resistant to depression. More stimulating environments, enhanced curiosity, better relationships with caregivers, and more exercise will undoubtedly help our kids to build brains that are less depression prone. The influence of circulating maternal hormones (reflecting the mother's emotional state) on the fetus' brain development is becoming another exciting area of research.

Learning more about the fuels and activities that keep brains healthy should trigger changes in how humans lead their lives. For depressed adults, future prescriptions might include travel and activities aimed at increasing exposure to novel experiences and new challenges for the memory apparatus. Therapies aimed at improved relationships or at decreasing our eternal preoccupation with striving for status may become as respected as medications--especially if neuroscience provides the means to document that they evoke similar changes in brain functioning.

For now, psychiatrists will continue to prescribe anti-depressant medications with little regard for the factors that may have led to the depressive illness. In the future, however, our task will be to develop multidimensional treatments that are specifically tailored to the needs of the individual. Specialized environments may be developed to carry out the assessments and varied therapies that a more complex understanding of depression will require. Perhaps, ultimately, psychiatrists will be concerned with helping people to live more memorable lives.

Dr. Kevin Turnquist is a board certified psychiatrist, employed full time for Hennepin County and State of Minnesota outpatient programs. A 1984 graduate of the New York Hospital/Cornell Medical Center, he has lectured widely and received the 1996 Exemplary Psychiatric Award from the National Alliance for the Mentally Ill.
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Author:Turnquist, Kevin
Publication:The Humanist
Geographic Code:1USA
Date:Sep 1, 2002
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