Feeling Good: The New Mood Therapy (54 page)

NOTE: Numbered Notes and References for Chapters 17–20 can be found on pages 682–687. Because some References are cited more man once, the superscript numbers assigned to those References will appear in these chapters more than once.

(Notes and References appear on pages 682–687
.
)

Some day, scientists may provide us with frightening technology that will allow us to change our moods at will. This technology may be in the form of a safe, fast-acting medication that relieves depression in a matter of hours with few or no side effects. This breakthrough will represent one of the most extraordinary and philosophically confusing developments in human history. In a sense, it will almost be like discovering the Garden of Eden again—and we may face new ethical dilemmas. People will probably ask questions like these: When should we use this pill? Are we entitled to be happy all the time? Is sadness sometimes a normal and healthy emotion, or should it always be considered an abnormality that needs treatment? Where do we draw the line?

Some people think such technology has already arrived in the form of a pill called Prozac. When you read the next few chapters, you will see that this is not really the case. Although we have large numbers of antidepressant medications that work for some people, many people do not respond to antidepressant medications in a satisfactory way, and when they do improve, the improvement is often incomplete. Clearly, we are still a long way from our goal.

In addition, we still do not really know how the brain
creates emotions. We do not know why some people are more prone to negative thinking and gloomy moods throughout their lives, whereas others seem to be eternal optimists who always have a positive outlook and a cheerful disposition. Is depression partially genetic? Is it due to some type of chemical or hormonal imbalance? Is it something we’re born with, or something we learn? The answers to these questions still elude us. Many people wrongly believe we already have the answers.

The answers to questions about treatment are equally unclear. Which patients should be treated with medications? Which patients need psychotherapy? Is the combination better than either type of treatment alone? You will see that the answers to questions as basic as these are more controversial than you might expect.

In this chapter, I address these issues. I discuss whether depression is caused more by biology (nature) or the environment (nurture). I explain how the brain works, and review evidence that depression might be caused by a chemical imbalance in the brain. I also describe how antidepressant drugs attempt to correct this imbalance.

In Chapter 18, I discuss the “mind-body problem” and address the current controversies about treatments that affect the “mind” (for instance, cognitive therapy) versus treatments that affect the “body” (for instance, antidepressants.) In Chapters 19 and 20, I will give you practical information about all the antidepressant drugs that are currently prescribed for mood problems.

Although much research is being conducted to try to tease out the relative strengths of the genetic and environmental influences on depression, scientists do not yet know which influences are the most important. With regard to bipolar (manic-depressive) illness, the evidence is quite
strong: genetic factors seem to play a strong role. For example, if one identical twin develops bipolar manic-depressive illness, the odds are high that the other twin will also develop this disorder (50 percent to 75 percent). In contrast, when one of two nonidentical twins develops bipolar (manic-depressive) illness, the odds that the other twin will develop the same illness are lower (15 percent to 25 percent). The odds of developing bipolar illness if a parent or nontwin sibling has this disorder are around 10 percent. All these odds are considerably higher than the odds that someone in the general population will develop bipolar illness—the lifetime risk is estimated at less than I percent.

Keep in mind that identical twins have identical genes, whereas nonidentical twins share only half their genes. This is probably why the likelihood of bipolar (manic-depressive) illness is so much higher if you have an identical twin than if you have a nonidentical twin with this disorder, and why these rates are so much higher than the rates for bipolar illness in the general population. The increased risk for bipolar illness among identical twins is even true if the identical twins are separated at birth and raised by different families. Although the adoption of identical twins by separate families is rare, it does happen on occasion. In some cases, scientists have been able to locate the twins later in life to determine how similar or different they are. These “natural” experiments can tell us a great deal about the relative importance of genes versus environment because the separately raised identical twins have identical genes but their environments are different. Such studies highlight the importance of strong genetic influences in bipolar disorder.

With regard to the far more common garden-variety depression without episodes of uncontrollable mania, the evidence for genetic factors is still quite fuzzy. Part of the problem facing genetic researchers is that the diagnosis of depression is much less clear-cut than the diagnosis of bipolar
(manic-depressive) illness. Bipolar manic-depressive illness is such an unusual disorder, at least in its more severe forms, that the diagnosis is often obvious. The patient has a sudden and alarming change in personality that comes on without drugs or alcohol, along with symptoms such as:

    • intense euphoria, often with irritability;

    • incredible energy with constant exercising or restless, agitated body movements;

    • very little need for sleep;

    • nonstop, pressured talking;

    • racing thoughts that skip from subject to subject;

    • grandiose delusions (for example, the sudden belief that one has a plan for world peace);

    • impulsive, reckless, and inappropriate behaviors (such as spending money foolishly);

    • inappropriate, excessive flirtatiousness and sexual activity;

    • hallucinations (in severe cases).

These symptoms are usually unmistakable and often so uncontrollable that the patient may require hospitalization with medication treatment. Following recovery, the individual usually returns to absolutely normal functioning again. These distinct features of bipolar illness make genetic research relatively straightforward, since it is usually not difficult to determine when individuals have the disorder and when they do not. In addition, this disorder usually begins fairly early in life, with the first episode often occurring by the age of twenty to twenty-five.

In contrast, the diagnosis of depression is much less obvious. Where does normal sadness end and clinical depression begin? The answer is somewhat arbitrary, but the decision will have a big impact on the results of research.
Another difficult question genetic researchers face is this: How long should we wait before we decide whether or not a person has developed a clinical depression during his or her life? Suppose, for example, that an individual with a strong family history of depression dies in an auto accident at the age of twenty-one without ever having had an episode of clinical depression. We might conclude that she or he did not inherit the tendency for depression. But if that individual had not died, she or he might have developed an episode of depression later on in life, since a first episode of depression can often occur when you are older than twenty-one.

Problems like this are not insurmountable, but they do make genetic research on depression difficult. In fact, many previously published studies on the genetics of depression are quite flawed and do not permit us to make any unambiguous conclusions about the importance of heredity versus environment in this disorder. Fortunately, more sophisticated studies are now under way, and we may have better answers to these questions during the next five to ten years.

Throughout the ages, humans have searched for the causes of depression. Even in ancient times there was some suspicion that blue moods were due to an imbalance in body chemistry. Hippocrates (460–377
B.C.
) thought that “black bile” was the culprit. In recent years scientists have spearheaded an intensive search for the elusive black bile. They have tried to pinpoint the imbalances in brain chemistry that might cause depression. There are hints about the answer, but in spite of increasingly sophisticated research tools, scientists have not yet discovered the causes of depression.

At least two major arguments have been advanced to
support the notion that some type of chemical imbalance or brain abnormality may play a role in clinical depression. First, the physical (somatic) symptoms of severe depression support the notion that organic changes might be involved. These physical symptoms include agitation (increased nervous activity such as pacing or hand-wringing) or enormous fatigue (motionless apathy—you feel like a ton of bricks and do nothing). You also may experience a “diurnal” variation in your mood. This refers to a worsening of the symptoms of depression in the morning and an improvement toward the end of the day. Other physical symptoms of depression include disturbed sleep patterns (insomnia is the most common), constipation, changes in appetite (usually decreased, sometimes increased), trouble concentrating, and a loss of interest in sex. Because these symptoms of depression “feel” quite physical, there is a tendency to think that the causes of depression are physical.

A second argument for a physiologic cause for depression is that at least some mood disorders seem to run in families, suggesting a role for genetic factors. If there is an inherited abnormality that predisposes some individuals to depression, it could be in the form of a disturbance in body chemistry, as with so many genetic diseases.

The genetic argument is interesting but the data are inconclusive. The evidence for genetic influences in bipolar manic-depressive illness is much stronger than the evidence for genetic influences in the more common forms of depression that afflict most people. In addition, lots of things that do not have genetic causes run in families. For example, families in the United States nearly always speak English, and families in Mexico nearly always speak Spanish. We can say that the tendency to speak a certain language also runs in families, but the language you speak is learned and not inherited.

I don’t mean to discount the importance of genetic factors. Recent studies of identical twins who were separated at birth and raised in different families show that many traits we think of as being learned are actually inherited.
Even such personality traits as a tendency toward shyness or sociability appear to be partly inherited. Personal preferences, such as liking a particular flavor of ice cream, may also be strongly influenced by our genes. It seems plausible that we may also inherit a tendency to look at things either in a positive, optimistic way or in a negative, gloomy way. Much more research will be needed to sort out this possibility.

The brain is essentially an electrical system that is similar in some ways to a computer. Different portions of the brain are specialized for different kinds of functions. For example, the surface of the brain toward the back of your head is called the “occipital cortex.” This is where vision takes place. If you had a stroke mat affected this region of the brain, you would have trouble with your vision. A small region on the surface of the left half of your brain is called “Broca’s area.” This is the part of your brain that allows you to talk to other people. If this part of your brain were injured by a stroke, you would have difficulty talking. You might be able to think of what you wanted to say, but find that you had “forgotten” how to speak the words. A primitive part of your brain called the “limbic system” is thought to be involved in the control of emotions such as joy, sadness, fear, or anger. However, our knowledge of where and how the brain creates positive and negative emotions is still very limited.

We do know that nerves are the “wires” that make up the electrical circuits in the brain. The long thin part of a nerve is called the “axon.” When a nerve is stimulated, it sends an electrical signal along the axon to the end of the nerve. A nerve is much more complex than a simple wire, however. For example, a nerve may receive input from tens of thousands of other nerves. Once it is stimulated, its axon may send out signals to tens of thousands of other nerves.