The steep path of self-development is... as mournful and gloomy as the path to Hell.
Mysteriously, in ways difficult to accept by those who have never suffered it, depression comes to resemble physical anguish. Such anguish can become every bit as excruciating as the pain of a fractured limb, migraine or heart attack.
Do hills get higher when valleys sink deeper? Periods of depression and despair commonly occur before religious experiences, as was confirmed in Hardy's sur-vey.3 Indeed, many accounts over the centuries have suggested that the depths of depression can be a prelude to enlightenment. To St. John of the Cross, the aspirant would go through "a dark night of the soul," a preliminary period of intense mental and physical anguish.4 To Master Han-shan, people appeared like "dead logs."5 This chapter provides plausible explanations for those dark nights when no moon lights up the steep and slippery path.
Are only certain kinds of people prone to have dark nights on their meditative path? If so, could they (and we) embark on a somewhat different style of meditative practice so as to encourage the preludes of depression to evolve toward the most positive, creative outcomes? We need longitudinal studies to answer these questions. Meanwhile, some reports suggest that the most creative persons are not the ones afflicted by a bipolar manic-depressive disorder. Instead, the creative outcomes tend to occur among their close relatives, in those family members who seem better able to direct their energies more constructively into that fruitful zone between the two polar extremes—the heights so pressured and distracted, the depths so gloomy with blank despair.6
Normal people of all ages undergo ups and downs in their biological cycle. Many learn to identify their transient high points and their blahs, especially when the blues go on to last for several days. Some dark thoughts express a specific dissatisfaction; other pessimisms are a disillusion with things in general. The person whose discontents pile up into a large knot may be stimulated to seek relief by adopting a very different set of values.
Those who then choose to take up the meditative path could have several other reasons for manifesting their low spirits. Let us consider some of them in sequence.
1. Too much sitting can be enervating. Overzealous meditation which leads to too much loss of sleep can also contribute to low spirits. Both conditions imply that meditation has been improperly performed, usually for too long. Interim physical work and hard exercise provide the necessary change of pace.
2. Closing the eyes during prolonged meditation may lead to sluggishness and depression in susceptible persons.
3. Beginners get discouraged, because the spiritual search is long and demanding.
4. Insights can have painful consequences. It is difficult to live in the everyday imperfect world. It is hard to give up all of one's old illusions and delusions. Most everyone on the path becomes discouraged sooner or later.
5. Finally, the brain will respond to a rigorous retreat with a variety of stress responses (see chapter 53).
The fifth item leads us to ask: Could some of the stress responses which arise during retreats invoke the same mechanisms which cause nonmeditating people to become clinically depressed during three other conditions of interest? These other situations are (1) our normal brief ups and downs; (2) the terminal depressions which evolve into an open acceptance of dying; and (3) those more pathological forms of depression.
Some answers are now coming in. Recent studies are beginning to clarify the mechanisms underlying several subtypes of depression. One subgroup of patients appears to have a reduced functional level of serotonin activity7 Their spinal fluid shows low levels of a breakdown product of serotonin called 5-hydroxyindoleacetic acid. The low functional level of ST activity is believed to render these patients vulnerable to recurrent depressions and suicide attempts. Indeed, most studies do find evidence that brain ST metabolism is reduced in persons who show suicidal behavior.8'9 Moreover, most depressed patients who had earlier responded successfully to antidepressant drugs will relapse into depression within a few hours after their plasma tryptophan levels are lowered.10 Note that measures which reduce this precursor, tryptophan, would soon reduce ST levels in the brain (see chapter 44).
Now the ST systems normally hold some norepinephrine activities in check. It follows that an ST underactivity might then lead, secondarily, to an overactivity of certain noradrenergic functions. Moreover, the breakdown products of dopa-mine also drop to low levels in the spinal fluid of depressed patients. The levels become almost as low as they are in Parkinson's disease, and they rise as the patients recover. So one factor which might contribute to the slow movements of depressed patients is a reduction in their motoric functions related to dopamine.11
Many depressed patients improve after they have been treated with drugs such as the tricyclic antidepressants.12 But tricyclics do more than increase the synaptic levels of ST and NE. They also have anticholinergic effects. These block the actions of acetylcholine as well. Endless speculation has arisen about what kinds of roles ST, NE, DA, histamine, and ACH play in causing depression. Much of this speculation has been based on the fact that, in practice, certain drugs which affect these messengers greatly improve many depressed patients. The reader may find it interesting to note how very specific some researchers have become in weaving biogenic amines into their current hypotheses. For example, some would now postulate that there exist two general types of depression, each of which has a definite profile of NE, ST, and DA.13-14
The first type, anxiety depression, is believed to reflect a predominance of excitatory activity coming from the locus ceruleus NE, dorsal raphe ST, and meso-cortical DA systems. The second type, anergic depression, is postulated to occur because inhibitory activity predominates. It is speculated that this inhibition might arise from separate NE nerve cells farther down in the ventral medulla, from ST activity of the median raphe, and from DA activity within the mesolimbic system.
In contrast, still other evidence suggests that ACH overactivity makes the major contribution to the symptoms, signs, and biochemical aspects of depression.15-16 This is called the "cholinergic overdrive" hypothesis. Indeed, some persons who are prone to melancholy do appear to be supersensitive to cholinergic agents even before their depressions occur.
Endorphins and other peptides are also candidates for some aspects of depression. Clearly, opioids yield positive feelings of pleasure. Therefore, depleting endogenous opioids, or not releasing them, might lead the person to feel that nothing yields pleasure. This anhedonic state of no pleasure is a major complaint in depressed patients. Suppose that low opioid levels earlier had prompted the brain to develop a (compensatory) increase in the number of its opioid receptors (a process called upregulation). Later, a pulse of opioids arrived. When these opioids then activated many of these new receptors, the subject could perceive the experiential impact as extraordinarily effective.
First the lower valley. Then the higher peak. And, as we have noted elsewhere, this principle of compensatory upregulation is not limited to opioids. It applies whenever the brain drops its ST, NE, DA, or other neuromodulators to low levels. Researchers can now measure receptor levels and localize them with the aid of brain mapping techniques. So it is now possible to test the following hypothesis, which centers on this potentially important receptor mechanism: after the earlier phase of an extended dark night, upregulation could help set the stage for a depressed brain to shift up into that rare state which illuminates by the pale light of the moon.
Some patients do shift quickly, from the depths of depression up to hypoma-nia. What causes the shift? Emotional or environmental stresses, or drugs that increase the turnover of biogenic amines.17 Among such drugs are levodopa, and others that raise amines to higher levels.18 Still other patients, just before they begin their hypomanic phase, enter a transition period for a number of hours. During this interim period they spontaneously reduce their time spent in REM sleep and their total sleep time.16
A new procedure, called "chronotherapy," helps some patients recover from their endogenous depression. It is of interest that they too are deprived of sleep, like those meditators who lose sleep during a sesshin. However, in the depressed patients, the sleep loss has already been appreciated to be a mode of "therapy."19 This therapy proceeds in the following way. Note that it begins by getting the patients up much earlier. The first night, they still go to sleep at their usual time, say 11 P.M. But now they are awakened at 2 A.M. This is five hours earlier than the usual 7 A.M. awakening their biological clock had previously been set for. Next comes a shift in the hour they drop off to sleep. Lights go off at only 6 P.M., so sleep now occurs five hours earlier than it did before. The patients then "adjust." Now, having reset their biological clock, they'll awaken when the lights go on again, eight hours later at 2 A.M. The result? Their mood lifts, later during the next day. Indeed, in the course of such shifts in their sleep-wake cycle, some 25 to 30 percent of these previously depressed subjects "overshoot," and switch up into a hypomanic or even a manic phase.20
In part V we considered the mechanisms underlying surges and quick-enings. Now, these patients are presenting us with a specific example of how a delayed overshoot is prompted by a shift in the sleep-wake cycle. What causes the long delay before the depression lifts? Delay raises the possibility that slower metabolic events might be taking place in second-messenger systems (see chapter 48). Among the current candidates are a special class of soluble proteins. These bind guanine nucleotides, and are therefore called G proteins. They are one of the steps in that cascade which starts with the release of glutamate and finally goes on to increase cAMP.21-22 One other interesting line of evidence suggests that the subjects in the particular subgroup of depressed patients who do respond to sleep deprivation tend to have increased functional activity in the limbic regions of their brain.23
Chronotherapy means rescheduling more than a patient's rest-activity and light-dark cycles. It also shifts other major synchronizers. These include mealtimes, caffeine intake, and social activities. When these change, the patient's old biological clock is reset, and a "new" twenty-four-hour day begins. Wouldn't Linnaeus be fascinated if he could see how humans shift their personal clocks to "bloom" at different times! (see chapter 77).
More is involved than simply getting out of the old rut. This five-hour phase advance in chronotherapy is a jolt equivalent to the jet-lag of flying east from New York to London. The whole body-brain must shift biochemical and physiological gears in almost a literal sense. So this is a major stressful process of adjustment. And it is in this dynamic setting that the patient's mood becomes elevated as the depression lifts. Two further points are of special note: (1) The type of sleep lost is predominantly D-sleep. It will, however, be made up. (2) Rigorous Zen retreats cause similar kinds of rescheduling. Again, the meditators awaken early, sometimes around 3 or 4 A.M. Many will also advance their formal sleep times (i.e., go to bed earlier), but others stay up late to meditate.
How would meditators be affected during a long retreat if they underwent a well-controlled, systematic phase advance, or an equal phase delay, as opposed to no change in the setting of their biological clocks? Would the time change make the states of absorption or kensho more likely or less likely to occur? In theory, a phase advance of a kind used in chronotherapy could help the brain uncouple its former cycles, allowing several of their functions to reassemble into more energized alternate states of consciousness. It is time to investigate this carefully.
Some persons' behaviors cycle with the seasons. The more the ambient light, the more active they are, mentally and physically. Full of energy between March and August, they feel more emotional and develop racing thoughts. Only a few weeks later, the darker months begin. Then, light-deprived from September to February the subjects become so moody and sluggish that they warrant a diagnosis of seasonal affective disorder (SAD), or seasonal depression. If you were a person overly prone to such depression, it would not be appropriate to meditate in the dark or to close your eyes too long. Light treatments (phototherapy) seem to help patients avoid seasonal depression. Some of them improve after receiving bright light during the evening hours from 7 to 9 P.M.24 Others are helped by exposure to bright light in the morning.25
Depression hurts. Styron points out that one of its very real constituents is a sense of physical anguish. A reduced activity within ST systems might contribute to depression's prominent symptoms of pain and suffering. Recalling this possibility, the therapeutic effect of imipramine is noteworthy. This drug is known to increase the synaptic levels of ST. And it also helps relieve not only human depression but also a variety of other painful states. Even so, the latest antidepres-sants—which also enhance the synaptic levels of ST—are not yet considered to be the ideal drugs.26
Do the two cerebral hemispheres show different vulnerabilities to depression? This remains moot.23-27-28 It also remains to be clarified how the increased release of ACTH and cortisol, as evidenced in the blood of many severely depressed patients, relates to their depression. PET scan studies have been performed on patients who have the particular kind of pure monopolar depression that runs in families. These earlier neuroimaging scans suggested that an active amygdala somehow made these patients vulnerable to their basic mood disor-der.29 Subsequent studies, performed in similar patients, showed that one part of the left anterior cingulate gyrus was reduced in volume.30 This region lies under the anterior bend (the "knee") of the corpus callosum. (Figure 3 represents this region within the crosshatched zone of the cingulate gyrus. It lies above and to the right of the large dot specifying the gyrus rectus.) Other patients have been studied who had other kinds of gross lesions in this ventromedial part of the prefrontal cortex.31 These patients did not respond appropriately to complex personal and social stimuli, but their primary emotions were not impaired.
To sum up: a broad, dynamic research interface has opened up. Brain mechanisms have now been identified that help to explain certain aspects of depression, of anguish, and of rapid shifts in mood. Relatively simple measures can cause a major shift in the tidal rhythms of our biological clocks. Procedures that reset these clocks will go on to destructure what would otherwise be an orderly rise and fall of our transmitter functions. It will be crucial to focus techniques from these fertile fields of research on selected human subjects who are undergoing long, grueling meditative retreats. Only the results of WM/h'disciplinary studies can help clarify why certain persons shift into enlightened states after having endured a very dark night and a gloomy meditative prelude.
Then, someday, will we understand why, as Basho's beautiful haiku once predicted:
The gloomy storm-clouds crumble, and behold: The mountains in the moonlight, clear and cold.32
Was this article helpful?