It is well known in our lives that losses happen – from minor ones, such as not getting the last piece of chocolate to major ones, such as the death of a loved one. How we react to these losses is what is important in determining how the rest of our lives will go. Emotions that are proportional to what is actually happening in our lives are felt as clean and right for the time. We appear to be going with the flow of our lives. Looking back, we can all remember episodes of sadness that had this quality of the right intensity, the right amount of time and a sense of integrity.
We have all had other experiences of excessive sadness with a ruminative painful, sticky quality, that lasted far beyond what seemed to be appropriate and affected our lives in significantly negative ways. Some of us may also have had periods of our lives where all of the colors were dark gray to black, where sounds were muted and somber, and where it seemed we could only play the bottom ten notes of an 88 key piano.
We may have had to take prescription medications or do therapy to lift of this veil from our lives. Some of us may have had wild rides from crazed euphoria to abject depression, wreaking havoc with our relationships and professions.
In this article, we will explore what neuroscience, psychology, and spiritual practice have to tell us about how we can assist ourselves to recover from these kinds of episodes, how we can rebalance our lives, and how we can inoculate ourselves against future events.
Overall maintenance of mood is dependent on continuous and coordinated input from brainstem neurons to the limbic system and cortex. This is summarized as the monoamine hypothesis of depression. The important monoamine transmitters are norepinephrine, serotonin, and dopamine.
Norepinephrine, derived from tyrosine in the diet, is produced in two regions of the brainstem—the locus ceruleus and the lateral tegmentum.
The locus ceruleus neurons send their axons to the cerebellum, spinal cord, amygdala, and the frontal lobes and cingulate cortex. They influence a lot of consciousness and planned actions in response to emotional stimuli. The Lateral tegmental neurons send their axons to the basal forebrain, the hypothalamus, and the amygdala, coordinating memory and autonomic/endocrine responses. Any disturbance in norepinephrine synthesis or metabolism will disrupt limbic and cortical functioning, will reduce neuroendocrine activity and alter the stress response, and will alter the pleasure/reward component of social/affective expression. Norepinephrine deficient depression may be more labile and demonstrative.
Dopamine, also derived from tyrosine, has three major sources. The substantia nigra in the brainstem projects to the caudate and striatum in the basal ganglia, smoothing out motor control systems (Parkinson’s disease). The ventral tegmentum projects to the ventral limbic system, the nucleus accumbens, and the prefrontal cortex. The hypothalamic dopamine neurons project to the pituitary and suppress prolactin secretion.
Dopamine is the precursor to norepinephrine in the synthetic pathway, so deficiencies in dopamine production can affect norepinephrine production as well. Dopamine problems can cause lassitude, a lack of energy, and difficulty in initiating action. There may also be psychotic behaviors due to excess dopamine in the frontal lobes.
Serotonin, derived from tryptophan, also has three sources in the brainstem that are involved in mood regulation. Small collections of neurons near the midline, called the raphe nuclei, are responsible for the bulk of the serotonin production. The dorsal midline raphe project to the striatum and the hypothalamus—these neurons are most affected by MDMA (3,4-methylenedioxymethamphetamine).
The median midline raphe project to the hippocampus and are involved in the memory components of mood disorders. These systems are overlapping in their distribution and create some of the different disorders through their receptor systems. The caudal raphe nuclei in the lower brainstem are involved in sleep regulation. With deficient serotonin, individuals become depressed, tend to continue to respond to non-rewarding situations regardless of punishment, tend to become involved in frightening/abusive situations, and may seem helpless in altering their behavior (learned helplessness).
Suicide and violent ends can be associated with deficient serotonin levels. Paradoxically, with a different receptor abnormality, the serotonin depression may exhibit motor retardation, social withdrawal, and confusion/sensory overload.
The hypothalamus also may be involved in some depressions. There is a reciprocal involvement of the amygdala and the hypothalamus. A predominant locus for pleasurable feelings is the lateral hypothalamus, and if this is damaged, the experience of pleasure and emotional responsiveness is markedly diminished.
The medial hypothalamus is associated with aversive and unpleasant sensations. In deep psychotic depressions, there is loss of appetite, sleep disturbance (insomnia), lack of energy, and loss of libido. The overall organization of the hormonal and autonomic nervous system is clearly involved, and the circuits of the hypothalamus are strongly affected by norepinephrine and serotonin.
The Hypothalamic-Pituitary-Adrenal axis is involved also in the hypersecretion of cortisol, which suppresses norepinephrine synthesis and leads to damage to multiple neuronal systems, such as the caudate and hippocampus.
The cortex of the brain is also involved in depression, independent of the brainstem systems described above. Studies of EEG, PET, and fMRI, as well as clinical correlations from patients with stroke, trauma, and tumor, have described a fairly consistent picture.
In the frontal lobes, increased activity in the right prefrontal cortex or decreased activity in the left lateral prefrontal cortex results in depression. The right frontal lobe increases its actions in response to negative events or negative moods. The left prefrontal cortex appears to modulate the time course of the emotional response, especially the recovery time. It projects to the amygdala and the hippocampus to suppress the memory cycle, otherwise, the amygdala stays active and maintains the aversive response. Therefore, the left PFC shortens negative affect and lengthens positive affect, by suppressing amygdala activity. The right PFC appears to do the opposite. Therefore, you have to be in your left brain to be in your right mind.
There are also important changes in the cingulate cortex and anterior insula which occur during both normal sadness and pathologic depression. These regions are responsible for self-awareness and for error detection, both of which are distorted in depressive episodes.
Some good news in the midst of this is that the changes in the cortex and brainstem are reversible with successful treatment, either with psychotherapy or with medication. PET studies with an antidepressant showed increases in left anterior cingulate activity and left insular activity with successful relief of the depressive symptoms. So activities that increase the left frontal lobe and cingulate function would be likely to ameliorate depression and sadness.
The overall integrative model of mood disorders starts with a predisposing hereditary component. In identical twins, there is a 69% concordance for depression, regardless of whether the twins are raised together or apart. The risk in first degree relatives, such as siblings, is 13%.
In this genetic environment, there is then a developmental predisposition. Parental conflict in parents with similarly affected genetics results in increased rates of separation and divorce as well as intrafamily violence and aggression. With these poor coping skills and poor parenting skills in the environment, there is a developmental object loss and poor development of the individual affected. The earlier the onset of this loss, the increased severity of the episodes of depression, and more likely the development of personality disorders and refractoriness to treatment.
With the development of this damaged temperament, a dysthymic approach to life (think of Eeyore in Winnie-the-Pooh), or a cyclothymic roller coaster mood style is fostered. These temperaments can persist for years before the onset of clinical major depression. They can predispose people to interpersonal friction, abnormal emotional arousal, sleep loss, and drug use. Life events and environmental adversities then impact a person with poor interpersonal support. This results in changes in the brain described above, with consequent major depression and potentially psychosis.
Even in normal people, there is a positive/negative asymmetry in experience. A single negative event requires multiple good events to counteract and rebalance the individual. People have more words for negative emotions, in all languages tested, than they have for positive emotions, and they use them more frequently. Studies of cognitive processing show that bad events and emotional experiences tie up more brain activity and have greater behavioral effects than pleasant emotions. In tests of how people regulate their own affect, people spend more time escaping bad emotions than in fostering good emotions.
In relationships, observations of marital interactions show the same heavy weighting to negative events. Gottman’s work on videotaped interactions of couples and the ability to predict marital discord and divorce from even subtle negative cues is a great example of this. In these relationships, decreasing the negative interactions was a much more powerful agent of change and improvement than increasing the positive interactions. Gottman’s ratio for evaluating interactions in relationships turns out to be greater than five positive interactions for every negative interaction in order to avoid future discord. It seems rational to conclude that handling oneself would require at least that ratio of positive to negative experiences in order to facilitate emotional health.
Good needs to triumph by sheer force of numbers.
It also helps to hold the number of choices to the minimum necessary. People who like to maximize their choices, in contrast to people who are satisfied with a few options, are not necessarily happier. There is a negative correlation between seeking all of the available options and happiness, optimism, self-esteem, life satisfaction. There is a positive correlation between maximizing the options and depression, perfectionism, and regret. People who are searching for all of the options tend to suffer from social comparison syndrome.
This is Part One of a two-part series.