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Depression may be one of the most misperceived of disease;
it certainly is approached in many different ways. Take into concentration the
variation in neurotransmitters, hormone ratios and genetics in depressive
individuals and you might be in accord with the biologist. Deem the cognitive
attributes of the depressive, a pessimistic and hopeless attitude about their
own skill and life, and you might side with the psychologists. Or, as many
undoubtedly wonder if depressed people simply experience the same hum-drumness
as the rest of us but simply overindulge in it, you might fall into another
perspective category altogether.
Depression is
quite a commonly used word and its clinical meaning can sink into the
over-usage of it. Life can deliver upsetting or disappointing events that make
us depressed feeling, however this is different than a major depressive state,
as it would be diagnosed. There
are in fact parameters that have distinct biological signifiers of depression.
The concentration of this blog is on stress and its effects
on health and disease. Depression is a peculiar disease in this case, though
powerfully correlated to the stress response, whether causally or
consequentially, it is less often viewed in this way. Before, however, I get
into that correlation, I’ll reference a bit of the diagnostic factors that
distinguish a major depressive state from the absence of one.
What do the symptoms of depression look like?
The foremost distinguishing factor of depression is an
inability to feel pleasure. Whether from food, humor, sex, achievement, hobbies
or friendships, the feeling towards these things are typically as inert as any unmemorable
moment would deliver. The depressed person will often feel nothing. In some
cases something, but a negative something - that it doesn’t count, or that the
thing or event is undeserved.
In fact, these repercussions compare to what is called
vegetative symptoms, in which eating and appetite decline, as well as sleep and
sleeping patterns. A depressed individual will typically have no trouble
falling asleep, but for short spurts of time and with disturbed sleeping cycles
between deep, shallow, and dream sleep states. Similarly, depressed people
commonly feature what is called psychomotor retardation, in which the person
has to exert immense effort and concentration in the littlest things. The
person may speak slower because simply adding to a conversation is arduous. Or
they may take twice the amount of time putting on their socks in the morning,
because lifting their leg to their hands requires exhaustive amounts of energy.
There are defining parallels between cognitive patterns and
depressive states quite naturally. For the majority of non-depressed people,
there is a complex array of emotion. Strongly positive emotion and strongly
negative emotion are not inversely related; they can be felt simultaneously to
different degrees. As in a depressed state, this emotional relationship
collapses inversely, often characterized by few positive emotions and many
negative emotions, though not felt simultaneously. Depression is also
characterized by a distorted view of facts, over- or under- analyzed to the
extent that conclusions are drawn that things are awful, getting worse and with
a loss of agency to do anything about it.
Family Profile B: Stress and Depression
Before I begin to annotate the stress-depression
relationship, let me present Family Profile B, a young adult female family
member of mine who has experience depression for much of her life adolescent
and adult years. She does not believe in taking medication for her depression.
Her symptoms seem to come and go regularly in waves. ‘B’ would describe herself
as being prone to depression because she stresses easily. To cushion this
proneness she finds, eating well, exercising, thinking positively and working
incessantly on stress-management benefits her the most.
She also considers this proneness due to hereditary, because
she handles stress similarly to the rest of the family. She has always been a
very emotionally responsive person, which ‘B’ believes has to do with
initiating depressive moods. Similarly, she finds herself sometimes wallowing
in despairing thoughts – about her abilities, about her emotions, about her
relationships, about her prospects. She explains that she is an overly analytical
person as well, basically picking herself apart and arriving at negative
conclusions.
‘B’ describes that she experiences physical symptoms often
times. She fits well into the depressed-person’s sleeping patterns: falling
asleep quick, waking up often and tired. Many times she feels general muscle
achiness all over. This may be related to psychomotor retardation, which she
agrees that she experiences exhaustiveness in small, easy tasks. She explains
how she is always hungry but never for anything in particular. And food does
not taste that good when she is eating. This corresponds with a lack of feeling
pleasure in any and everything that is characteristic of depressive people.
In describing the stress-depression correlation, she agrees
that this is accurately fits her general idea of her depression. ‘B’ even says,
quite understandably, that her depressive symptoms seem to spiral out of
control when she is stressed. She even explains that high-strung, jittery yet
exhausted feeling inside, as she says, it’s like “too much energy and no
outlet.”
What causes depression?
You likely have heard that depression is related to imbalances
in neurotransmitters – the most probable focus being on dopamine,
norepinephrine, and serotonin. These imbalances are not easily understood.
Basically, these neurotransmitters have been held responsible because drugs
that increase the level of signaling by these neurotransmitters seem to assist
in treating depression. Though surely, other neurotransmitters and factors are at
work here.
There are two theories involved here in how drugs treat
depression. The first states that its too high levels of neurotransmitters,
which generate depressive symptoms. So when these drugs, that increase these
levels of neurotransmitters, are given, one would think the depressive symptoms
would increase. And they do, at first. After a certain amount of time, the
receptor cells to these neurotransmitters decrease, or down-regulate,
decreasing excessive signaling and balance the recognized levels. And the
person feels better. (Sapolsky, 2004)
The second theory states that its really too little
neurotransmitters communicating between neuron A and neuron B. Not only does
neuron B have receptor sites for neurotransmitters, but neuron A has them as
well as a means of regulating the amount of neurotransmitters it releases. If
it recognizes too much, it will produce less. If it recognizes too many, it
will produce more. But what happens when neuron A decrease or down-regulates
its receptor sites or autoreceptors? It would recognize too low amounts of
neurotransmitters released and accordingly, release more. (Sapolsky, 2004)
Though the problem gets increasingly more complicated. If
neuron A starts synthesizing more amounts of neurotransmitters, then neuron B
may down-regulate its receptor sites. We’re now back close to the first theory.
Why do these neurotransmitters cause depression?
It helps to know what function these neurotransmitters help
to regulate. Serotonin is thought to relate to incessant ideation in
depression, the looped thought patterns of failure, doom and despair.
Norepinephrine plays a role in alerting other areas of the brain – activating
them or lowering their threshold for response. This is thought to perhaps
explain how psychomotor retardation in depressed people makes small daily tasks
exhaustive. Dopamine is related to the ‘pleasure pathway.’ Robert Sapolsky sums
up this stimulate pathway quite well:
“Something along the lines of “Aaaaah, boy, that feels good.
It’s kind of like getting your back rubbed but also sort of like sex or playing
in the backyard in the leaves when you’re a kid and Mom calling you in for hot
chocolate and then you get into your pajamas with the feet…”” (Sapolsky, 2004)
Of course the complication with treating depression arises
since there are many other factors that can contribute to it. Things like the
body inducing a stress response over a sad abstract thought (Sapolsky, 2004).
Genetics are also heavily at play in the manifestation of depression. However,
genetics rarely destine the health of an individual, it depends on the
environment in how they are expressed. Certain hormones often go hand in hand
with depression.
Perhaps most interestingly, depression and stress are
closely linked. In some instances, people who are prone to depression
experience stressors at a higher rate. On the other hand, people who are
enduring many stressors are more likely to give way to depressive states.
It is common to find elevated levels of glucocorticoid (one
of those stress hormones) in depressed individuals (Sapolsky, 2004). Often, people
with depression are viewed as lethargic, mopey and perhaps even lazy. In fact,
it is more accurate to see them as high-strung, strenuous, alert and on edge,
but all internally. This creates a dynamic and overwhelming battle within a
person where they feel exhausted and drained with every little task but at the
same time, overflowing with panicky apprehension.
So what does the stress-depression relationship look like?
Typically, clinically depressed people have abnormal levels
of glucocorticoids, whether abnormally low or high. It is more often the case
that these levels are too high, coupling an overactive stress-response and an
overactive sympathetic nervous system. That ‘jittery yet exhausted’ feeling
fits like a glove over the chronic stress-response profile. These elevated
levels of glucocorticoid found in depressives appear to arise from too much of
a stress signaling in the brain.
The brain is less effective at shutting off the
glucocorticoid-secreting stress response, activated by the sympathetic nervous
system. Glucocorticoids have a strong influence of those neurotransmitters
described earlier – serotonin, norepinephrine, and dopamine – namely in the
amount of each synthesized, how fast they are broken down, how many receptors
there are for the neurotransmitters and how well the receptors work. It is easy
to see, in this case, how chronically high levels of glucocorticoid in a
depressed person’s system would throw this delicate chemical balance off.
A sustained stress response depletes dopamine from that
‘pleasure pathway’ and norepinephrine from alerting other areas of the brain.
Furthermore, stress modifies all sorts of areas of synthesis, release, efficacy
and recycling of serotonin. Sustained high levels of glucocorticoids can alter
manifold of other mechanisms in the body, but specifically in relation to
depression, it has been found to damage the hippocampus, which deals with,
among other things, memory – specifically, declarative memory. The frontal
cortex of the brain seems to be markedly sensitive to glucocorticoids as well.
Decreased volume of the frontal cortex and the hippocampus is commonly found in
depressed individuals and may have a detrimental correlation with glucocorticoids.
(Sapolsky, 2004)
All of these aspects and more make depression so sufferable
and tricky to climb out of. This is why it is all to commonly heard of that
depression reaches a vicious cyclical nature in which individuals will
continually fall back into depression soon after relief of it. Similarly, being
in a depression is enormously stressful in and of itself, stimulating more
glucocorticoid secretion and deepening that chaotic cycle.
On a lighter note though, it may be hopeful to consider that
depression can often be triggered by stress and not just a mysterious imbalance
in brain chemicals. Although this imbalance ensues with the stress response, it
may be easier and less detrimental to practice better methods of
stress-management rather than find the right antidepressant that best represents
your body’s optimal levels of neurotransmitters.
Reference:
Sapolsky, Robert M. (2004). Why Zebras Don’t Get Ulcers: The
Acclaimed Guide to
Stress,
Stress-Related Diseases, and Coping. New York: St. Martin’s Griffin
Press.
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