Wednesday, March 27, 2013

Family Profile B: Stress & Depression


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found at {http://www.flickr.com/photos/ruthanddave/}

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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