The Day Goes On …

659px-MonoamineOxidase-1GOS

Monoamine Oxidase, Slayer of Neurotransmitters!

I really intended to be blogging more often – or at the very least more regularly … my brain, however, had other ideas.

I’ve been dealing with perhaps the worst, and certainly the longest-lasting, depression of my life. A couple of weeks ago, I began to suspect that the medications I was taking might be contributing to it – there sure as hell wasn’t any real reason for me to be so morose … nothing wrong with my finances, no particular pressure at work, no pressure from my family – they’re in Birmingham, and hardly ever have any contact with me (my fault more than theirs). I’m lonely, and that’s certainly sad: I’m 56 and alone, and the manner in which I live my life makes it exceedingly likely that this won’t change … but that’s a long-since accepted fact, and hardly a justification for depression …

As soon as that thought crossed my mind, I realized that the unfair assumptions of society toward the mentally ill can come from me, as much as anyone.

Depression is not only and exclusively a response to “real” stress! It certain can be a response, as in the death of a loved one, the loss of a long-standing job, the departure of the children from the nest – each of these are real reasons to be depressed and no one would deny for a second that depression in such cases is justified 

Depression does not require a real stressor, though. Depression is a biochemical reaction in the brain (we can talk about the spirit a little later – it does have an effect, but the neurological fact is, if your brain chemistry is fucked, no amount of positive thinking is going to help!) More importantly, I shouldn’t have to justify it! If you have the flu, you don’t have to explain to your boss the actions of antigens, or the reasons why yours are too low to deal with the virus! You just say “I’m enmiserated … miserified … miserablated – look, I’m sick, ok?”

And he sends you home. Just like that.

In America, you freaking can’t go to your boss and say “I’m too depressed to work” – he’ll certainly ask, if he’s a fair and decent person, “What’s the problem? What’s making you so down?”

A reply of “I’m bipolar”, or “I have Major Depressive Disorder” is going to leave him staring blankly at you. “But isn’t there some sort of trigger?” he’ll likely ask – and remember, this is a good guy, he’s not consciously prejudiced, he’s not consciously discriminating: he just freaking doesn’t understand! He’s in good company, too:  most physicians, while they do know slightly more about mood disorders than the general public, still have a really hard time understanding a completely endogenous depression – that is, one without a visible cause – despite that being one of the distinguishing marks of this illness!

Endogenous Depression is essentially the result of too little serotonin in the brain … that’s a gross over-simplification, but it’s the nearest most of us can get to grasping the facts, unless you have a degree in Neuroscience, Psychiatry, or Biochemistry (I sure as hell don’t! ). Serotonin is a neurotransmitter – a chemical produced at the end, or axon, of certain nerve fibers. Serotonin is responsible for transmitting a signal from that nerve, to the dendrite, or receiver, of the next nerve. The Axons and Dendrite’s don’t touch: there’s a microscopic space between them – and this space, known as the Synaptic Cleft, or Synapse – is the reason we need neurotransmitters: electrical charge can’t cross that gap … instead, an electrical charge stimulates production of the neurotransmitter, and it bridges the gap just long enough to transmit the signal. The really cool thing about this mechanism is the way in which neurotransmitter production is stimulated – it’s a miracle of design/evolution (whichever of those you accept):  the greater the electrical charge, the more neurotransmitters are produced, and the longer the connection is maintained in the synapse … the longer the connection is maintained, the greater the electrical charge generated in the dendrite to carry the signal along …

People usually think of the brain working like a computer: if they imagine activity at the level of nerves at all, they tend to think it’s a simple on/off kind of deal – it’s not, though. The mechanism I just described makes the process analog, not digital, and an analog process is the only kind that can make life possible: nerves transmit signals weakly, or strongly … if the signal is strong enough, it goes through the synapse – but the dendrite then ‘decides’ whether it’s strong enough to pass on, and, if it is, how strongly to send it …

Think of sorting your e-mail: some messages are junk and you trash them … some are of very low priority, or don’t have much impact on you, so you note them, and put them away … some messages are important and require a reply … the dendrite evaluates how ‘important’ the signal is, based on signal strength, but instead of replying, it passes the message on forward, to the next nerve.

Now imagine this process happening in huge bundles of nerves, called pathways – each dendrite in that pathway makes its own decision … it allows for an incredible degree of sensitivity, and an enormous range of responses – it’s what makes it possible for you to hate, dislike, be indifferent to, like, really like, or love an experience, and every shade in between!

Except, in depressives, that mechanism is broken … without enough serotonin, signals don’t go through, or they go through very weakly … instead of that range of hate through love, everything comes through flat, as unsatisfying

Diagram from Wikipedia article 'Neurotransmitter', Public Domain

Diagram from Wikipedia article ‘Neurotransmitter’, Public Domain

It may not be just a matter of neurons not producing enough: it could be that serotonin is being consumed before it can act, or taken back up by the axon before it transmits its signal – each of these mechanisms have been suggested, and each would account for the activity that’s been observed or theorized. It would be entirely in keeping with the nature of life if all of these mechanisms are active. (Scientists love to treat their hypotheses as exclusive of any other hypothesis – and time after time discover that the truth is somewhere between Scientist A’s idea, and his arch-enemy Scientist B’s idea … or that both ideas are correct, or that neither idea is correct and the truth is far more improbable than either A or B ever imagined (but they’ll each teach the newly-proven truth as being self-evident, and conveniently forget that they ever thought anything different! Theories of light are a terrific example: Newton was certain light was composed of particles, Huygens was just as certain it was made up of waves – Quantum Theory showed it to be BOTH …)

The thing is, serotonin, like other neurotransmitters, gets re-absorbed by the axon that produced it incredibly quickly … if it’s not reabsorbed right away, it gets destroyed (metabolized) in the synapse almost as quickly … and if, for any reason, the  axon is slow in replacing the destroyed serotonin, it’s unable to transmit signals as efficiently …

So maybe the axons in a particular part of my brain (the Limbic System, if you’re curious) don’t produce serotonin quickly enough … maybe the enzymes that destroy serotonin are present in unusual quantities in my brain … or maybe my axons are especially good at sucking serotonin back out of the synapse … any or all of these may be true, and the nerves of my Limbic System won’t be as active as they should be – and that lack of activity translates to depression!

That’s some pretty freaking heavy neurochemistry to explain to even the most patient and supportive of bosses.

The most effective anti-depressants work on one of those theories. Some prevent the cells from reabsorbing serotonin ( the SSRI’s or selective serotonin re-uptake inhibitors, like Prozac, Celexa, Lexapro, Paxil, and Zoloft.) Others inhibit the enzymes that destroy serotonin in the synapse (the MAOI’s or Monoamine Oxidase Inhibitors.) Still others act to both inhibit re-uptake, and block inappropriate receptors so that more serotonin remains available (these are the Tricyclic Anti-depressants.) All of these have been proven effective in fighting depression – the thing most people just don’t get is that these drugs don’t make people happier:  some prevent the obsession … the tendency to brood over unpleasant subjects … others seem to have the effect of enabling people to have pleasure (by enabling transmission on those pathways) … that’s the symptom “normal” people have the most difficulty with: the idea that a person is simply, physically, unable to enjoy, or take pleasure in things!

Try to explain it till you’re blue in the face, but most people, faced with declarations like I can’t enjoy anything … nothing feels fun anymore … everything’s an effort … will simply assume that you’re being childish, weak, whiney, etc …

Most Americans will never accept that there’s a physical cause to such things, no less valid than the physical lack of Insulin that causes diabetes, the physical degradation of nerves that causes Parkinsonism, or the physical damage that makes a paraplegic unable to use his legs!  None of the latter people have to justify their condition – and no one would ever claim that any of them was being ‘whiney’!

Worse still, there are some psychiatrists who claim the entire neurotransmitter theory of mood disorders is wrong … personally, I find it disturbing that A) most of these guys are psychotherapists (you can’t talk a neurotransmitter imbalance away, so anti-depressants are killing their businesses), B) they seem unwilling or unable to suggest why anti-depressants work, and C) they have no better theory to offer!

Look, I’m not a doctor, not a neuroscientist, not a biochemist or a chemist, or any sort of scientist at all – but, in my opinion, if someone screams that a useful theory is wrong, and doesn’t offer a theory equally as useful, they can just shut the fuck up!

It’s possible to put someone on the edge of a diabetic coma, using medication. It’s possible to make people hallucinate using the psychedelics. It’s possible to paralyze people in whole or in part, to simulate paraplegia, and quadriplegia. It’s possible to reproduce any number of medical conditions, so that other people can feel what any of those conditions are like (and usually their imaginations are adequate enough that they don’t need such demonstrations) … but I’m not aware of any way of duplicating the sensation of anhedonia – the inability to experience pleasure … and I think that goes a long way toward explaining the lack of understanding! I said something along these lines to a friend who immediately scoffed that barbiturates, or ‘downers’ duplicated depression, and he’d actually enjoyed those back in the 60’s …

I wanted to punch his stupid face. Instead, I explained quietly, “Barbs, do not mimic the effects of depression – most of them are hypnotics that put you in a dreamlike state, or just flat reduce you to unconsciousness … they do not keep you from enjoying things. They do not keep you awake at night. They don’t make the effort of brushing your teeth something that brings tears to your eyes! THEY DO NOT FUCKING MAKE YOU OBSESS OVER EVERY MISTAKE YOU’VE EVER MADE IN YOUR FUCKING LIFE!!!!”

Obviously, at some point during my discourse, my quiet, patient, tone changed. My friend moved back from me. His eyes were the size of dinner platters. I could actually see my reflection in them …

I walked away. He tried to talk to me the next day. Tried to apologize. I was well into a dysphoric state by then, and didn’t want to hear anything from him … Eventually things were ok between us, but, in the back of my head, I could still see the look of wide-eyed fear on his face, and I felt ashamed nearly every time I looked at him. Three months later his mother and little sister died in a car wreck … I didn’t see him or hear from him for a month, as he was in his home state dealing with things. When he came back, I offered my condolences.

He said, “I never believed you – about depression, I mean … I’d seen people suffering, but some part of me always thought that’ll never happen to ME: I’d handle things better … I get it now.”

I said, “I’m sorry you had to learn about it …”

But I wasn’t. I was sorry his kin had died. I was sorry he was suffering. I genuinely wished there was something I could do to comfort him – but I knew that time would take his pain away.

Time only makes me older.

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~ by dourscot on January 27, 2015.

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