Why do we get depression?

Why do we get depression?

We still don’t really know what causes depression well enough for us to pinpoint the mechanism to treat depression with one particular thing. We can often see correlations between things to deduce more or less from what someone gets depressed, but that isn’t exactly the same thing. The mechanics of it and the physiology is still too tricky for us to answer in a good way. Easily said, neurotransmitters and activity in some areas of the brain seem to be part of the answer, but that’s practically the answer to everything related to the brain, so that doesn’t tell us anything now, does it?

I love questioning why. That’s not just my profession, but also my hobby. Practically a lifestyle if I get to say so myself. Questioning why here, isn’t just amusing, however. It’s often REALLY tricky – but in return, it could be life-changing.

The answer to why we get depressed depends on who you ask. If you ask people interested in the brain and small things, they are more likely to go for neurotransmitter theories or something similar. Some behaviorists look at behaviors, obviously. Those interested in lifestyles look at whole populations and how they live. This isn’t odd in any way. If you focus on one area, you’ll see things with that filter. If you just bought a new car – you’ll compare cars for a while, because you happen to be interested in that right now. If you’re nose deep in any subject and interested there – that’s what you’ll focus on and that’s how you’ll look at the world and things in it. Bias isn’t strange. People are good at – and interested in –  different things. That doesn’t affect why we get depressed. Perhaps it’s more complex?

The Serotonin Theory

We can’t possibly suffer from depression like this simply because we lack pills, can we?

If so, how come more pills are being prescribed simultaneously as people suffer more and more?

There’s got to be something else..?

There are a lot of models to explain the why of depression. Sometimes levels of dopamine need to increase. Perhaps the activity level somewhere is wrong. The most known one is, without a doubt, the serotonin theory. Since selective serotonin reuptake inhibitors, SSRIs, work for some in some cases depression must be because we lack a portion of serotonin in the synaptic cleft… right?

When this is the theory, I love to question why. Why the heck would we lack some serotonin there? And if there’s a great answer to why, which I’ve never gotten, I’m still curious if that isn’t quite… unpractical. But sure, pathologies are. But is depression something pathological or is it rather a function of some sort?

In short, this theory seems to be quite outdated. It doesn’t really cut it anymore. It would be great if it did, but if this was spot on we would be done with depression since we prescribe more SSRIs now than ever before.

The theory started circulating about fifty years ago and we used more or less the same substances then, as we do now… despite the uncertainty of their excellence.

Do we use them because it’s simple?

Because a lot of others do?

Is it because we’ve done so for so long and it sometimes works?

It is because we lack the resources to give every depressed patient a better option?

If kids get them it can’t be particularly dangerous, can it?

In the cases where they do work I don’t mind them the least. I like what works. But this is kind of the go-to solution most of the time, and it seems as if they don’t work most of the time. This is, in a lot of cases, the first – and the last – treatment method to do something about depression. And it’s not the last because they work, but because that’s it. That’s what you get.

The side effects of these obviously tell us that they do something. That’s for sure. Which ones you get slightly depends on what substance you get, but common ones are:

Fatigue and an increased need to sleep.

Trouble sleeping.

Nausea and vomiting, which could make it troublesome to dose these things right. “Did I throw up my pill?” If you did you’ll be uncomfortable because you didn’t get your dose. If you didn’t, but add another pill, you’ve increased your dose.

A constant feeling of stress, agitation, anxiety and restlessness that come with abnormal sweating.

Emotional numbness, rather than increased happiness. This one might be a net-positive, but it’s not straight out a mood-enhancer.

More or less hunger and increased or decreased weight.

Sexual dysfunction, lack of interest or inability to orgasm.

Is anything familiar there from the “what is depression”-chapter? How many of the side effects match the symptoms of depression itself? Being fine and getting too many of these could practically get you a depression diagnosis.

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Counter evidence?

If we look at what Irving Kirsch concluded in 2014 in “Antidepressants and the Placebo Effect” in Zeitschrift fur Psychologie. 2014; 222(3): 128–134, it seems as if most people could manage fine without the SSRIs.

The abstract of the study tells us the following:

“Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.”

They went through practically everything relevant to SSRIs, published or not, and deduced that placebo seems to be the effect… Which isn’t bad in and of itself. An effect is an effect, regardless of how it works, but according to this, it won’t magically solve any serotonin troubles. If you do believe in the effect, they could make a great change. If that’s the case, ignore everything I’ve gone through this far and ignore what I tell you about the subject in the future.

The first result when I google “serotonin theory of depression” right now takes me to pub med and a text with the title “What has serotonin to do with depression?” by Philip J Cowen and Michael Browning. It tells us this:

“The “serotonin hypothesis” of clinical depression is almost 50 years old. At its simplest, the hypothesis proposes that diminished activity of serotonin pathways plays a causal role in the pathophysiology of depression. This notion was based on the depressogenic effects of amine depleting agents such as reserpine, as well as the actions of antidepressant drugs such as monoamine oxidase inhibitors and tricyclic antidepressants, discovered by clinical serendipity, but later found in animal experimental studies to potentiate the effects of serotonin and other monoamines at the synapse (1).

This pattern of theory making – moving from the pharmacological actions of drugs with some efficacy in treatment to biochemical notions of causation – has been common in biological psychiatry. In such an undeveloped field this approach, though logically precarious, has been a useful heuristic and, in the case of the dopamine hypothesis of psychosis, has been strikingly upheld by advanced brain imaging techniques (2). However, the serotonin hypothesis of depression has not been clearly substantiated. Indeed, dogged by unreliable clinical biochemical findings and the difficulty of relating changes in serotonin activity to mood state, the serotonin hypothesis eventually achieved “conspiracy theory” status, whose avowed purpose was to enable industry to market selective serotonin reuptake inhibitors (SSRIs) to a gullible public (3).”

Since SSRI works for so few,

despite how much we use it,

I don’t think this outdated theory should have its place in the spotlight anymore.

I think it’s more complex.

Is the answer environmental?

There is a theory about depression where the thought is for it to actually depress us, as a sort of hibernation. The point and the plan are to depress you enough to withdraw from others and rest. That’s not entirely crazy, is it? If you’re in an environment good enough to thrive, you’re likely not depressed. If you’re in an unfit environment, you get depressed – and then you withdraw, escape, rest, and hide.

I wouldn’t mind thinking there’s something to this.

Is the answer behavioral?

Jordan B Peterson uses lobsters to make a point about hierarchies in his book “Twelve rules for life”. He tries to disprove the point or argument that hierarchies are social constructs “invented to allow certain people (such as white men) to have power over others”.

Bear with me and relax here. My point is, in fact, not about hierarchies. If you’re curious about the sources about lobsters and Peterson, they do their best to flood the internet. It’s just a google-search away.

Anyway, he says that hierarchies are natural to some extent and prove this point by using the example of lobsters, with whom we share a common evolutionary ancestor. “Like humans, lobsters exist in hierarchies and have a nervous system attuned to status which “runs on serotonin” (a brain chemical often associated with feelings of happiness). The higher up a hierarchy a lobster climbs, this brain mechanism helps make more serotonin available. The more defeat it suffers, the more restricted the serotonin supply. A lower serotonin level is associated with more negative emotions – perhaps making it harder to climb back up the ladder.”

According to Peterson, hierarchies in humans work similarly – we are wired to live in them. But the interesting point for someone who’s not interested in hierarchies, such as me? The research itself, and the behavior-loop we see in those lobsters, rather than their conclusion. The facts included in the story tell us that serotonin is highly connected to dominance and aggressive social behavior in said lobsters. “When free moving lobsters are given injections of serotonin, they adopt aggressive postures similar to those displayed by dominant animals when they approach subordinates”.

Is that one point to anti-depressants? Not necessarily. The entire neurology field is complex, likely (hopefully) more so in humans than in lobsters as they lack brains and have an “agglomerate of nerve endings” instead. But as said, I’d like to steal the small facts that come out of how they behave.

So here’s my point: two lobsters start with the same amount of serotonin and they fight since that’s what lobsters do.

One wins – more serotonin makes him confident, aggressive, and dominant so he keeps winning. Positive feedback loop to grow, get more food, ladies, and seawater. This first one will keep acting and trying, which will lead to the fact that it might keep winning, and that’s a lovely positive feedback loop compared to the one who loses. The loser will get less serotonin equals shy, small, suppressed, and fearful so he keeps losing. Still a positive feedback loop, but to get less and less, he’ll continue to shrink and despise life. The spiral continues to strengthen the slippery slope, but one of failure, instead of the one of success the first lobster had.

When I treat people I often do so by changing behaviors as a part of it, so I definitely believe there’s something to this.

Learned helplessness

Learned helplessness could be one part of it all and goes hand in hand with the behavioral parts, but it feels as if it’s worth mentioning on its own. I won’t cover it in length here, but the point of it is that you tried – and learned that everything is hopeless. Trying again and again, and getting nothing but drawbacks, beatings, and negative outcomes. That makes you smaller, like the losing lobster I mentioned. This turns into a positive feedback loop where you fail, care less, try worse, get worse results, and on and on it goes.

The more time we do something, the better we get at it. The more this happens, the more it continues to happen. Unless there’s a thought-through solution that you actively try to go for to change that path. Behaviors work the same way. Do something, and you’ll likely do it more and more. The further you go on with behaviors, the harder they stick, and they get harder to change. It’ll work with the thought patterns of depression, anxiety, and everything you did to get you there.

Is the answer related to chemistry and physiology?

We are complex creatures, so we could be influenced and affected by an incredible amount of variables. A lot of mechanisms need to work in harmony for us to work decently. Those need to work even better for us to work ideally. This is proven when we get a tiny flaw in our genome to get deformed or handicapped. Cell division going wrong gives us cancer, which could kill us unless the immune system saves us before it’s too late.

There’s a tremendous amount of chemistry and physiology going on inside us, where one thing affects the other and a bunch of them together keeps a system going and working as it should. Then there’s a vast number of systems, where just one faltering is enough for us to die. It’s astonishing that we’ve got the average age we do when thinking of this.

For all of this to work decently enough for you, you’ll need input from a lot of different things. Nutrition, to start with something obvious. For a plant, that is more or less water, carbon dioxide, and some minerals. For you, the input necessary from nutrition consists of a bizarre number of different molecules in comparison. That is to get all the energy you need and to keep all of your functions working, to keep you alive – or thriving.

Too little of something necessary and functions will falter. They might work to some degree – or not at all. Blood should go around and around by having the heart beating, muscles should be functional by contracting and relaxing when they should and growing when necessary, the brain and nervous system got to do their thing – and that’s a lot of things, in a really delicate system. There are hormones and there are tissues where everything needs their building blocks, signals from something, and enough energy to actually do their thing. Everything needs to come from somewhere, be broken down into appropriate enough parts, transported, modified, and rebuilt to turn into something useful.

That’s one thing, nutrition. Then there are signals from other things, like light, to keep us updated about when we ought to be up and running or when we should wind down. Both light, preferably sunlight, and sleep has been shown to be a big deal when it comes to depression, which could be relevant for those who are most affected by the seasonal affective disorder, SAD. Those who are affected by SAD usually get worse when it gets darker, but then there are those who get their worst period in the spring. Is that confusing? It most definitely is.

To influence this one could use bright lights, which ought to decrease melatonin to make you less sleepy. Darkness increases the amounts and signals to you that it’s time to go to bed. But some things show that darkness decreases the amount of serotonin as well. Does that matter? If it does, how much?

Actual pathologies and physiological troubles are not to be neglected, but I’m having a hard time looking at depression as the pathology itself. I’m sure there is something going on inside the organism and in the brain to cause all the symptoms, but is that the core problem or the symptom? It’s definitely a handicap, but since we don’t know why, it’s hard to pinpoint if it’s a bug or a feature.

ADHD or ADD could increase the risk of getting depression.

Hormonal troubles like hypothyroidism could cause depression. With that malfunction, all of you get slower and closer to hibernation because you’re not using the gas pedal – your metabolism – enough. When that’s the case, depression seems to be close at hand. The same thing goes for premenstrual troubles for women, where hormones go completely haywire.

These are relevant factors, but which one is the hen and the egg? Does one cause the other as a symptom… or do you get another disease, depression, with the first?

Other factors and reasons why could be

As mentioned everywhere, too much stress or long-term pain are great reasons.

But there’s also a fair share of genetics, which could be quite unfair. Unfortunately, that’s life.

Medication, too much alcohol, or using the wrong kinds of drugs in the wrong way could greatly increase the risk.

Some mention diet as one factor. If the diet causes inflammation, that’s not necessarily a terrible thought. Gluten is one thing some people point at. Some do so with everything; when that’s the case it sounds less reliable. Some are extremely sensitive and allergic to gluten on the other hand, in their cases, it’s completely rational to keep far away. If it’s easy to avoid and you think it’s worth doing, that’s a small cost to check another maybe-box. Other diet-related things could be sugar, red meat and things that increase the insulin levels a lot, since those might be pro-inflammatory.

So WHY?

It seems as if more people thought it was worth living a few years ago. We don’t even have to back up that much. I might, of course, be totally wrong about this, but I think people suffered from the concept of depression less some time back. There is definitely evidence that depression was around, but I think it was far from as common then as it is today.

I think it’s not a question of pills, and I do believe that it’s something that increased with the modern world. If that’s right this ought to be a question of life somehow, right?

People and their lives and all their aspects are vast and complex. Life is hard. It’s full of troubles, issues, problems, and hassles: Murphy’s law, war, and evil. But plenty of us seem to find that it’s worth living anyway. Some even seem… provocatively content.

Is our high standard of living a problem today? Did people have less existential dread and angst before we got this wealthy? When people had to work in the fields and do things manually they didn’t have the time to bother with the higher levels of Maslow’s hierarchy of needs. Could that be it? Could we suffer more because we’re quite fine physically – but suffer more in imagination than in reality, as Seneca says?

I think it’s reasonable to think holistically about this. In some cases, one thing might be what bothers you, and that’s fine, but when speaking about a general why, that can’t be the answer. You might be bullied or threatened – and that’s reason enough to be depressed. Perhaps you’re ill in some way or grieving. You don’t necessarily have to be depressed because of a thousand reasons. But there are likely a thousand to get depressed from. There’s the difference.

I think it’s reasonable to keep all of it in mind, because every and any single on could be the reason. How we’re created and how we work with anatomy and physiology in relation to our habits, behaviors and everything else that might be relevant. Again with the bio-psycho-social perspective.

We’ve evolved to function in a specific way and in a more or less specific environment, even though we’re quite adaptable. We’re likely better suited in a hunter-gatherer society than in the modern world. But now we’re here, so we’ll have to make the best of it. But if we drift too far from what we’ve created for I think depression might very well be a consequence.

A good question, to begin with, could be “Is your life in order or are you depressed for a good reason?”

If you’re curious there’s more about it in the book found at www.mbdolor.com/book!

Full series:
The Big Three: What Is Depression?
Why Do We Get Depression?
Treat Depression

Why do we get depression?

It’s too complex to answer that easily. It could be a vast amount of things, but in some sort of way we’re not satisfied with life. Not giving the organism enough in one area could be enough; we need to look at everything when answering this, biological, psychological and social aspects.
We still don’t really know what causes depression well enough for us to pinpoint the mechanism to treat depression with one particular thing. We can often see correlations between things to deduce more or less from what someone gets depressed, but that isn’t exactly the same thing. The mechanics of it and the physiology is still too tricky for us to answer in a good way. Easily said, neurotransmitters and activity in some areas of the brain seem to be part of the answer, but that’s practically the answer to everything related to the brain, so that doesn’t tell us anything now, does it?

What is the Serotonin Theory?

The theory started circulating about fifty years ago, and the point, in short, is that we lack serotonin in the synaptic cleft. Irving Kirsch writes, in relation to the subject: “Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory.

Is the Serotonin Theory right?

It’s pretty outdated, I’d say. If anti-depressants can either increase or decrease the serotonin levels… Or do nothing and still get the same effect, whether positive, negative, or just a bunch of side effects, said serotonin levels seem irrelevant.

Irving Kirsch writes, in relation to the subject: “… analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin.Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong.”

Are anti-depressants dangerous?

They are volatile medications where things could go both ways. With suicidal patients, they are, to the degree where some physicians do get more careful to prescribe them if the patient seems prone to end their life.
Irving Kirsch writes, in relation to the subject: “Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.”
Personally, I sure hope not when I see how many of them get prescribed. My guess is that the most dangerous thing about them is all of the side effects. The suicides because of the pills themselves are likely relatively few, but most people eating them will get side effects.

Are there counter evidence to the serotonin theory?

If we look at what Irving Kirsch concluded in 2014 in “Antidepressants and the Placebo Effect” in Zeitschrift fur Psychologie. 2014; 222(3): 128–134, it seems as if most people could manage fine without the SSRIs.
The abstract of the study tells us the following:
“Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.”
They went through practically everything relevant to SSRIs, published or not, and deduced that placebo seems to be the effect… Which isn’t bad in and of itself. An effect is an effect, regardless of how it works, but according to this, it won’t magically solve any serotonin troubles. If you do believe in the effect, they could make a great change. If that’s the case, ignore everything I’ve gone through this far and ignore what I tell you about the subject in the future.

The first result when I google “serotonin theory of depression” right now takes me to pub med and a text with the title “What has serotonin to do with depression?” by Philip J Cowen and Michael Browning. It tells us this:
“The “serotonin hypothesis” of clinical depression is almost 50 years old. At its simplest, the hypothesis proposes that diminished activity of serotonin pathways plays a causal role in the pathophysiology of depression. This notion was based on the depressogenic effects of amine depleting agents such as reserpine, as well as the actions of antidepressant drugs such as monoamine oxidase inhibitors and tricyclic antidepressants, discovered by clinical serendipity, but later found in animal experimental studies to potentiate the effects of serotonin and other monoamines at the synapse (1).

This pattern of theory making – moving from the pharmacological actions of drugs with some efficacy in treatment to biochemical notions of causation – has been common in biological psychiatry. In such an undeveloped field this approach, though logically precarious, has been a useful heuristic and, in the case of the dopamine hypothesis of psychosis, has been strikingly upheld by advanced brain imaging techniques (2). However, the serotonin hypothesis of depression has not been clearly substantiated. Indeed, dogged by unreliable clinical biochemical findings and the difficulty of relating changes in serotonin activity to mood state, the serotonin hypothesis eventually achieved “conspiracy theory” status, whose avowed purpose was to enable industry to market selective serotonin reuptake inhibitors (SSRIs) to a gullible public (3).”

Are there environmental reasons to get depressed?

There is a theory about depression where the thought is for it to actually depress us, as a sort of hibernation. The point and the plan are to depress you enough to withdraw from others and rest. That’s not entirely crazy, is it? If you’re in an environment good enough to thrive, you’re likely not depressed. If you’re in an unfit environment, you get depressed – and then you withdraw, escape, rest, and hide.
I wouldn’t mind thinking there’s something to this.

Are there behavioral reasons to get depressed?

Jordan B Peterson uses lobsters to make a point about hierarchies in his book “Twelve rules for life”. He tries to disprove the point or argument that hierarchies are social constructs “invented to allow certain people (such as white men) to have power over others”.
Bear with me and relax here. My point is, in fact, not about hierarchies. If you’re curious about the sources about lobsters and Peterson, they do their best to flood the internet. It’s just a google-search away.
Anyway, he says that hierarchies are natural to some extent and prove this point by using the example of lobsters, with whom we share a common evolutionary ancestor. “Like humans, lobsters exist in hierarchies and have a nervous system attuned to status which “runs on serotonin” (a brain chemical often associated with feelings of happiness). The higher up a hierarchy a lobster climbs, this brain mechanism helps make more serotonin available. The more defeat it suffers, the more restricted the serotonin supply. A lower serotonin level is associated with more negative emotions – perhaps making it harder to climb back up the ladder.”
According to Peterson, hierarchies in humans work similarly – we are wired to live in them. But the interesting point for someone who’s not interested in hierarchies, such as me? The research itself, and the behavior-loop we see in those lobsters, rather than their conclusion. The facts included in the story tell us that serotonin is highly connected to dominance and aggressive social behavior in said lobsters. “When free moving lobsters are given injections of serotonin, they adopt aggressive postures similar to those displayed by dominant animals when they approach subordinates”.
Is that one point to anti-depressants? Not necessarily. The entire neurology field is complex, likely (hopefully) more so in humans than in lobsters as they lack brains and have an “agglomerate of nerve endings” instead. But as said, I’d like to steal the small facts that come out of how they behave.
So here’s my point: two lobsters start with the same amount of serotonin and they fight since that’s what lobsters do.
One wins – more serotonin makes him confident, aggressive, and dominant so he keeps winning. Positive feedback loop to grow, get more food, ladies, and seawater. This first one will keep acting and trying, which will lead to the fact that it might keep winning, and that’s a lovely positive feedback loop compared to the one who loses. The loser will get less serotonin equals shy, small, suppressed, and fearful so he keeps losing. Still a positive feedback loop, but to get less and less, he’ll continue to shrink and despise life. The spiral continues to strengthen the slippery slope, but one of failure, instead of the one of success the first lobster had.
When I treat people I often do so by changing behaviors as a part of it, so I definitely believe there’s something to this.

What is learned helplessness?

The point of it is that you tried – and learned that everything is hopeless. Trying again and again, and getting nothing but drawbacks, beatings, and negative outcomes. That makes you smaller, like the losing lobster I mentioned. This turns into a positive feedback loop where you fail, care less, try worse, get worse results, and on and on it goes.
The more time we do something, the better we get at it. The more this happens, the more it continues to happen. Unless there’s a thought-through solution that you actively try to go for to change that path. Behaviors work the same way. Do something, and you’ll likely do it more and more. The further you go on with behaviors, the harder they stick, and they get harder to change. It’ll work with the thought patterns of depression, anxiety, and everything you did to get you there.

Do we get depressed because of neurotransmitters, chemistry and physiology?

We are complex creatures, so we could be influenced and affected by an incredible amount of variables. A lot of mechanisms need to work in harmony for us to work decently. Those need to work even better for us to work ideally. This is proven when we get a tiny flaw in our genome to get deformed or handicapped. Cell division going wrong gives us cancer, which could kill us unless the immune system saves us before it’s too late.
There’s a tremendous amount of chemistry and physiology going on inside us, where one thing affects the other and a bunch of them together keeps a system going and working as it should. Then there’s a vast number of systems, where just one faltering is enough for us to die. It’s astonishing that we’ve got the average age we do when thinking of this.
For all of this to work decently enough for you, you’ll need input from a lot of different things. Nutrition, to start with something obvious. For a plant, that is more or less water, carbon dioxide, and some minerals. For you, the input necessary from nutrition consists of a bizarre number of different molecules in comparison. That is to get all the energy you need and to keep all of your functions working, to keep you alive – or thriving.
Too little of something necessary and functions will falter. They might work to some degree – or not at all. Blood should go around and around by having the heart beating, muscles should be functional by contracting and relaxing when they should and growing when necessary, the brain and nervous system got to do their thing – and that’s a lot of things, in a really delicate system. There are hormones and there are tissues where everything needs their building blocks, signals from something, and enough energy to actually do their thing. Everything needs to come from somewhere, be broken down into appropriate enough parts, transported, modified, and rebuilt to turn into something useful.
That’s one thing, nutrition. Then there are signals from other things, like light, to keep us updated about when we ought to be up and running or when we should wind down. Both light, preferably sunlight, and sleep has been shown to be a big deal when it comes to depression, which could be relevant for those who are most affected by the seasonal affective disorder, SAD. Those who are affected by SAD usually get worse when it gets darker, but then there are those who get their worst period in the spring. Is that confusing? It most definitely is.
To influence this one could use bright lights, which ought to decrease melatonin to make you less sleepy. Darkness increases the amounts and signals to you that it’s time to go to bed. But some things show that darkness decreases the amount of serotonin as well. Does that matter? If it does, how much?
Actual pathologies and physiological troubles are not to be neglected, but I’m having a hard time looking at depression as the pathology itself. I’m sure there is something going on inside the organism and in the brain to cause all the symptoms, but is that the core problem or the symptom? It’s definitely a handicap, but since we don’t know why, it’s hard to pinpoint if it’s a bug or a feature.
ADHD or ADD could increase the risk of getting depression.
Hormonal troubles like hypothyroidism could cause depression. With that malfunction, all of you get slower and closer to hibernation because you’re not using the gas pedal – your metabolism – enough. When that’s the case, depression seems to be close at hand. The same thing goes for premenstrual troubles for women, where hormones go completely haywire.
These are relevant factors, but which one is the hen and the egg? Does one cause the other as a symptom… or do you get another disease, depression, with the first?

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