SSRI Medication Explained

Standard of Care

Every day, millions of prescriptions are being filled for antidepressant medication. Every day, people all over the world head to their psychiatrist’s office for a visit, call in to their primary care doctor for a refill, and head to the pharmacy to pick up the refill awaiting them. Every day, millions of Americans are taking antidepressant medication (1). The majority of these antidepressant medication prescriptions are for SSRI’s (selective serotonin reuptake inhibitors).


But, it’s not everyday that any one of us feels totally ready and up for asking their doctor to start an antidepressant medication. It requires us enduring a lot of pain, suffering, and confusion to get to that point. For most of us, things have to not only be bad, but reach a boiling point for us to decide to finally take that next step and ask our doctor for help. Things have to become bad enough. That’s when we are finally pushed to open up about anxiety, depression, or other deeply personal and very dark experiences. This is often how people come to start taking an SSRI medication.


For many, antidepressant medications do offer help. They do reduce the intensity of anxiety, sadness, anger, and other uncomfortable symptoms. These medications are not perfect. They are not silver bullets. But, they do help.
Despite that helpfulness, that initial conversation with the doctor can be really hard. Patients walk in to their psychiatrist/doctor’s office fully intending to let it all out. Once inside the office, instead of a crystal clear, pre-rehearsed explanation of what’s going on, what usually comes out are vague descriptions of being “worried a lot” or “feeling down sometimes.” That obviously doesn’t match what’s really going on at home. So it’s odd, but not that odd, that whatever we reveal is typically expressed casually with no real urgency.


How come? Well, it takes courage to share aloud with another person the true extent of one’s mental illness. This is often due to stigma and the prevalent perception that symptoms are a form of weakness. Even if we don’t think that way about other people, when it comes to us, it’s too much to ask ourselves to just say it aloud. It’s embarrassing, even shameful for some. We feel an urge inside us to talk, to get it out. But, in that moment, it can be really scary and overwhelming.
On the receiving end of that apprehension and discomfort is the doctor or psychiatrist. Despite sometimes talking like a robot, all doctors are people too. Like any human, they can feel what their patients are feeling. Even without a patient saying it, doctors can tell when someone’s in pain. And, there is that human urge in them to try and make it better.


That’s a common scenario. A patient desperate for help, but unable to explain things fully. A doctor who’s listening, but also really busy. And a health care system that is putting pressure on the doctor to prescribe the right solution, and quickly. Needless to say, there’s a mismatch here between what is needed and what is available.

Chemicals in Balance

Out of empathy for patient’s suffering and pressure to solve the problem quickly, the mystical, yet highly palatable, “chemical imbalance” theory was born.  For the better part of the last three decades, psychiatry has been offering the chemical imbalance theory as an explanation to patients coming in with complaints about anxiety and depression.
The basic theory goes like this: For reasons we don’t fully know, sometimes people’s brain chemistry becomes imbalanced. This imbalance causes depression and anxiety. But, there are medications that science has developed to correct the imbalance, so we’re all good.


The word imbalance is technical-sounding enough to make it seem like really smart biochemists understand exactly what’s going on, but don’t have a way to explain it to the average person without a degree in neuroscience. It’s also just vague enough to not be so specific that the theory could ever be proved wrong. It’s an imbalance. We got meds to fix it. What else do you need to know?


The term imbalance generally refers to not having low serotonin levels in the brain. In reality, not having enough serotonin is an oversimplification of the problem. Our brains are not like cars, where if you didn’t have enough oil or gas, the car would break down. In the human brain, there’s layers of complexity. Even with the neurotransmitter serotonin, there are multiple unique types of receptors that can be activated by serotonin. In addition, the receiving neurons that get activated by serotonin, then go on to activate other neurons which use other kinds of neurotransmitters like dopamine, glutamate, GABA, etc. It’s a massive network of interconnections likely too complex for us to ever fully understand.


As we take a closer look at brain chemistry, however, things don’t seem as simple as “my doctor says my brain has a chemical imbalance.” The more we dig into brain chemistry, the fuzzier things become. Even in the package inserts for SSRI’s and many other psychiatric medications notes “the exact mechanism… is unknown.” (2) Even the exact cause of depression and anxiety are not fully understood. (3)


Yet, this chemical imbalance theory simplifies things, and makes treatment quick and easy. Quick and easy is what’s needed in the appointments when a person finally musters up the courage to ask their very busy doctor for help. Actually, over time, the chemical imbalance theory has made it easier for people to come and ask for help with mental illness. It turns the focus away from themselves and on to something else… chemicals. Another solution that required more time, investigation, and for that matter, effort, would not work as well in this scenario. With the chemical imbalance theory, all it takes is one sweep of the pen and doctor can feel confident that the patient will feel better. As a bonus, this trimmed down approach still allows the busy doctor to save enough time in their day to take a lunch.


The chemical imbalance theory sounds good, especially when he original reason for coming to the doctor was that everything felt out of balance. Patients tell the doctor how they have been feeling off. The doctor regurgitates that same message, but colors it with technical sounding terms. Thus, chemical imbalance theory carries the benefit of sounding true. It sounds all the more true when it’s coming from a doctor.


Like it or not, SSRI medications, which increase the availability of serotonin in parts of the brain, have been prescribed for, and taken by, millions of people in the past several years. Despite all the concerning shortcuts described above, is it actually true the they help with anxiety and depression? Do they work? Well, yes. So, are things as simple as the chemical imbalance theory says it is? No.
 

The American Way: If Some Is Good More Must Be Better

For some patients I’ve treated, it does seem that using serotonin boosting medications worked. We started the serotonin boosting medications, and a month later those particular patients walk back into the office smiling and seeming 10lbs lighten and 2in taller. They report that their anxiety and low moods are almost completely gone. The relief they have experienced is palpable, and sometimes even surprising to me.


For other patients, unfortunately, the outcome is quite the opposite. They started taking the medication daily, and within a few weeks, their symptoms became worse. Or, after a week or two, they began experiencing some intolerable side effects. The side effects either accompany some mild benefits, or just presents without any benefits to make continuing seem worthwhile at all.


And, there’s a not-so-small minority of patients, for whom the SSRI medication didn’t produce any change - positive or negative. On the one hand, nothing happening is a good thing. No agitation, no shakes, not stomach aches, no headaches… no harm, no foul. But, without any change in their mental health, they are still feeling mentally and emotionally unwell.
It’s not 100% of patients who take SSRI’s who get better. The percent that get better is less than that. I won’t say how much less. This should definitely put into question the chemical imbalance theory that supports the use of these medications. One could say, “oh well, we tried, and it didn’t work, so what… what’s the big deal?’


We could ask, what is the harm of relying solely on medication. What happens if the doctor just prescribes the SSRI, but doctor and patient do not address the anxiety or depression with any other means? Is is possible that delay in making progress was a harm? It likely depends upon how you think about it, but this would be the subtle and hidden harm baked into the cake with the chemical imbalance theory. The same confidence that may have helped some start an SSRI medication, could also be the same confidence that permits them to neglect the basics, like therapy and self-care.


What’s worse, many doctors, strapped for time, respond to the SSRI not working by just doubling the dose. Without a comprehensive understanding of the problem and variety of treatment approaches, it’s is a roll of the dice. Sometimes the SSRI works, sometimes it doesn’t, often it produces side effects.


Start at the Beginning

Let’s take closer look at the science behind these medications that boost serotonin activity.

Anti-depressant medications have been around for several decades. Pharmaceutical companies have been developing newer and supposedly better ones throughout that time. Although the mechanism of action of the various medications has changed over time, what they all share in common is that they target a select set of neurotransmitters.


Neurotransmitters are chemicals messengers in the brain that are needed for one neuron to communicate with another. There’s over 100 neurotransmitters working in the human brain. However, there is a small number of specific neurotransmitter, called amines, that pharmaceutical industry has focused on with psychiatric medications. This group of amines includes the infamous serotonin, as well as norepinephrine and dopamine (4).

The first antidepressants, monoamine oxidase inhibitors (MAOI’s) worked by reducing the breakdown and elimination of  neurotransmitters. MAOI’s targeted the enzymes that naturally existed in the brain. These enzyme are there to dispose of neurotransmitters that neurons just squirted out. In Nature’s infinite wisdom, this elimination of neurotransmitters is a really important for our mental and emotional balance. Too much neurotransmitters hanging around and pinging our receptors would be overwhelming for us. There would be just too much mental and emotional activity going on in our brains and bodies.


MAOI’s worked by inhibiting (slowing down) the activity of these enzymes. The result? More neurotransmitters hanging around for longer in between neurons. As you may have guessed, these medications worked for some, and caused a lot of side effects for others. If the MAOI’s overshot the boost in neurotransmitters in an individual, then they would experience all kinds of bodily disruptions, including nausea, diarrhea, insomnia, headaches, and possibly a dangerous spike in blood pressure (5).
That was problematic. So, the pharmaceutical industry went back to the drawing board and came up with the next generation of anti-depressants, called the Tricyclics (TCA’s). Instead of boosting the amount of serotonin, norepinephrine, and dopamine, these antidepressants worked by blocking the transporters for just serotonin and norepinephrine.


Transporters are proteins that sit at the end of the sending neuron. They are sucker-backer-uppers. Neurons get stimulated and squirt out neurotransmitters in the space in between neurons. Again the point of that is to stimulate the nearby, receiving neuron, so the message can continue on… from one neuron to the next, across the brain. But, once the neurotransmitter is squirted out, these transporters are there to scoop them back up into that sending neuron. This recycling of neurotransmitters helps the brain conserve resources, and protects us from being overstimulated.


In blocking the recycling of these neurotransmitters, the tricyclics essentially made the neurotransmitters more available to trigger responses in the brain. The TCA’s worked fairly well for most with depression. But, similar to the MAOI’s, patients often experienced strong, unwanted side effects with TCA’s. These included dry mouth, blurry vision, constipation, impaired thinking, and even feeling emotionally blunted (6). These medications helped countless people resurface from devastating depression and anxiety. Yet, these medications also come with some problems. Psychiatry and the pharmaceutical industry was on the right track, just not quite there yet.

Then in 1987, along came fluoxetine (Prozac). It was the first anti-depressant that was ‘selective’ for serotonin. Hence, this new category was named selective serotonin reuptake inhibitors (SSRI’s). This was the first antidepressant to just focus primarily on serotonin.


Later, in 1991, sertraline (Zoloft) was released to the US market. These two all-stars spawned a cultural movement. These medications were better tolerated than the previous generations of antidepressants - as they targeted just one neurotransmitter versus two or three at once. Additionally, these two blockbusters came along at the right time. As the pharmaceutical industry, medicine, and our Western culture started working in sync to create and promote an ideological shift towards “a pill for every ill” (7). Capitalism pushed marketing that helped make taking SSRI antidepressant medication cool, or at lease less shameful.
An obvious good news, bad news situation emerged. It was a good thing that people were feeling more comfortable to ask for help, and at the same time they were able to more easily access that help. Likely a net negative that the marketing behind the SSRI’s encouraged simplistic view of anxiety and depression, distilling it down to just a serotonin deficiency.


Adjusting mostly just serotonin helped to reduce the adverse effects that was seen with the prior generations of anti-depressants. With SSRI’s there are still side effects, but less so compared to the MAOI’s and TCA’s. Excess serotonin activity in the wrong places, at the wrong times, in the wrong amounts can lead to headaches, digestive upset, restlessness, and some degree of feeling numbed.


The simple math here is that if you mess around with neurotransmitter levels, stuff will happen. Some of that stuff will be welcomed. Some of it will not. If you mess around with less neurotransmitters in the brain (just serotonin, but not norepinephrine or dopamine), less stuff will happen. You’ll get less unwanted side effects. On the flip side, you may also get less wanted, helpful effects.


Again, serotonin deficiency is not the one and only cause of depression or anxiety. There’s a lot of evidence that dopamine and norepinephrine activity in certain brain pathways are very much involved in mood, thinking, motivation, and social behaviors. Dopamine and norepinephrine are important chemicals in depression too (8, 9). 

The SSRI’s, which are the predominate anti-depressants prescribed today, do not alter dopamine or norepinephrine directly (sertraline is an exception, as it does somewhat slow down the recycling of dopamine as well as serotonin). There are SNRI’s now that enhance both serotonin and norepinephrine activity, but doctors don’t typically reach for them first. And, note that SNRI’s don’t boost dopamine activity. In truth, all of this picking and choosing neurotransmitters may not be that helpful. It’s just not that simple. As noted above, there’s no evidence out there Serotonin is the be-all-end-all of depression and anxiety treatment.
This is where the “you’re deficient in serotonin” theory begins to break down. There is no evidence that a deficiency of serotonin is the one and only thing that matters. It’s not as simple as how eating food cures starvation, or how drinking water solves dehydration. However, increasing the amount of serotonin available, or increasing the activity of the serotonin receptors, will produce an effect. What we need to realize is that this tool (SSRI medication) is crude and blunt. It may get the job done, but it’s not as clean and easy as the commercials on TV make it out to be. On the other side, these medications are also not as evil and poisonous as some online discussion threads make it seem.


So, there is some after-the-fact logic at play with the chemical imbalance theory. Neurotransmitters are figuratively (as well as literally) just the messengers. Neurotransmitters just react to those other things and mediate the response. Neurotransmitters are not the cause. It’s unlikely that anxiety and depression are caused by any one thing. What’ more likely is that anxiety and depression come about from a number of contributing factors - psychological stress, physical and emotional trauma, lack of stimulation/activity, nutrient deficiencies, inflammation in the body that reaches the brain, even imbalances in our gut bacteria.
But, with the chemical imbalance theory, the fact that a number of contributing factors have to come together to produce symptoms of anxiety and depression is discarded. SSRI’s shoot the messenger.


But, enough people get better, or at least seem to get better, with the use of SSRI’s, so a simple conclusion was drawn. The field of psychiatry concluded that if adding serotonin helped relieve depression, then it must have been a lack of serotonin that was the original problem. It seems as though once Medicine had the answer, it went back and redefined the problem. Unfortunately, that’s not how science is supposed to work. It is, however, how marketing and advertising work.
In considering if an SSRI may help, it is really important to know that these medications can help, but it also true that this solution (SSRI and other antidepressant medications) helped to redefine the problem (anxiety and depression). SSRI’s need to be just one part of an overall treatment approach, which should include some form of therapy, increased socialization, and the old sleep, diet, exercise, stress reduction self-care protocol.

Nerd Alert: Neuroscience Lesson

We could end here. Now you know that SSRI medications help most, but not all, with anxiety and depression. They improve symptoms, but the benefits come along with side effects. They move the ball forward, but we also need to be engaged in other forms of treatment. Recovery from anxiety and depression is like trying to fend off a bear from your campsite. Scream, shout, throw everything you can at it, and hope it eventually goes away.


The other things that you can throw at anxiety and depression (therapy, meditation, exercise, socializing, nutrition, good sleep, etc) is another article for another day. For now, if you’re curious about what exactly these SSRI medications do in the brain, then read on to learn more!


To review, serotonin does activate parts of the brain that help us to feel better. SSRI medications do increase serotonin availability and activity in the brain. For most, SSRI medications boost serotonin, and that helps them feel and function better. For some, nothing seems to be happening, good or bad. For many, that increase in serotonin activity comes with a cost.
But how exactly do the SSRI medications and the extra serotonin levels and activity lead us to feel less anxious and less sad? To begin to understand all that, let’s start with some basic human biology rules.

First rule: the body is constantly seeking balance (10). You can’t just shove the body or brain in a one direction and expect it obey. When challenged with a stressor, the human body will compensate with a swift movement in the opposite direction. We adapt so that we can survive. Think of a pendulum being pushed in one direction, pausing momentarily, then effortlessly dipping back towards the direction from which it just came. The body automatically functions in the same manner. Push it in one direction with a specific stressor, it will soon initiate a compensatory counter movement.


One example is the way our bodies regulate blood sugar levels. Eat a donut and you’ll experience a spike in blood sugar. The body will respond with a release of insulin to grab all that extra sugar in the blood and stuffs it into muscle and fat cells, which then lowers the blood sugar levels back down.


What happens when we push serotonin in one direction with SSRI’s? Neurons eventually push back in the other direction by reducing the amount of receptors on the receiving neurons that can be stimulated by all that extra serotonin (11).

Second rule: the body is also conservative. It conserves energy and resources wherever and whenever possible. Related to this discussion, neurotransmitters are a resource that the brain seeks to conserve (12). SSRI’s directly disrupt the brain’s conservation efforts. The main target of SSRI’s are those transporters - the sucker-backer-uppers - that recycle the serotonin that was just squirted out in an effort to stimulate nearby neurons. Once the neurotransmitters are releases, they float across the space between the sending neuron and the receiving neuron.


Some of those neurotransmitter dock with the receptors on the receiving neuron. Some of them float away and are lost forever. Some are broken down and eliminated by those same enzyme the MAOI’s block. And, many of them are naturally sucked back up into the sending neuron. Why does that happen? Easy answer here. If the neuron can recycle a neurotransmitter, it doesn’t have to spend it’s limited energy and resources on making new ones. This is why recycling rocks. Less waste, more efficiency, greater ability to dedicate resources toward other important stuff.


Third rule: the brain functions via circuits (13). There are billions of single neurons, but trillions of connections between all the neurons. It’s a big bowl of spaghetti up there in the brain. Connections between neurons are organized in specific ways. For anything to happen - a thought, feeling, memory, sensory perception - one part of the brain has to talking to another part. When you see a family member, the visual center of the brain receives the image, then passes the message through the memory center, which then runs it through the emotional center to tag it with meaning.
 

Circuit Training

Every thought, feeling, memory, sensory perception is a specific combination of connections… also known as a circuit. A brain circuit is a unique signature. It’s a one-of-a-kind pathway of neuronal connections across the brain. Thoughts, feelings, memories, and sensory perceptions, and all kinds of experiences are unique combinations of neurons that have branched together over time, thus forming a circuit (14).


The connections between neurons are not pre-set at birth. They are formed through experience, after repeated messages are shared between two neurons. So circuits are shaped over time. They become stronger with repeated use as well. They mediate our reactions to various situations. Once established through repeated experience, they predetermine how we think and feel about things. Experience shapes our circuitry, as well as our reactions to life.


In this way, circuits allows us to process what’s happening in life - quickly. Processing means taking in information through our senses, combining that information with past experiences (memories), and making meaning out of the experience. The more we have processed an experience, the quicker we can process it the next time. That efficiency helps us in our quest to at least survive, and at best thrive, in life. Inventing the wheel was hard enough the first time. Imaging having to reinvent the wheel every time you needed to get something done. You’d be toast by Tuesday.


Healthy, functional circuits help maintain automatic processes in the brain, which is often a good thing. Activation of brain circuits over time helps the circuits to operate on autopilot. This frees us up to focus on other things. Think of your commute to work. If you take it every day, pretty soon the brain doesn’t need to dedicate much mental energy towards deciding where, and when, to turn. This is how we can listen to podcasts, have deep thoughts, and do our make-up all while driving 75 mph down the highway. It’s a uniquely human capacity.


Neurotransmitters have to be available and at the ready in between neurons to keep those circuits firing. This is how increasing neurotransmitter levels and activity can have such broad-reaching effects on our minds and bodies. Increasing the availability of neurotransmitters means that those circuits are more likely to fire and be active. More activity in the circuits can be a good thing or bad thing, depending on which circuit is being activated.


SSRI medication, in boosting the availability of serotonin (and a little bit of dopamine for Zoloft), help certain brain circuits to be more active. When certain circuits are more active, they gain an upper hand over other circuits that are vying to be heard as well. The brain is always very active. And, it’s a big competition. Strengthening the signal of any one circuit helps us to hear what that circuit is trying to say over all the noise of the other circuits.

Stop, Collaborate, & Listen

So what does serotonin have to do with processing? How does processing relate to depressed moods and episodes of anxiety? Two separate questions, but the answers for both are related.

Emotions stem from processing. Sometimes that processing occurs below the level of our awareness. We can walk into a room, and get a funny feelings. We look around and try to figure out what is giving us that gut feeling. For the life of us we can’t figure it out. But, our intuition is strong. So, if feasible, we walk out of the room. What’s happening in the brain in this scenario is that our body and brain is picking up on something in the environment. It may not register in our conscious awareness, but some part of our brain is reading the room. That sends a signal along the circuits that run through the fear center in our brain and then we suddenly become aware that we feel uneasy.


That feeling response has been evolutionarily refined to help us stay safe and well. It’s usually wise to listen to those gut feelings. Sometimes they lead us astray, but often they are just trying to protect us.  What can happen over time, however, is those signals going to and coming from the fear center strengthen (15). The circuits that carry those signals become too active. Too much fear leads us to feel worried, sad, and even angry. Eventually, after frequently feeling the feelings that the protective fear mechanism makes us feel… we become stuck. We can get stuck in fear and it’s descendants, anxiety and depression.
So, if we experience negative feelings too much, there can be a danger that we continue to be triggered by things and go down the pathway of fear, sadness, and anger that much easier and quicker the next time. It’s a slippery slope.
If only there was to pull back the throttle on that runaway fear train.


Well, in the brain, there are other circuits that were built in to quiet these fear circuits. There are circuits that run from the fear center in our brain (amygdala) to the rational thinking center (prefrontal cortex). In fact, these calming, inhibitory circuit run on serotonin. In these particular circuits, serotonin is inhibits (slows down) activity of the fear circuit (16).
In the brain, to inhibit means to slow down or stop an electrical message from being sent along. The opposite of inhibition in the brain is excitation. Excitation is exactly the process of messages being passed along. Balance between the two is needed to keep us mentally balanced. Some examples: Kids with ADHD and hyperactivity could use more inhibition (but they don’t necessarily need more serotonin). People with social anxiety, experience too much inhibition.


Here’s how it all goes down: The fear center notices something in environment and gets activated. The result is the fear center tells the rest of the brain to watch out because something dangerous is coming. There is an urgent need to protect oneself. We tend to feel this as fear, anger, angst, or defensiveness. However, the rational thinking center in the front of our brain can kick in once the fear center gets activated. It will send an inhibitory signal to the fear center to inhibit it’s activity.


The result is that the fear is muted, interrupted just long enough for our rational thinking center to kick into gear. We have all experienced this. Something makes us feel afraid, worried, really self-conscious, or very angry. For a moment or two we are drowning in fear, sadness, or anger. But, a few moments later, we can start to talk ourselves through the fear. We calm down and start to breathe again. That signal from the rational thinking center to the fear center is mediated by circuits that use a few different serotonin receptors (17, 18).
 

Momma Raise Me Right

More specifically, serotonin participates in activity called behavioral inhibition. Behavioral inhibition is avoidance of things that could be bad for you or could go wrong. It may sound like sophisticated brain process, but it’s actually kind of like how is sounds. Behavioral inhibition is about stopping yourself from doing things that would work out poorly for you, such as blurting out an inappropriate comment in the wrong social group, or resisting the urge to eat the entire container of ice cream. Both of those behaviors would may make you feel sick to your stomach in the end. Serotonin knows that, and it’s actively working the brain to stop you from engaging in behaviors that would lead to bad outcomes for yourself.


Serotonin participates in the circuits that offer us the awareness of how things we do could lead to outcomes that we wouldn’t like. That circuit doesn’t necessarily cross over into the circuits that manage our conscious awareness of things. This circuit mediates a subconscious self-protective process.


That actually saves us from freaking out all the time in two key ways. First, the serotonin’s behavioral inhibition, if functioning properly, keeps us from doing things that work out poorly in the end. As a result, we are better off in life, and thus have less problems to stress over. With less problems to stress over, there is less activation of that sticky fear circuit that can lead to anxiety and depression.


Second, this serotonin activity in these behavioral inhibition circuits operate in the background, below the level of our conscious awareness. The negative feelings of disgust (over awful behavior that we might potentially engage in if it were not for this serotonin circuit), fear, and anger are humming along, doing their thing, keeping us in line, all without our full conscious awareness. Strange that we can feel or experience fear without actually really feeling it. But, that disgust, fear, and anger drive the avoidance of doing things that would later on work out poorly for us (19).


Behavioral inhibition is about how well can you navigate the world. How well do you take advantage of opportunities, but also avoid obvious dangers? You're probably a lot better at it than you give yourself credit for. That's because serotonin is working in specific circuits in the brain, keeping you away from dangers automatically and without you being aware of it.
Serotonin doesn’t stop there. This particular neurotransmitter, and it’s related brain circuitry, mediates another important process. That is the automatic, subconscious predicting of negative events (20). The brain is constantly evaluating the environment, scanning for situations or things around that could produce harm to the individual. While this is vital for survival in the woods, in our modern world of electronics, fast moving cars, highly competitive marketplace, and barrage of images of attractive, near perfect people, being aware is potentially anxiety inducing.


In sum, serotonin keeps you doing good.


Serotonin’s role in these specific brain centers and circuits is the constant scanning for threats in the environment. If all goes well, this activity happens below the level of our awareness. Threats are noticed by the brain, but not necessarily brought to our conscious awareness and attention. The rational thinking prefrontal cortex presses mute on whatever environmental stimuli that is attempting to trigger us. It stops the fear from bubbling up to our conscious awareness. It prevents negative thought patterns related to fearful emotional states. Therefore, we don’t feel the need to freak out. That’s a pretty darn awesome feature of the human brain.


This obliviousness offers us the opportunity in life to pretend like everything is all good. Meanwhile, life is never all good, nor easy, nor absent of threats to our well-being. But, this kind of serotonin-induced inhibition favors optimism, (or least neutrality) over fear and pessimism.


The end result? When that automatic suppression of fear and negativity is running in the background of your mind (which means that the fears do not reach forefront of your thinking), you are less likely to focus on the potential for negative things happening in your life. Essentially, serotonin helps us move on with our day and be oblivious to how crappy our life actually is, or could be in the future.

Better Living Through Chemistry

Perhaps, as we evolved during the hunter-gatherer days, serotonin helped us tolerate some tough stuff. Imagine trying to negotiate, on a daily basis, a harsh environment full of uncertainty - tigers, bears, violence, starvation, inclement weather, and serial childbirths adding up to just more and more mouths to feed.



 

Maybe serotonin was there at times to let us be in denial about our mortality and just get on with it. Maybe serotonin’s influence helped us make it through tough times. Maybe it still does just that. Humans are indeed very resilient when push comes to shove. Ever wonder what that’s about? How are some of us able to endure hardship and maintain hope and belief in a brighter future? Maybe it has something to do with serotonin.


With an understanding of all of this science, it is easier to see how a person may not have an actual chemical (serotonin) deficiency, but could still benefit from an SSRI. The increase in serotonin activity may serve to limit conscious negativity. That kind of negativity could be experienced by a person as their depression or their anxiety. Alternatively, that negativity might just be a stressor that contributes to the development of a depressive or anxiety disorder.


The unfortunate part is that, for some, it is also true that SSRI’s cause more harm than good (21). I have seen this happen many times in treating patients over the years. In my experience, I would argue that one of the more insidious and subtle side effects of SSRI’s is that they do their job a little too well. For some, I have seen the effect of SSRI’s make patients too numbed. This limits the effort and energy that patients put into addressing important issues in their lives and subdues their urgency for self-care activities. Thus, the reasons to start a SSRI are very individual and depend on the person’s situation at the moment.

 

In sum, serotonin and the SSRI’s help us to suppress intense emotional reactions that are distressing, so we can get on with life. For some, SSRI’s are a life-saving tool. For others, not so much. Knowing when and how and why we should use SSRI’s is an important discussion to have with one’s medical/psychiatry provider. Framed with this understanding of the science, a conversation about how fear and negative predicting impacts the individual, often leads to greater insight about what is really bothering us and what else we can do about it.

References:

(1) https://www.cdc.gov/nchs/products/databriefs/db283.htm


(2) https://www.tevagenerics.com/globalassets/products/pi/fluoxetine-tablets-20mg_pi.pdf


(3) Syme, K., Hagen, E. (2019). Mental health is biological health: Why tackling "diseases of the mind" is an imperative for biological anthropology in the 21st century. American journal of physical anthropology 171 Suppl 70(S70), 87-117. https://dx.doi.org/10.1002/ajpa.23965


(4) Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Chapter 6, Neurotransmitters. Available from: https://www.ncbi.nlm.nih.gov/books/NBK10795/

 



(5) Sathyanarayana Rao, T. S., & Yeragani, V. K. (2009). Hypertensive crisis and cheese. Indian Journal of Psychiatry, 51(1), 65–66. http://doi.org/10.4103/0019-5545.44910



 

(6) Remick, R. A. (1988). Anticholinergic side effects of tricyclic antidepressants and their management. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 12(2-3), 225-231

(7)Busfield, J. (2010). ‘A pill for every ill’: Explaining the expansion in medicine use Social Science & Medicine 70(6), 934-941. https://dx.doi.org/10.1016/j.socscimed.2009.10.06

(8) Chantal Moret, M. B. (2011). The importance of norepinephrine in depression. Neuropsychiatric Disease and Treatment, 7(Suppl 1), 9–13. http://doi.org/10.2147/NDT.S19619

 



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