In my last article about oxytocin I mentioned that increasing the release and uptake of this hormone turned neurotransmitter helps combat feelings of low mood and depression. However, oxytocin is hardly the neurotransmitter thought off when thinking of longer-term (un)happiness. When we are talking happiness, we are talking serotonin.
Are you happy yet? When thinking of happiness, or lack thereof, we think of serotonin as the one neurotransmitter that controls this. However, it’s not really clear what exactly causes low mood and depression. A key theory in the past years is that depression is caused by an imbalance of neurotransmitters or hormones in the body. Following from this, depression has been linked to low levels of serotonin.
Unsurprisingly then, the happier we feel, the higher our levels or serotonin tend to be. The lower our levels of serotonin are, the lower our mood is. But this leads to a way of thinking that is just too simple. Let’s dive into what else serotonin does:
Are you functioning? Serotonin is mainly associated with happiness. But there is so much more to this neurotransmitter. I think of serotonin as a manager, or a controller if you will. Why? Because it is involved in almost EVERYTHING. It doesn’t just regulate mood, it also regulates most things (in)directly related to mood, such as sleep. You know how bad your mood gets when you are sleep deprived. Well, continuous sleep deprivation is directly related to serotonin misfunctioning.
Sleep isn’t the only thing that goes out the window when serotonin isn’t functioning properly. Your memory goes too. Memory processing is very important in day-to-day life. Memory is what makes us learn, it facilitates social interactions and well, it makes us function properly. There is a reason that memory-degenerative diseases are considered to be one of the worst diseases of the mind.
It’s not strange that memory goes, general cognition is impaired when serotonin falters. Now cognition is a massively general term. And that is exactly the problem. Serotonin is so complex it affects us all-over, so general cognitive functioning can be impaired. It is hardly surprising that people who suffer from depression and anxiety cannot focus on their studies/work/social life and report feeling calmer, more focused, less anxious and more emotionally stable when on SSRIs (Selective Serotonin Reuptake Inhibitors).
Beyond the mind, there is the body. Serotonin has also been linked to the following processes: digestion and appetite (Beattie & Smith, 2008), bone metabolism (Frost, et al, 2011; Frost, et al, 2010; Mödder et al, 2010; Rosen, 2009), organ development (Hahn, 1984; Ozanne & Hales, 2004) and cardiovascular growth (Glassman, 1998).
Poppin’ Pills and Stigma I have just mentioned SSRIs. These are pills increasingly prescribed when people suffer from long(er)-term low moods, depression and anxiety. But what does an SSRI do?
The brain communicates through sending signals from neuron to neuron. Between two neurons there is the synaptic cleft through which the signal has to travel as well. It does so by releasing chemicals (neurotransmitters) from the one neuron to the other. So, there is release and uptake. The longer neurotransmitters are in the synaptic cleft, the stronger the signal, without an additional release. This is what SSRIs do. They stimulate prolonged staying in the synaptic cleft. If this is going too fast for you, maybe read my article introducing neuroeconomics, in which I describe this process in more detail.
SSRIs have a cumulative effect. So “popping” one pill is not going to cut it. Most people are prescribed this form of medication when experiencing depression, but anxiety can also be treated this way. Issue is, people who are experiencing low moods, need not experience any of the other side-effects. Yet increasing your levels of serotonin can mess with everything, because serotonin seems to be involved with everything. So, if you didn’t have sleeping issues before, you might have them now!
Although I fully understand the need for this type of medication when experiencing depression and anxiety, I’m becoming increasingly worried with the frequency of prescription (Wong, et al, 2004). Most people I know have been on this medication at least once. I have no intention of invalidating mental health concerns, but my concern is over-prescription of a medication that can both fix and cause problems that are equally bad (Cascade, et al, 2009; Ferguson, 2001). If you didn’t have sleeping problems before, but have them when on the medication, you can hardly be surprised if you’re still as depressed. Sleep is directly linked to mood, because of serotonin. There is also an increasing literature showing that neonatal and/or young exposure to SSRIs is causing a whole load of issues of their own (Maciag, et al, 2006; Popa, et al, 2008).
So, fixing the one thing is not helping. There have been other issues with some SSRIs. People with suicidal ideation when prescribed SSRIs might finally have the motivation and the energy to complete their goal (Möller, et al, 2008). This happens because some of the medication increases energy levels before it elevates the mood. Not all SSRIs have this is issue, but it is something to take into account.
Another issue is that we as a society have moved towards looking at medication as a solution in itself. When the problem is truly neurological (some people are born with serotonin pathway deficiencies), medication might be the best and only option. But most people do not suffer this type of depression. They suffer something that has been mainly induced by nurture, rather than nature. How have we moved to making a quick-fix that is supposed to support the healing process the ultimate solution? It is hardly surprising the stigma is lifting when all of us are in on it!
If you are experiencing depression or anxiety, especially combined with suicidal or self-destructive tendencies, or know someone who is, do not think medication is enough. It is a quick fix that can help, but is unable to replace diving into the true root of the problem, which can often only be done through therapy. As miserable as that sounds.
References Beattie, D. T.; Smith, J. A. M. (9 April 2008). "Serotonin pharmacology in the gastrointestinal tract: a review". Naunyn-Schmiedeberg's Archives of Pharmacology. 377 (3): 181–203. doi:10.1007/s00210-008-0276-9
Cascade, E., Kalali, A. H., & Kennedy, S. H. (2009). Real-world data on SSRI antidepressant side effects. Psychiatry (Edgmont), 6(2), 16.
Ferguson, J. M. (2001). SSRI antidepressant medications: adverse effects and tolerability. Primary care companion to the Journal of clinical psychiatry, 3(1), 22.
Frost M, Andersen TE, Yadav V, Brixen K, Karsenty G, Kassem M (March 2010). "Patients with high-bone-mass phenotype owing to Lrp5-T253I mutation have low plasma levels of serotonin". Journal of Bone and Mineral Research. 25 (3): 673–5. doi:10.1002/jbmr.44. PMID 20200960
Frost M, Andersen T, Gossiel F, Hansen S, Bollerslev J, van Hul W, Eastell R, Kassem M, Brixen K (August 2011). "Levels of serotonin, sclerostin, bone turnover markers as well as bone density and microarchitecture in patients with high-bone-mass phenotype due to a mutation in Lrp5". Journal of Bone and Mineral Research. 26 (8): 1721–8. doi:10.1002/jbmr.376
Glassman, A. H. (1998). Cardiovascular effects of antidepressant drugs: updated. The Journal of clinical psychiatry, 59, 13-18.
Hahn P (July 1984). "Effect of litter size on plasma cholesterol and insulin and some liver and adipose tissue enzymes in adult rodents". J. Nutr. 114 (7): 1231–4. doi:10.1093/jn/114.7.1231. PMID 6376732.
Maciag D, Simpson KL, Coppinger D, Lu Y, Wang Y, Lin RC, Paul IA (January 2006). "Neonatal antidepressant exposure has lasting effects on behavior and serotonin circuitry". Neuropsychopharmacology. 31 (1): 47–57. doi:10.1038/sj.npp.1300823. PMC 3118509
Mödder UI, Achenbach SJ, Amin S, Riggs BL, Melton LJ, Khosla S (February 2010). "Relation of serum serotonin levels to bone density and structural parameters in women". Journal of Bone and Mineral Research. 25 (2): 415–22. doi:10.1359/jbmr.090721. PMC 3153390. PMID 19594297.
Möller, H. J., Baldwin, D. S., Goodwin, G., Kasper, S., Okasha, A., Stein, D. J., ... & Versiani, M. (2008). Do SSRIs or antidepressants in general increase suicidality?. European Archives of Psychiatry and Clinical Neuroscience, 258(3), 3-23.
Ozanne SE, Hales CN (January 2004). "Lifespan: catch-up growth and obesity in male mice". Nature. 427 (6973): 411–2. Bibcode:2004Natur.427..411O. doi:10.1038/427411b. PMID 14749819.
Popa D, Léna C, Alexandre C, Adrien J (April 2008). "Lasting syndrome of depression produced by reduction in serotonin uptake during postnatal development: evidence from sleep, stress, and behavior". The Journal of Neuroscience. 28 (14): 3546–54. doi:10.1523/JNEUROSCI.4006-07.2008. PMID 18385313.
Rosen CJ (February 2009). "Breaking into bone biology: serotonin's secrets". Nature Medicine. 15 (2): 145–6. doi:10.1038/nm0209-145. PMID 19197289.
Wong, I. C. K., Murray, M. L., Camilleri-Novak, D., & Stephens, P. (2004). Increased prescribing trends of paediatric psychotropic medications. Archives of Disease in Childhood, 89(12), 1131-1132.
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