A Pharmacodynamic Perspective on Antidepressants


A Pharmacodynamic Perspective on Antidepressants

In the study of pharmacology, there are two main fields of study, pharmacokinetics (PK), which examines a patient’s effect on a drug, how it is absorbed, distributed throughout the body, how it metabolized inside the body, and how it leaves the body through excretion. Pharmacologists use the acronym ADME to describe this process; an understanding of which is critical to determine the posology and toxicity (i.e. what is a safe dose) for new medicines. This article will examine the second field, the pharmacodynamics (PD) particularly in relation to antidepressants; a study of how the drug affects the body.

Relationship Between Serotonin & Clinical Depression

Contrary to popular belief, depression is not characterised by feeling sad all of the time. Sadness is a natural emotion which allows the brain to process psychological trauma by way of a healthy, self-healing process. Depression, by contrast, is a neurological disorder which inhibits emotional regulation and the ability to experience natural emotions like joy, caused by chemical imbalances in the brain.

Serotonin is a monoamine neurotransmitter. More simplistically, it is a compound which allows the brain to communicate complex internal functions, such as modulating mood, cognition, reward, learning and memory as well as various autonomic functions like vomiting and vasoconstriction. It would be overly simplistic to say that low levels of serotonin are what cause clinical depression. In fact, one review recently claimed that there is no convincing empirical evidence there even is a connection between clinical depression and serotonin depletion per se. This is because depression is far more complex than that, and stems from a wide variety of causes depending on each individual’s circumstances and neurological state at the time. For example, neurodegenerative diseases play a major role in affecting emotional regulation in most people, something stem cell researchers like bioxcellerator are working hard to address.

What is known, however, is that in a statistically significant number of cases, raising serotonin levels can improve symptoms of clinical depression and make patients more responsive to other types of treatment, such as cognitive behavioral therapy (CBT). For some people,

a rise in serotonin can break the cycle of depression long enough for other interventions like CBT to become effective.

Selective Serotonin Reuptake Inhibition (SSRI)

When serotonin has performed its function, it is usually reabsorbed by nerve cells; this is known in pharmacodynamics as reuptake. Selective serotonin reuptake inhibitors (SSRIs) are drugs which block these nerve cells. This strategically traps serotonin, meaning there is more of it to pass further messages to nearby nerve cells. In that context, increasing serotonin in the brain is akin to giving a body that is giving out during surgery a shot of adrenaline to keep it going. This does not solve the problem outright, but it can give medical practitioners invaluable time to intervene in other ways and, ultimately, save lives.

Examples of SSRIs

Most anti-depressants you will have heard of are SSRIs. These are drugs like citalopram (Cipramil), dapoxetine (Priligy), escitalopram (Cipralex), fluoxetine (Prozac or Oxactin), fluvoxamine (Faverin), paroxetine (Seroxat), sertraline (Lustral) and vortioxetine (Brintellix). Other common anti-depressants, like mirtazapine (Remeron), are not SSRIs, rather they are atypical anti-depressants with a different mechanism of action; mirtazapine, for instance, by blocking the serotonin receptors and inhibiting reuptake of norepinephrine rather than serotonin.

Adverse Effects of SSRIs

SSRIs can be problematic as a treatment, because they typically take a long time to produce the desired effects, whilst in the meantime introducing the patient to a litany of adverse reactions ranging over their mood declining even further, extreme nausea, agitation or anxiety, indigestion, diarrhea or constipation, loss of appetite and weight loss, dizziness, blurred vision, dry mouth, excessive sweating (which can be linked to serotonin syndrome), insomnia and sleep related problems, headaches, a complete loss of libido (sex drive), sexual dysfunction including erectile dysfunction, delayed ejaculation or vaginal dryness…to name just a few of the more common ones. Some of the less common ones are bruising or bleeding very easily, or vomiting blood, mental confusion, mobility problems including stiffness or shaking, visual and/or audible hallucinations and urological problems. Then there is serotonin syndrome, which happens when serotonin levels are too high. This is particularly common in patients who combine antidepressants or combine medication with herbs like St John’s wort. This can result in fever, seizures, arrhythmia or even a loss of consciousness, and in severe cases can easily become a medical emergency. SSRIs typically take about 3 months of regular use before the adverse reactions finally begin to subside, and the intended, controlled serotonin increasing effects begin to flourish. For some, SSRIs have been a literal lifesaver, and these are usually people who are over the age of 30 and have an extensive support network to help them cope with the first three months. Unfortunately, the majority of clinical trial data on the efficacy and effects of SSRIs are from >30s populations. Suicide rates in teenagers and adults in their early 20s on SSRI prescriptions are somewhat higher. Therefore, it is clear that careful discussion is needed before anyone embarks on this kind of treatment and to ensure that a support network is in place which understands all the problems involved.

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