The Chemistry of Love
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INTRODUCTION
Love is difficult to describe in words but is universally known - It is that warm and cozy feeling, the desire to be with that someone or the exhilarating feeling at the start of a relationship. In this article, we will look into the chemistry behind romantic love. Why does our hearts race when we see our significant other? Why do we get the feeling of ‘butterflies in the stomach’? What happens in the brain when we fall in love? Find the answers here!
BIOCHEMISTRY OF LOVE
Monoamines are a group of neurotransmitters that play a significant role in the way we feel, and many of them are involved in bringing about the emotions of love; they are noradrenaline, dopamine, serotonin and phenethylamine (PEA). Before we look into the mechanism behind it all, let us look at how we have discovered our answers - The story starts from Psychiatrist Michael Liebowitz, who gave the first biochemical perspective on love. Liebowitz described love as having two components: attraction (yearning) and attachment (the pleasant feeling of being with someone you love), and that love can be like an ‘addictive state’ and may end with ‘withdrawal-like symptoms’, referring to those in a breakup. In his study, he compared the feelings of euphoria when in love with the high from amphetamine use; where it was found that low amphetamine levels can lead to depressing withdrawal-like states, akin to those when experiencing a breakup [1].
Another scientist who studied the biochemistry of love was Dr. Helen Fisher, who brought the lust component into the picture of Romantic love. Fisher suggested that lust plays a huge part in romantic love as it is rare for someone to fall ‘head over heels’ with more than one person at the same, and she described the attachment phase of love as the years after marriage - which is a clear distinction as we all know that in the start of a relationship, everything is very exciting, and some would describe it like an ‘emotional rollercoaster’; however, after being with your partner for a long time, of course you continue to love them dearly, but the exhilarating factor will have weakened over time[1].
Both Liebowitz and Fisher performed many studies that supported their theory that monoamines play a huge part in the emotions of love, and we will look into them in the next section Monoamines.
MONOAMINES
Let us now look more into the monoamines that are involved in love. As I have introduced in the previous section, noradrenaline, dopamine, serotonin and phenylethylamine (PEA) all play an important part. Noradrenaline converts into Adrenaline and brings about the ‘fight or flight’ response involved when falling in love; dopamine and serotonin, the well-known neurotransmitters that are present in the pleasure centre of the brain; phenylethylamine (PEA). Moreover, there are other hormones like endorphins which promote attachment that are involved in love. We will now look into some of these monoamines in greater depth in each section: (1) Noradrenaline, (2) Dopamine and (3) Serotonin
Noradrenaline
Noradrenaline brings about the physiological changes that happen in your body when in love e.g. increased heart rate, enhanced ability to cope without sleep and sweaty hands. Noradrenaline is the demethylated version of adrenaline and it can trigger the ‘fight or flight’ response. It is almost ironic or paradoxical to describe love this way but the reason why we do is because both love and the ‘fight-or-flight’ response affect the sympathetic nervous system, so they bring about similar physiological changes [1].
So how does noradrenaline cause our heart to beat faster? Well, it triggers a signal cascade that produces a large amount of cyclic adenosine monophosphate (cAMP) in cardiac cells. It starts when noradrenaline binds to the G-protein coupled receptor (also known as β-adrenergic receptor [2]) and this receptor is coupled with a G-protein (it is located just right next to the receptor). The G protein interacts with guanosine triphosphate (GTP), and just like the famous Adenosine triphosphate (ATP), it is an energy carrying molecule. ATP is present and when the GTP is hydrolysed into guanosine diphosphate (GDP), it causes the ATP to be converted into cAMP. The Hydrolysis of GTP can act as a timer in this signal cascade (can control the timeframe at which cAMP is produced) because its interaction with the G-protein is composed of three different subunits: α, β, and γ. When the G-protein hydrolyses the GTP, there is a change in shape to the protein and this causes a single molecule of noradrenaline to bind to the receptor. The G protein is already bound to the GDP (product of the previous cycle of hydrolysis) therefore when the receptor binds back to the G-protein, the GDP that was embedded in the G protein is released and another GTP molecule then moves and binds to the G protein. This then leads to the α subunit to change shape and detach from the β, and γ subunits, and its new shape allows it to bind to adenylyl cyclase. Adenylyl cyclase is then able to convert ATP into cAMP and when this happens, the α subunit hydrolyses the GTP back into GDP. Once hydrolysis is complete, the α subunit returns back to its original shape, causing it to deactivate adenylyl cyclase and allowing it to rejoin with the β, and γ subunits [1]. (See Fig. 1)
Fig. 1 Noradrenaline signal cascade in the heart
Noradrenaline binds to the receptor.
Which causes the receptor to change shape so that it can bind to G-protein.
G-protein ejects GDP and binds GTP.
Binding GTP causes the α subunit of the G-protein to change shape so it detaches from the β, and γ subunits.
The α subunit binds to adenylyl cyclase which converts ATP into cAMP. At the same time, the α subunit hydrolyses GTP back into GDP.
When hydrolysis is complete, the subunits recombine and adenylyl cyclase is deactivated.
Source: [1]
So how does cAMP cause the heart to beat faster? Well, cAMP interacts with protein kinase A (PKA) which phosphorylates L-type calcium ion channels - this means that the activated PKA adds a phosphate group (P) to Rad, causing Rad to dissociate from the calcium ion channels [2]. Thus, these calcium ion channels are open, so a surge of calcium ions enters the cell. This influx of calcium ions is what causes the cardiac cell to contract [1]. (See Fig. 2)
[2]
SYNAPSE
Before we look into dopamine and serotonin in depth, let us first look into the mechanism for the release of neurotransmitters across a synapse. When an impulse arrives at the end of the presynaptic neurone, calcium ion channels open, so calcium ions will move out and diffuse towards the presynaptic knob. This triggers vesicles containing neurotransmitters to move towards the presynaptic membrane, releasing the neurotransmitters so that they diffuse across the synaptic cleft. These neurotransmitters will then bind to the receptors at the postsynaptic neurone, and this triggers sodium ion channels at the post synaptic neurone to open. This results in depolarisation of the post-synaptic neurone as there is an influx of sodium ions into the neurone, and if passes a threshold, an action potential will be generated - meaning that the neurone is stimulated. This is the case for dopamine and all the other neurotransmitters [3]. (See Fig. 3)
Fig. 3 How an impulse or action potential can be generated in the next neurone (postsynaptic neurone)
Image taken from [3]
2. Dopamine
Fig. 4 Chemical Structure of Dopamine
Source: Wikimedia Commons
Creator: Harbin
https://commons.wikimedia.org/wiki/File:Dopamine2.svg
Dopamine is known to be the neurotransmitter that is responsible for addiction - it is prevalent in the pleasurable centres of the brain; which is why when we fall in love, the dopamine levels in synaptic clefts are high - neurones are stimulated, resulting in feelings of happiness and enjoyment - which is the reason why we like to spend time with our significant other.
A study on the effect of dopamine agonist and antagonists on prairie voles was carried out by Brandon Aragon (Dopamine agonists are able to mimic dopamine and its effects; on the other hand, dopamine antagonists are able to bind to the receptors of dopamine, but don’t cause the dopamine effect). In the investigation, the drugs were injected into the nucleus accumbens (brain’s pleasure centre) and the results have shown that the dopamine antagonists made the voles lose interest in their significant others, whilst agonists made them more in love [4]. Therefore, dopamine plays an important part in mate selection for prairie voles and other studies have shown that it triggers lust in rats. This strongly suggests that it is the same case for us [1].
There are many more studies that have supported this hypothesis that dopamine is involved in the emotion of love - one of which is carried out by Dr. Fisher, Dr. Arthur aron and his colleagues. In their study, they scanned the brains of 17 people who had recently fallen in love. From the results, they identified that the brain reward’s centre: the ventral tegmental area (VTA) and the caudate are activated. These regions of the brain are known to be ‘dopamine-rich’ - further supporting their conclusion and the hypothesis that love can be ‘addicting’ - the rewarding feeling leaves you wanting more of it [1].
Dr Fisher also did a further study that strongly suggest the involvement of dopamine in the VTA (neurones can release more than one type of neurotransmitter). In this study, the study subjects took a dopamine antagonist that contained a radioactive tracer e.g. raclopride containing C-11 and underwent a PET Scan. The Scan was able to determine the location of the radiolabeled antagonist and results have shown that fewer raclopride molecules bind to receptors after a meal than when the study subjects were fasting. This suggests that the meal triggered a release of dopamine, and this dopamine binds to the receptors. When the raclopride molecules arrive, there are fewer available dopamine receptors so fewer will be able to bind to them [5]. Therefore, strongly suggesting that dopamine is present in large amounts in the VTA [1].
3. Serotonin
Fig. 5 Chemical Structure of Serotonin
Source: Wikimedia Commons
https://commons.wikimedia.org/wiki/File:Serotonin.png
Serotonin is another monoamine involved in the emotion of love and in a study by Donatella Marazitti and her colleagues, the role of serotonin was explored in not just love, but also in OCD. In the investigation, there were three groups: 20 people in love, 20 people with OCD and a control group of 20 members. The results show that in both the OCD and love group, the serotonin levels are lower in the blood than those in the control group (making the assumption that the serotonin levels in the blood were similar to that in the brain) - which supports the fact that when in love, we constantly think of a ‘crush’ or a partner [6]. This may seem contradictory when compared to Liebowitz’s theory (that MAO inhibitors increase the levels of all monoamines, which causes more stimulation of postsynaptic neurones and more ‘feel good’ sensations are created), but it may be because his hysteroid dysphorics had low levels of serotonin even before they fell in love, and that they were even lower when in love that made their levels of obsession unsustainable (In Liebowitz’s Study, Patients affected by hysteroid dysphoria took MAO inhibitors and found that it helped them alleviate their fear of rejection and their constant yearning for attention from their partners, this is due to the fact that they had very low serotonin levels that made them easily fall in love, so increasing serotonin levels actually helped them become less in need to be in a relationship and prevented them from just getting together with anyone [7]). Other studies also support the idea that higher levels of Serotonin dampens romantic love - In many studies where participants took Selective Serotonin Reabsorption inhibitors (SSRIs), they reported that they were feeling less in love with their significant other. Some reported that coming off the pills intensified their amorous feelings [1].
BIBLIOGRAPHY
[1] Husband, Thomas Mutrie. The Chemistry of Human Nature. Royal Society of Chemistry, 2017.
[2] Wang, Xiaohan, and Richard W. Tsien. “Suspect That Modulates the Heartbeat Is Ensnared.” Nature News, Nature Publishing Group, 22 Jan. 2020, www.nature.com/articles/d41586-020-00096-3?proof=t.
[3] “The Synapse (Article) | Human Biology.” Khan Academy, Khan Academy, www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/the-synapse.
[4] Aragona, Brandon J et al. “A critical role for nucleus accumbens dopamine in partner-preference formation in male prairie voles.” The Journal of neuroscience : the official journal of the Society for Neuroscience vol. 23,8 (2003): 3483-90. doi:10.1523/JNEUROSCI.23-08-03483.2003
[5] Small, Dana M et al. “Feeding-induced dopamine release in dorsal striatum correlates with meal pleasantness ratings in healthy human volunteers.” NeuroImage vol. 19,4 (2003): 1709-15. doi:10.1016/s1053-8119(03)00253-2
[6] Marazziti, D et al. “Alteration of the platelet serotonin transporter in romantic love.” Psychological medicine vol. 29,3 (1999): 741-5. doi:10.1017/s0033291798007946
[7] Liebowitz, Michael R. The Chemistry of Love. Berkley Books, 1984.
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