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group_4_presentation_2_-_love_and_hate [2018/03/02 15:45] chowds6 |
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| ====== Love and Hate ====== | ====== Love and Hate ====== | ||
| - | <box 35% right | > {{ :love-hate-art-print.jpg?400 |}} </box| Figure 1: Visual by Vilson (2016).> | + | <box 34% right | > {{ :love-hate-art-print.jpg?400 |}} </box| Figure 1: Visual by Vilson (2016).> |
| - | Love is comprised of various positive and strong emotional experiences and mental states. Driving love are three components: lust, attachment, and attraction. Each component of love is influenced by various hormones and neurotransmitters that affect our brain's reward circuit. Two regions that become active when in love include the caudate nucleus and the ventral tegmental area, also known as the reward circuit. This circuit is linked with the nucleus accumbens, with the function of operating dopamine and serotonin. Other structures that contribute to the reward circuit include the amygdala, the hippocampus, and the prefrontal cortex. In contrast, heartbreaks result from traumatic breakups or the death of a loved one. In extreme events the emotional distress can be so severe it can result in the alteration of the left ventricle. As a consequence, many symptoms arise and are known to be associated with the heartbreak syndrome, also known as Takotsubo Cardiomyopathy (TC). Neurochemical processes such a the m-opioid receptor and drastic declines in love neurotransmitters such as dopamine and oxytocin have been shown to cause the brain to react negatively and seek out social contact. Beyond heartbreak, hate is also a common emotion that is felt. Hate, in its simplest form, is to have a strong emotional response to extreme dislike. One can manifest a hatred for a variety of things, including an individual and certain groups of people. A study based on “the hate circuit” has proposed that the reason why we hate is due to the same four areas of the brain being activated, which is consistent across all individuals and which help with motor and decision planning when confronted with a hated person. Potential treatments include painkillers, opioids, placebo treatments, social support and even comfort food to demission activation of areas of the brain that cause both physical pain and emotional pain. | + | Love is comprised of various positive and strong emotional experiences and mental states. Driving love are three components: lust, attachment, and attraction. Each component of love is influenced by various hormones and neurotransmitters that affect our brain's reward circuit. Two regions that become active when in love include the caudate nucleus and the ventral tegmental area, also known as the reward circuit. This circuit is linked with the nucleus accumbens, with the function of operating dopamine and serotonin. Other structures that contribute to the reward circuit include the amygdala, the hippocampus, and the prefrontal cortex. In contrast, heartbreaks result from traumatic breakups or the death of a loved one. In extreme events the emotional distress can be so severe it can result in the alteration of the left ventricle. As a consequence, many symptoms arise and are known to be associated with the heartbreak syndrome, also known as Takotsubo Cardiomyopathy (TC). Neurochemical processes such a the μ-opioid receptor and drastic declines in love neurotransmitters such as dopamine and oxytocin have been shown to cause the brain to react negatively and seek out social contact. Beyond heartbreak, hate is also a common emotion that is felt. Hate, in its simplest form, is to have a strong emotional response to extreme dislike. One can manifest a hatred for a variety of things, including an individual and certain groups of people. A study based on “the hate circuit” has proposed that the reason why we hate is due to the same four areas of the brain being activated, which is consistent across all individuals and which help with motor and decision planning when confronted with a hated person. Potential treatments include painkillers, opioids, placebo treatments, social support and even comfort food to demission activation of areas of the brain that cause both physical pain and emotional pain. |
| ====== What is Love? ====== | ====== What is Love? ====== | ||
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| <box 55% | >{{ :figure-1-1.png?600 |}}</box|Figure 2. A study done by Harvard University found that during each component of love there are certain chemicals that take the lead as shown above (Wu, 2018).> | <box 55% | >{{ :figure-1-1.png?600 |}}</box|Figure 2. A study done by Harvard University found that during each component of love there are certain chemicals that take the lead as shown above (Wu, 2018).> | ||
| - | ====== Your Brain on Love ====== | + | ====== The Brain on Love ====== |
| There have been studies demonstrating functional MRI (fMRI) images of the brain of individuals when they were shown photos of people they romantically loved. As a result, the brain became active in regions rich with dopamine which is known as the “feel-good neurotransmitter” (Fisher 2005). Specifically, two regions became active including the caudate nucleus, associated with reward detection and integration of sensory experiences into social behavior, and the ventral tegmental area, also known as the reward circuit is associated with pleasure and focused attention and motivation to acquire rewards (Fisher 2005). Rewards are defined as the biological mechanisms that motivate behavior by events associated with pleasure. | There have been studies demonstrating functional MRI (fMRI) images of the brain of individuals when they were shown photos of people they romantically loved. As a result, the brain became active in regions rich with dopamine which is known as the “feel-good neurotransmitter” (Fisher 2005). Specifically, two regions became active including the caudate nucleus, associated with reward detection and integration of sensory experiences into social behavior, and the ventral tegmental area, also known as the reward circuit is associated with pleasure and focused attention and motivation to acquire rewards (Fisher 2005). Rewards are defined as the biological mechanisms that motivate behavior by events associated with pleasure. | ||
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| Takotsubo cardiomyopathy is the weakening of the left ventricle, which is the heart's main pumping chamber. This is usually caused by severe emotional or physical stress. The precise cause of this syndrome is unknown but experts think that surging stress hormones like adrenaline essentially "stun" the heart, triggering changes in heart muscle cells or coronary blood vessels or even both that prevent the left ventricle from contracting effectively (Fisher, Xu, Aron & Brown, 2016). Other hormone levels like norepinephrine and epinephrine also are elevated in individuals with broken heart syndrome. The echocardiograms of individuals with broken heart syndrome usually have a weakened contraction in the middle and upper portions of the heart muscle, and inverted T waves and prolonged Q-T intervals often associated with stress (Fisher, Xu, Aron & Brown, 2016). Heartbreaks can also jeopardize one’s health due to abandonment rage as it stresses the heart consequently raising blood pressure and suppressing the immune system. This can further induce clinical depression and in extreme cases even lead to suicide (Fisher, Xu, Aron & Brown, 2016). | Takotsubo cardiomyopathy is the weakening of the left ventricle, which is the heart's main pumping chamber. This is usually caused by severe emotional or physical stress. The precise cause of this syndrome is unknown but experts think that surging stress hormones like adrenaline essentially "stun" the heart, triggering changes in heart muscle cells or coronary blood vessels or even both that prevent the left ventricle from contracting effectively (Fisher, Xu, Aron & Brown, 2016). Other hormone levels like norepinephrine and epinephrine also are elevated in individuals with broken heart syndrome. The echocardiograms of individuals with broken heart syndrome usually have a weakened contraction in the middle and upper portions of the heart muscle, and inverted T waves and prolonged Q-T intervals often associated with stress (Fisher, Xu, Aron & Brown, 2016). Heartbreaks can also jeopardize one’s health due to abandonment rage as it stresses the heart consequently raising blood pressure and suppressing the immune system. This can further induce clinical depression and in extreme cases even lead to suicide (Fisher, Xu, Aron & Brown, 2016). | ||
| - | <box 60% | >{{ :28643253_10211372904986245_564440784_o.jpg?550 |}}</box|Figure 4. The heart on the left is the normal heart displaying the normal state of the left ventricle during contraction. The heart on the right shows the shape of the left ventricle when it contracts and as depicted it is enlarged during the TC syndrome (SVH, 2016).> | + | <box 47% | >{{ :28643253_10211372904986245_564440784_o.jpg?550 |}}</box|Figure 6. The heart on the left is the normal heart displaying the normal state of the left ventricle during contraction. The heart on the right shows the shape of the left ventricle when it contracts and as depicted it is enlarged during the TC syndrome (SVH, 2016).> |
| - | ====== Brain on Heartbreak ====== | + | ====== The Brain on Heartbreak ====== |
| The neurological process involved in the perception of heartache is not known but is thought to involve the anterior cingulate cortex of the brain, which during stress may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest. | The neurological process involved in the perception of heartache is not known but is thought to involve the anterior cingulate cortex of the brain, which during stress may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest. | ||
| - | |||
| - | <box 60% | >{{ :28535093_10211372980308128_709345701_n.png?500 |}}</box|Figure 5. This figure shows the Cingulate Gyrus which could be involved neurologically during a heartbreak. During stress it may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest (Cingulate cortex, 2018).> | ||
| Research published by the National Academy of Sciences showed that the pain we experience in moments like heartbreak is actually quite literal: our brains and bodies process the pain of emotional rejection in much the same way they do a sprained ankle or a broken leg (Vastag, 2003). Research participants viewed a photo of an ex after an unwanted breakup with that person and were told to think about the rejection of that breakup (Vastag, 2003). As they did, under neuroimaging the same regions of the brain that underpin the response to physical pain became active. Revealing that emotional pain such as social rejection and physical pain are similar as they share a common representation in somatosensory brain systems (Vastag, 2003). In the case of physical injury, there is first an adrenaline surge of stress hormones that prepare the body for flight or fight causing the individual to feel numb before the hormone surge dissipation and the pain reaction sets in. Researchers found the same reaction to occur after social rejection as well (Vastag, 2003). | Research published by the National Academy of Sciences showed that the pain we experience in moments like heartbreak is actually quite literal: our brains and bodies process the pain of emotional rejection in much the same way they do a sprained ankle or a broken leg (Vastag, 2003). Research participants viewed a photo of an ex after an unwanted breakup with that person and were told to think about the rejection of that breakup (Vastag, 2003). As they did, under neuroimaging the same regions of the brain that underpin the response to physical pain became active. Revealing that emotional pain such as social rejection and physical pain are similar as they share a common representation in somatosensory brain systems (Vastag, 2003). In the case of physical injury, there is first an adrenaline surge of stress hormones that prepare the body for flight or fight causing the individual to feel numb before the hormone surge dissipation and the pain reaction sets in. Researchers found the same reaction to occur after social rejection as well (Vastag, 2003). | ||
| + | |||
| + | <box 55% | >{{ :28535093_10211372980308128_709345701_n.png?500 |}}</box|Figure 7. This figure shows the Cingulate Gyrus which could be involved neurologically during a heartbreak. During stress it may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest (Cingulate cortex, 2018).> | ||
| ====== Biochemistry of Heartbreak ====== | ====== Biochemistry of Heartbreak ====== | ||
| + | |||
| + | ==== Reduced Neurochemical Activity ==== | ||
| As discussed previously, feelings of love and adoration have been observed to elevate certain neurochemicals, in particular, dopamine activity in the reward pathway and oxytocin which has also been both associated with feelings of trust and social connection in humans (Burnett, 2016). Over a period of time, the brain soon becomes accustomed to these elevated levels positive neurochemicals, however, when they unexpectedly end due to cases such as heartbreak, the brain turns to a state of shock (Burnett, 2016). All the positive neurochemicals the brain has come to expect due to being in a relationship and having them all drastically decline after a relationship ceases can negatively affect the brain by inducing this state of distress, uncertainty, and ambiguity (Burnett, 2016). Multiple studies have also shown that these sudden neurochemical decreases due to relationship breakups have also demonstrated to activate similar brain regions that process physical pain (Burnett, 2016). | As discussed previously, feelings of love and adoration have been observed to elevate certain neurochemicals, in particular, dopamine activity in the reward pathway and oxytocin which has also been both associated with feelings of trust and social connection in humans (Burnett, 2016). Over a period of time, the brain soon becomes accustomed to these elevated levels positive neurochemicals, however, when they unexpectedly end due to cases such as heartbreak, the brain turns to a state of shock (Burnett, 2016). All the positive neurochemicals the brain has come to expect due to being in a relationship and having them all drastically decline after a relationship ceases can negatively affect the brain by inducing this state of distress, uncertainty, and ambiguity (Burnett, 2016). Multiple studies have also shown that these sudden neurochemical decreases due to relationship breakups have also demonstrated to activate similar brain regions that process physical pain (Burnett, 2016). | ||
| + | ==== μ-Opioid Receptor ==== | ||
| + | |||
| Another mechanism that has been found to modulate heartbreak is the endogenous opioid system, a primary neurochemical system for regulating physical pain, as demonstrated in its ability to mediate social attachments in various animal and human studies (Tchalova & Eisenberger, 2015). In particular, it is proposed that social separation distress, much like the distress defined in heartbreak, can cause a painful low-opioid state. This low-opioid state can then motivate social proximity seeking, in other words, motivation to establish relationships/connections with other individuals (Tchalova & Eisenberger, 2015). This seeking behaviour ends once social contact is made, prompting the release of endogenous opioids and establishing regular opioid levels once again (Tchalova & Eisenberger, 2015). | Another mechanism that has been found to modulate heartbreak is the endogenous opioid system, a primary neurochemical system for regulating physical pain, as demonstrated in its ability to mediate social attachments in various animal and human studies (Tchalova & Eisenberger, 2015). In particular, it is proposed that social separation distress, much like the distress defined in heartbreak, can cause a painful low-opioid state. This low-opioid state can then motivate social proximity seeking, in other words, motivation to establish relationships/connections with other individuals (Tchalova & Eisenberger, 2015). This seeking behaviour ends once social contact is made, prompting the release of endogenous opioids and establishing regular opioid levels once again (Tchalova & Eisenberger, 2015). | ||
| - | To examine this phenomenon further, studies have been conducted to examine m-opioid, which has been known to be released as an emotional and physical painkiller during both types of events; when someone feels physical pain, as well as when a person experiences rejection and social detachment (Fisher, 2015). Moles and colleagues (2004) conducted a study on the m-opioid receptor, which attaches to opioid molecules to complete the endogenous opioid system and plays a key role in pain perception and addiction. In this study, m-opioid receptors (Figure 6) were genetically engineered and removed in mice models. The removal of this specific receptor resulted in an induced increase of distress vocalizations when mice pups were removed from their mother (Moles et al., 2004). Results from this study have thus helped indicate an associated molecular mechanism for abnormalities and deficits in social attachment behavior, as well as experiences of social distress (Moles et al., 2004). | + | To examine this phenomenon further, studies have been conducted to examine μ-opioid, which has been known to be released as an emotional and physical painkiller during both types of events; when someone feels physical pain, as well as when a person experiences rejection and social detachment (Fisher, 2015). Moles and colleagues (2004) conducted a study on the μ-opioid receptor, which attaches to opioid molecules to complete the endogenous opioid system and plays a key role in pain perception and addiction. In this study, μ-opioid receptors (Figure 8) were genetically engineered and removed in mice models. The removal of this specific receptor resulted in an induced increase of distress vocalizations when mice pups were removed from their mother (Moles et al., 2004). Results from this study have thus helped indicate an associated molecular mechanism for abnormalities and deficits in social attachment behavior, as well as experiences of social distress (Moles et al., 2004). |
| - | <box 50% | >{{ :screen_shot_2018-03-02_at_11.21.44_am.png?300 |}}</box|Figure 6. The normal interaction between opioid molecules and m-opioid receptors in the endogenous opioid system (Tchalova & Eisenberger, 2015).> | + | <box 35% | >{{ :screen_shot_2018-03-02_at_11.21.44_am.png?400 |}}</box|Figure 8. The normal interaction between opioid molecules and μ-opioid receptors in the endogenous opioid system (Tchalova & Eisenberger, 2015).> |
| - | The mutation of the m-opioid receptor gene, specifically A118G polymorphism, has also been observed in a study by Zhang and colleagues (2005) to validate the receptor’s effect on social behaviour and addiction. The A118G polymorphism of the m-opioid receptor gene is hypothesized to be a loss-of-function allele that lowers mRNA expression and receptor protein translation rates (Zhang et al., 2005). It was observed from studies such as these that there is a greater physical pain susceptibility in childhood withdrawal, and even primates showing more pronounced and persistent separation anxiety (Tchalova & Eisenberger, 2015). Altogether, these research findings support the idea of shared sensitivities to physical and social pain and make a sound argument for the involvement of the endogenous opioid system in the regulation of social pain. | + | The mutation of the μ-opioid receptor gene, specifically A118G polymorphism, has also been observed in a study by Zhang and colleagues (2005) to validate the receptor’s effect on social behaviour and addiction. The A118G polymorphism of the μ-opioid receptor gene is hypothesized to be a loss-of-function allele that lowers mRNA expression and receptor protein translation rates (Zhang et al., 2005). It was observed from studies such as these that there is a greater physical pain susceptibility in childhood withdrawal, and even primates showing more pronounced and persistent separation anxiety (Tchalova & Eisenberger, 2015). Altogether, these research findings support the idea of shared sensitivities to physical and social pain and make a sound argument for the involvement of the endogenous opioid system in the regulation of social pain. |
| Opioid receptor antagonists, which are known to aggravate physical pain have also shown to increase distress vocalizations in isolated animals and slow the reduction in distress vocalizations typically seen when animals are reunited with their companions (Fisher, 2015). From these findings, it can also be argued that those prone to social anxiety, panic attacks and depression release less opioid, therefore taking longer to recover from negative social experiences. These individuals may also struggle to gain as much pleasure from social support as those who release more opioid in comparison (Fisher, 2015). | Opioid receptor antagonists, which are known to aggravate physical pain have also shown to increase distress vocalizations in isolated animals and slow the reduction in distress vocalizations typically seen when animals are reunited with their companions (Fisher, 2015). From these findings, it can also be argued that those prone to social anxiety, panic attacks and depression release less opioid, therefore taking longer to recover from negative social experiences. These individuals may also struggle to gain as much pleasure from social support as those who release more opioid in comparison (Fisher, 2015). | ||
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| There are many other ideas of why individuals hate. One idea is that hate derives from fear of the unknown. The in-group out-group theory postulates that in times of fear or conflict our natural survival mechanism is to turn towards our ‘in group’, which are individuals who they identify with, love, or recognize. Thus, the ‘out-group’ are individuals who are collectively unrecognized and aggressed towards- thus leading to hate (Halevy, Bornstein, & Sagiv, 2008). Another idea is almost a mirror of the previous, where individuals hate others based on insecurities and fears of themselves. This is better known as ‘projection’, where individuals perceive their undesirable qualities onto others (Govorun, Fuegen, & Payne, 2006). | There are many other ideas of why individuals hate. One idea is that hate derives from fear of the unknown. The in-group out-group theory postulates that in times of fear or conflict our natural survival mechanism is to turn towards our ‘in group’, which are individuals who they identify with, love, or recognize. Thus, the ‘out-group’ are individuals who are collectively unrecognized and aggressed towards- thus leading to hate (Halevy, Bornstein, & Sagiv, 2008). Another idea is almost a mirror of the previous, where individuals hate others based on insecurities and fears of themselves. This is better known as ‘projection’, where individuals perceive their undesirable qualities onto others (Govorun, Fuegen, & Payne, 2006). | ||
| - | ====== Your Brain on Hate ====== | + | ====== The Brain on Hate ====== |
| - | The reason why exactly we hate has been under discussion for decades, yet the exact cause has yet to be determined. However, in a groundbreaking study conducted by neurobiologists Zeki and Ramava (2008) they uncovered what they called, “The Hate Circuit.” In their study, 17 adults were scanned via fMRI while they first observed at the face of an acquaintance who they had neutral feelings towards, and then again when observing the face of someone they professed to hate. The areas activated in by the neutral faces were the same as when one would look at a blank face such as a mannequin, creating a baseline and control for the study (Zeki & Ramava, 2008) as seen in Figure 7. | + | The reason why exactly we hate has been under discussion for decades, yet the exact cause has yet to be determined. However, in a groundbreaking study conducted by neurobiologists Zeki and Ramava (2008) they uncovered what they called, “The Hate Circuit.” In their study, 17 adults were scanned via fMRI while they first observed at the face of an acquaintance who they had neutral feelings towards, and then again when observing the face of someone they professed to hate. The areas activated in by the neutral faces were the same as when one would look at a blank face such as a mannequin, creating a baseline and control for the study (Zeki & Ramava, 2008) as seen in Figure 9. |
| - | <box 50% | >{{ :journal.pone.0003556.g002_1_.png?500 |}}</box|Figure 7. The areas activated in by the neutral faces were the same as when one would look at a blank face such as a mannequin, creating a baseline and control for the study - the fusiform face area and right and left fusiform gyrus (Zeki & Ramava, 2008).> | + | <box 40% | >{{ :journal.pone.0003556.g002_1_.png?400 |}}</box|Figure 9. The areas activated in by the neutral faces were the same as when one would look at a blank face such as a mannequin, creating a baseline and control for the study - the fusiform face area and right and left fusiform gyrus (Zeki & Ramava, 2008).> |
| - | However, when individuals were faced with the image of someone they hated, all 17 participants had the same four areas activated, in other words, a consistent “hate circuit” amongst the medial frontal gyrus, right putamen, premotor cortex and medial insula, as seen in Figure 8. Through further observations, these areas all we correlated linearly with the level of hatred participants felt, as well as activity for the initiation of aggressive behaviour, significantly different than anger or aggression itself (Zeki & Ramava, 2008). In particular, the premotor cortex and subcortex that was activated are related to the generation of aggressive behaviour, such as when combatting an individual or walking away from them, as well as general motor planning. Areas of the frontal cortex that were activated however were related to predicting the actions of others, which is key when in the decision-making processes when confronting a hated individual. In addition, it was observed the same two areas, the putamen, and the insula were activated when an individual is feeling either love or hate, indicating a biological connection between the two (Zeki & Ramava, 2008). | + | However, when individuals were faced with the image of someone they hated, all 17 participants had the same four areas activated, in other words, a consistent “hate circuit” amongst the medial frontal gyrus, right putamen, premotor cortex and medial insula, as seen in Figure 10. Through further observations, these areas all we correlated linearly with the level of hatred participants felt, as well as activity for the initiation of aggressive behaviour, significantly different than anger or aggression itself (Zeki & Ramava, 2008). In particular, the premotor cortex and subcortex that was activated are related to the generation of aggressive behaviour, such as when combatting an individual or walking away from them, as well as general motor planning. Areas of the frontal cortex that were activated however were related to predicting the actions of others, which is key when in the decision-making processes when confronting a hated individual. In addition, it was observed the same two areas, the putamen, and the insula were activated when an individual is feeling either love or hate, indicating a biological connection between the two (Zeki & Ramava, 2008). |
| - | <box 70% | >{{ :journal.pone.0003556.g003.png?500 |}}</box|Figure 8. The areas activated by all 17 participants when observing hated faces were the medial frontal gyrus, right putamen, premotor cortex and medial insula (Zeki & Ramava, 2008).> | + | <box 50% | >{{ :journal.pone.0003556.g003.png?600 |}}</box|Figure 10. The areas activated by all 17 participants when observing hated faces were the medial frontal gyrus, right putamen, premotor cortex and medial insula (Zeki & Ramava, 2008).> |
| ====== Potential Treatments ====== | ====== Potential Treatments ====== | ||
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| Opioid drugs are considered painkillers, but it has been found not to only diminish physical pain, but social pain as well. In several animal studies, it has been found that animals administered low-dose morphine, a type of opioid drug, lowered the frequency of social separation distress calls, while opioid receptor agonists increased the vocalizations from the isolated animals (Tchalova & Eisenberger, 2015). Painkillers are also effective at reducing both physical and social pain. To illustrate this, acetaminophen, also known generically as Tylenol, a common painkiller, was tested to see if it would reduce social pain as well as physical pain. Sixty-two healthy undergrad students were recruited for a study, in which they were instructed to take a 500-mg pill after waking up and before going to bed. 30 of the participants were given 1000mg Tylenol, while 32 were given a placebo. The participants were also instructed to use the Hurt Feelings Scale to report how much social pain they had endured that given day. The participants were to do this consecutively for 3 weeks. Following this, the patients were subjected to a functional MRI scale with efforts to observe differences in neuronal responses associated with social rejection in the brain. It was found that acetaminophen was associated with reduced social pain on a daily basis, and also reduced neuronal activation in the dorsal anterior cingulate cortex, and anterior insula- which are areas of the brain which are found to be associated with both physical and social pain (DeWall et al., 2010). | Opioid drugs are considered painkillers, but it has been found not to only diminish physical pain, but social pain as well. In several animal studies, it has been found that animals administered low-dose morphine, a type of opioid drug, lowered the frequency of social separation distress calls, while opioid receptor agonists increased the vocalizations from the isolated animals (Tchalova & Eisenberger, 2015). Painkillers are also effective at reducing both physical and social pain. To illustrate this, acetaminophen, also known generically as Tylenol, a common painkiller, was tested to see if it would reduce social pain as well as physical pain. Sixty-two healthy undergrad students were recruited for a study, in which they were instructed to take a 500-mg pill after waking up and before going to bed. 30 of the participants were given 1000mg Tylenol, while 32 were given a placebo. The participants were also instructed to use the Hurt Feelings Scale to report how much social pain they had endured that given day. The participants were to do this consecutively for 3 weeks. Following this, the patients were subjected to a functional MRI scale with efforts to observe differences in neuronal responses associated with social rejection in the brain. It was found that acetaminophen was associated with reduced social pain on a daily basis, and also reduced neuronal activation in the dorsal anterior cingulate cortex, and anterior insula- which are areas of the brain which are found to be associated with both physical and social pain (DeWall et al., 2010). | ||
| - | <box 60% | >{{ :screen_shot_2018-03-02_at_11.44.29_am.png?500 |}}</box|Figure 9. Both treatment (acetaminophen) and placebo group individuals were subject to fMRI full brain scans to observe neuronal activity. To highlight, the dorsal anterior cingulate cortex (dACC) (a) and right anterior insula (b) were both seen to have heightened activity in the acetaminophen group than the placebo group. (DeWall et al., 2010).> | + | <box 55% | >{{ :screen_shot_2018-03-02_at_11.44.29_am.png?500 |}}</box|Figure 11. Both treatment (acetaminophen) and placebo group individuals were subject to fMRI full brain scans to observe neuronal activity. To highlight, the dorsal anterior cingulate cortex (dACC) (a) and right anterior insula (b) were both seen to have heightened activity in the acetaminophen group than the placebo group. (DeWall et al., 2010).> |
| ==== Placebo Treatments ==== | ==== Placebo Treatments ==== | ||
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| Social support- Social support helps alleviate the emotional and social distress, but also helps the physical pain. To highlight how social support helps with the physical pain, a study was conducted that observed females being subjected to thermally induced pain. Some individuals were either holding the hand, of their romantic partner or looking at a photo of their romantic partner. It was found that the women who were looking at the photos of their loved ones or holding their hand, experienced less pain compared to women who were alone. It is also found that social support during painful situations has led to decrease signaling in the dorsal anterior cingulate cortex and anterior insula, which are regions of the pain that perceive physical pain (Tchalova & Eisenberger, 2015). | Social support- Social support helps alleviate the emotional and social distress, but also helps the physical pain. To highlight how social support helps with the physical pain, a study was conducted that observed females being subjected to thermally induced pain. Some individuals were either holding the hand, of their romantic partner or looking at a photo of their romantic partner. It was found that the women who were looking at the photos of their loved ones or holding their hand, experienced less pain compared to women who were alone. It is also found that social support during painful situations has led to decrease signaling in the dorsal anterior cingulate cortex and anterior insula, which are regions of the pain that perceive physical pain (Tchalova & Eisenberger, 2015). | ||
| - | <box 60% | >{{ :screen_shot_2018-03-02_at_11.44.38_am.png?500 |}}</box|Figure 10. Both treatment (acetaminophen) and placebo group individuals were subject to fMRI full brain scans to observe neuronal activity. To highlight, the dorsal anterior cingulate cortex (dACC) (a) and right anterior insula (b) were both seen to have heightened activity in the acetaminophen group than the placebo group. (DeWall et al., 2010).> | + | <box 50% | >{{ :screen_shot_2018-03-02_at_11.44.38_am.png?500 |}}</box|Figure 12. Both treatment (acetaminophen) and placebo group individuals were subject to fMRI full brain scans to observe neuronal activity. To highlight, the dorsal anterior cingulate cortex (dACC) (a) and right anterior insula (b) were both seen to have heightened activity in the acetaminophen group than the placebo group. (DeWall et al., 2010).> |
| ==== Comfort Food ===== | ==== Comfort Food ===== | ||
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| ====== Conclusion ====== | ====== Conclusion ====== | ||
| - | In summary, love is a deeper experienced emotional and mental states ranging from affection to pleasures. Influences by our desire or lust for someone, attraction, and attachment. The more we experience these positive affections or pleasures, the more activated our brain’s reward circuit becomes. This acts as a positive feedback loop which is affected by multiple neurotransmitters and hormones. There are many structures involved with the feeling of love including the caudate nucleus and the ventral tegmental area known as the reward circuit. These are also linked with the nucleus accumbens, the hippocampus, amygdala, and the prefrontal cortex. Within these structures, chemicals and hormones such as dopamine, norepinephrine, serotonin, vasopressin, oxytocin, testosterone and estrogen play an important role in the emotion of love. The mechanism of heartbreak is yet to be fully understood, but many journal articles propose sudden declines in dopamine and oxytocin, increased cortisol, as well as low opioid levels to be correlated to feelings of social separation distress as observed in heartbreak.The hate circuit has shown groundbreaking evidence on how certain areas of the brain, specifically the medial frontal gyrus, right putamen, premotor cortex and medial insula to be correlated to motor planning and predicting other’s behaviour when feeling hate towards someone. | + | In summary, love is a deep emotional experience and comprises of mental states ranging from affection to pleasures, influenced significantly by our desire or lust, attraction, and attachment towards someone. The more we experience these positive affections or pleasures, the more activated our brain’s reward circuit becomes. This acts as a positive feedback loop which is affected by multiple neurotransmitters and hormones that affect different components of love. There are many structures involved with the feeling of love including the caudate nucleus and the ventral tegmental area, also known as the reward circuit. These are also linked with the nucleus accumbens, the hippocampus, amygdala, and the prefrontal cortex. Within these structures, chemicals and hormones such as dopamine, norepinephrine, serotonin, vasopressin, oxytocin, testosterone and estrogen play an important role in the emotion of love. The mechanism of heartbreak is yet to be fully understood, but many journal articles propose sudden declines in dopamine and oxytocin, increased cortisol, as well as low opioid levels to be correlated to feelings of social separation distress, similarly observed in heartbreak. The "hate circuit" has also shown groundbreaking evidence on how certain areas of the brain, specifically the medial frontal gyrus, right putamen, premotor cortex and medial insula, are correlated to motor planning and predicting other’s behaviour when feeling hate towards someone. Overall love, heartbreak, and hate are complex human emotions that are equally as different, as they are similar. |
| ====== Presentation ===== | ====== Presentation ===== | ||
