Pain and suffering are often confused; learning to differentiate them can help us live a better life
Understanding suffering is crucial to live a meaningful life. For that reason, suffering a fundamental concept in many religions, particularly in Buddhism, which is built around a reflection on suffering and its overcoming. The same can be said for philosophies like Stoicism and Epicureanism. However, in today’s culture there is a simplistic interpretation of suffering that confuses it with pain, to the point where these two words are often used interchangeably. I have gained a deep comprehension of the difference between pain and suffering from three sources. First, by doing scientific research on pain neuroscience. Second, from my interest in sadomasochism. Third, from my practice of Zen Buddhism.
A few facts about pain from neuroscience
Pain and nociception are different things. Strictly speaking, the detection of noxious (harmful) events in the body by the central nervous system is called nociception, not pain . Nociception gives rise to pain only when it becomes a subjective experience, that is, when it becomes conscious. For example, under general anesthesia there is nociception but not pain: all nociceptive pathways from the body to the brain are active, but there is no pain because the anesthesia keeps us unconscious . In contrast, if a peripheral anesthetic like lidocaine is applied to the surgery site, there would be neither nociception nor pain, because lidocaine keeps the pain nerves from sending signals to the nervous system. The converse is also true: there can be pain without nociception. This happens in a disorder called “central pain” in which pain originates in a dysfunction of the brain , and in phantom limb pain [2,14]. My point here is that pain is part of our conscious experience.
Pain is a sensation of its own, different from tact, itch and other sensations coming from the body. This was controversial for a while , but now we know that pain has its own pathways: sensory nerves contain non-myelinated C fibers and thin myelinated A-delta fibers  that are specialized in sending noxious signals from the body to the dorsal horn of the spinal cord . From there, neurons send axons to different brain areas (mainly the parabrachial nucleus and the thalamus), which then relay pain signals to the cortex. Although pain is different from tact (which is carried by thick myelinated A-beta fibers), it interacts strongly with it. Usually, tactile sensations inhibit pain. This is why we rub a knee we just bumped or kiss our child’s boo-boo. However, in chronic pain disorders normal tactile sensations become painful. This is because there is a neuronal “gate” in the spinal cord that connects neurons that process tact with neurons that process pain. Normally, the gate is inhibitory, so tact inhibits pain. But in chronic pain disorders the gate becomes excitatory, so tactile sensations become painful .
The brain exerts a large control over the intensity of pain. Apart from this modulation by tactile sensations, the intensity of pain is also controlled by “descending pathways”: neurons in the brain send axons down the spinal cord [4,13]. The best know descending pathway is the one that links the periaqueductal grey (PAG) area in the middle of the brain with the rostral-ventral medulla (RVM) in the brain stem, and uses endorphins and opioid receptors to inhibit pain . The analgesic effect of morphine and other opioids is largely mediated by this pathway. Another pain inhibition pathway uses noradrenaline as its neurotransmitter and links the nucleus coeruleus with the spinal cord [21,22,27]. The noradrenergic and the opioid pathways inhibit each other, so they are not active at the same time: the noradrenergic one is active in fight/flight situations, whereas the opioid one is linked to the freeze response , social defeat and relaxation. A third descending pathway increases pain instead of decreasing it [29,35], and a fourth uses dopamine as the neurotransmitter [16,17]. The modulation of pain by these systems is not trivial: the inhibitory pathways can completely abolish the pain caused by a major injury, whereas the stimulatory ones can deliver excruciating pain from a minor one. The take-home message here is that our mental state and attitude towards pain regulates the intensity of pain.
Fear affects pain. One of the main triggers for these descending pathways is fear. Counter-intuitively, fear inhibits pain ; except in some chronic pain disorders in which fear increases pain [15,20]. There is an evolutionary reason for this: if an animal is in a fight/flight situation, pain would be a distraction that will hinder its escape or its ability to fight. This inhibition of pain by fear is mediated by the amygdala (the brain region that processes fear) and the noradrenergic descending pathways [7,24,34,36]. This explains why we feel less pain while doing sports and other activities that trigger our fight/flight response.
Pain has a sensory component and an emotional component. Nociceptive signals from the spinal cord arrive at the thalamus, and there split into three pathways. One goes to the somatosensory cortex, which produces the sensation of pain: where it is located and what kind of pain it is (sharp, dull, etc.). The other two pathways go to the anterior cingulate cortex and the insula [8,11]. The anterior cingulate serves to motivate behavior, in this case to avoid the pain. The insula is responsible for the emotional aspect of pain: its unpleasantness. Drugs like ketamine and PCP (called “dissociative anesthetics”) are able to block the emotional component of pain while leaving its sensory component intact: under their influence people feel the pain, know where it is, but do not care about it. The key link between pain and suffering is in this emotional component of pain.
Pain is an emotion
Although we all have a strong intuition about what is an emotion, there is quite a bit of controversy about their exact definition. I am going to go out on a limb and provide my own, which I think is informative and in accordance with novel concepts in neuroscience: Emotions are states of the brain that provide valence and salience in order to filter sensations, drive ideation and motivate behavior. “Valence” refers to whether a mental content is attractive or aversive (we like it or not). “Salience” refers to the ability of a mental content to claim attention to itself over other mental content.
According to this definition, pain is clearly an emotion because it has valence, salience and is a strong drive for ideation and behavior: if we are in pain we tend to go out of our way to stop it. Even if you disagree with my definition of emotion, there is a consensus among pain neuroscientists that pain is an emotion or has an “emotional component” . Pain is not the only sensation with an emotional component, others are itch, tickle, hunger, thirst and pleasure. Itch can be as salient as pain and motivates us to scratch. Pleasure makes us want to continue doing whatever we are doing .
The emotional component of pain is based on its activation of the insula and the anterior cingulate cortex. The insula is a place where multiple emotions converge including pleasure, itch and disgust . It also plays a role in positive emotions such as love and empathy, even orgasm! But all this refers to the posterior insula. Throughout the evolution from monkeys to humans, there was a rapid development of the anterior insula. According to neuroscientist Bud Craig [11,12], the right anterior insula has an important and very specialized function in humans: it simulates hypothetical states of the body. Thus, if you imagine what a kick in the butt would feel like, that’s your right anterior insula doing the work. This means that we can also imagine sensations that other people may be feeling: the right anterior insula mediates empathy. It may even participate in another unique property of the human mind: theory of mind, which consists of modeling what goes on in other people’s minds [19,26].
Pain and suffering
Pain not always has negative valence. In lay terms, this means that sometimes pain can feel good. There are many examples. You may remember when you were 6 years old and had to continually move with our tongue that dangling tooth about to fall (and the Tooth Fairy has nothing to do with it). It hurt, but it hurt so good! Billions of people in nations like Mexico, Thailand, and India love spice food. The compound that makes food spicy is capsaicin, which activates a protein called TRPV1, the one that mediates the sensation of painful burning [6,32]. Hence, spicy food actually causes pain. Another use of capsaicin is to make Maze and tear gas. All mammals except us avoid capsaicin — birds do not have TRPV1, that’s why they eat chili peppers like candy. Another instance where pain feels good is sports. People love to “feel the burn” while running or working out. Personally, I love to twist my feet and hands inside the crack in a rock face to climb it , or to keep doing those hard turns while skiing regardless of the pain in my quads. Zen meditation was always painful for me, but I learned to explore the ways pain affects my consciousness. Then there is sexual masochism. Millions of people around the world love to be spanked. Some even like being caned, paddled and whipped to levels of pain that would be considered torture by most people. Clearly, a lot of activities that we consider joyful or fulfilling entail a certain level of pain, which we tolerate or even appreciate for its own sake.
Why are we able to enjoy pain? First of all, when we are doing an exciting activity like skiing or rock climbing, this activates the noradrenergic descending pathway that inhibits pain. Pain also mixes up with other emotions in the insula, and the resulting effect may be that pain enhances the positive emotions, including pleasure. In the case of sexual masochism, not all forms of pain are enjoyable. Masochists tend to favor a burning, stingy kind of skin pain, similar to the sensation that capsaicin from spicy food leaves in the mouth. Muscular, bone and visceral pain are much less enjoyable. Some masochists do not enjoy the pain but its psychological context as punishment or as a sign of dominance.
Of course, I am not denying that pain can be a significant source of suffering. I am well aware of the suffering of people with chronic pain, of the grinding effect of having to endure excruciating levels of pain for days on end. The goal of my research was to find a cure for chronic pain. But even for chronic pain patients, beliefs about pain and coping mechanisms can have a great impact on their suffering. Since in these disorders fear increases pain, letting it take over the mind increases pain. Positive emotions and cognitive strategies can interact with pain in the insula, dampening its emotional impact.
Cognition and culture can influence the intensity and valence of pain. Therefore, the ability to induce suffering depends on our education and values. Whereas our culture teaches children to fear and avoid pain, other cultures teach indifference to pain or stoicism. Pain would make us suffer less if we change the way we think about it.
As we have seen, pain is an emotion that is often unpleasant but that sometimes can be joyful, so pain is not sufficient for suffering. Neither is pain necessary for suffering, because a lot of suffering occurs in the absence of pain. Therefore, pain and suffering are different things.
Emotions and suffering
What about emotional pain? Somehow, it has become fashionable to talk about physical and emotional pain as if they were the same thing, perhaps because both of them engage the insula. However, negative emotions do not use the pain pathways that I described above, so we should avoid confusing them with pain. But, for simplicity, I am going to use “emotional pain” to refer to emotions with negative valence, that is, emotions we rather not have. These would include fear, sadness, disgust, shame and guilt. Anger, contempt and indignation present a peculiar problem because they feel good more often than not.
One could be tempted to say that suffering is having negative emotions , pain being one of them. But, again, this idea does not withstand close scrutiny. Most movies, plays and novels move us to fear, sadness, anger, and other negative emotions. And, still, we love them and seek them out.
Another issue is that, if we were to avoid emotional pain we would not become friends with people who may suffer, and we would not seek love. We value romantic love above many other things in life, knowing full well that by seeking it we will get our heartbroken. As Paul Simon sings in “I am a rock”:
I have no need of friendship friendship causes pain Its laughter and its loving I disdain. I am a rock, I am an island! Don’t talk of love Where have I heard that word before? It’s sleeping in my memory I don’t disturb the slumber Of feelings that have died If I’d never loved, I never would have cried I am a rock, I am an island!
If our goal is to avoid as much emotional pain as possible, this sort of attitude would be entirely rational. Yet, we know Paul Simon is saying all that sarcastically. Few people are as cynical about love and friendship as to avoid them. But perhaps we seek them because the final balance would bring us more happiness than suffering.
Let’s do a thought experiment, then. Person A is passionate: he constantly falls in madly in love, but after a period of bliss he suffers a painful break-up. Then he starts over again. Person B marries a woman he is comfortable with but doesn’t feel particularly passionate about, and spends all his life with her. Which would you rather be?
Perhaps the rational decision would be to be Person B, but many of us would choose to be Person A. A passionate, interesting life sounds more appealing than a dull, boring one.
Clearly, when it comes to negative emotions we are in a similar situation as with pain: they often hurt, but not always. And we certainly do not live our lives trying to avoid them. Whether an emotion causes suffering does not depend on the emotion itself, but on what causes it. Sadness from a tear-jerking movie is great, sadness from losing a loved one is tragic. What causes suffering is not the emotion itself, but something deeper that has to do with what we value in life. Suffering is not an emotion, it cuts deeper than that.
Suffering and happiness are states of being
Living an interesting, passionate, meaningful life has little to do with physical or emotional pain. Emotions are temporary mental states, whereas these things are cognitive experiences that are related to cultural values and extend through long periods of time. Of course, I am not denying that if we had to live in constant pain (like chronic pain) or in a negative emotional state (like depression) this would make us suffer. These diseases can cause extreme suffering, to the point of inducing suicide. But there is much more to suffering than that.
Here are some things that would make us suffer and have little to do with pain: a hostile social environment, psychological abuse, the suffering of others, loss of a loved one, lack of social status, lack of freedom, boredom, regrets, dread of the future, existential angst and lack of meaning. You may argue that most of these things entail emotional pain, but that emotional pain is an effect of an underlying cause, not the cause itself. These are things that we need to live a meaningful life because they are basic needs of human beings. They are not temporary emotions but long-term states of mind related to our values and our culture. These states of mind drive our behavior, affect our relationships, evoke our emotions and depend on our knowledge. That is why I think that suffering should be considered a state of being, something that pertains to the entirety of the human mind and not to particular emotions or sensations. The same can be said of the opposite of suffering: happiness — happiness is a state of being and not just an emotion.
Realizing this can serve to guide us to live lives with less suffering and more happiness. We do not achieve happiness by avoiding pain, either physical or emotional, but by leading a meaningful existence. How we define that is up to us, but educating ourselves and getting to know ourselves seem to be the path to follow. In that, Buddhism, Epicureanism and Stoicism are fundamentally right.
Basbaum, A I, D M Bautista, G Scherrer, D Julius. Cellular and molecular mechanisms of pain. Cell 139: 267–284 (2009)
Bloomquist, T. Amputation and phantom limb pain: a pain-prevention model. AANAJ 69: 211–217 (2001)
Bunting, C J, M J Little, H Tolson, G Jessup. Physical fitness and eustress in the adventure activities of rock climbing and rappelling. J Sports Med Phys Fitness 26: 11–20 (1986)
Bushnell, M C, M Ceko, L A Low. Cognitive and emotional control of pain and its disruption in chronic pain. Nat Rev Neurosci 14: 502–511 (2013)
Butler, R K, D P Finn. Stress-induced analgesia. Prog Neurobiol 88: 184–202 (2009)
Caterina, M J, M A Schumacher, M Tominaga, T A Rosen, J D Levine, D Julius. The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature 389: 816–824 (1997)
Chen, W, Y Taché, J C G Marvizon. Corticotropin Releasing Factor in the brain and blocking spinal descending signals induce hyperalgesia in the latent sensitization model of chronic pain. Neuroscience 381: 149–158 (2018)
Craig, A D. Interoception: the sense of the physiological condition of the body. Curr Opin Neurobiol 13: 500–505 (2003)
Craig, A D. A new view of pain as a homeostatic emotion. Trends Neurosci 26: 303–307 (2003)
Craig, A D. Pain mechanisms: labeled lines versus convergence in central processing. AnnuRevNeurosci 26: 1–30 (2003)
Craig, A D. The sentient self. Brain Struct Funct 214: 563–577 (2010)
Craig, A D. Significance of the insula for the evolution of human awareness of feelings from the body. Ann N Y Acad Sci 1225: 72–82 (2011)
Heinricher, M M, I Tavares, J L Leith, B M Lumb. Descending control of nociception: Specificity, recruitment and plasticity. Brain Res Rev 60: 214–225 (2009)
Iacono, R P, J Linford, R Sandyk. Pain management after lower extremity amputation. Neurosurgery 20: 496–500 (1987)
Jennings, E M, B N Okine, M Roche, D P Finn. Stress-induced hyperalgesia. Prog Neurobiol 121: 1–18 (2014)
Kim, J Y, D V Tillu, T L Quinn, G L Mejia, A Shy, M N Asiedu, E Murad, A P Schumann, S K Totsch, R E Sorge, P W Mantyh, G Dussor, T J Price. Spinal dopaminergic projections control the transition to pathological pain plasticity via a D1/D5-mediated mechanism. J Neurosci 35: 6307–6317 (2015)
Koblinger, K, T Fuzesi, J Ejdrygiewicz, A Krajacic, J S Bains, P J Whelan. Characterization of A11 neurons projecting to the spinal cord of mice. PLoS One 9: e109636 (2014)
Kringelbach, M L, K C Berridge. Towards a functional neuroanatomy of pleasure and happiness. Trends Cogn Sci 13: 479–487 (2009)
Krupenye, C, F Kano, S Hirata, J Call, M Tomasello. Great apes anticipate that other individuals will act according to false beliefs. Science 354: 110–114 (2016)
Le Roy, C, E Laboureyras, S Gavello-Baudy, J Chateauraynaud, J P Laulin, G Simonnet. Endogenous opioids released during non-nociceptive environmental stress induce latent pain sensitization via a NMDA-dependent process. Journal of Pain 12: 1069–1079 (2011)
Maeda, M, M Tsuruoka, B Hayashi, I Nagasawa, T Inoue. Descending pathways from activated locus coeruleus/subcoeruleus following unilateral hindpaw inflammation in the rat. Brain Res Bull 78: 170–174 (2009)
Maire, J J, L N Close, M M Heinricher, N R Selden. Distinct pathways for norepinephrine- and opioid-triggered antinociception from the amygdala. Eur J Pain (2015)
Mason, P. Contributions of the medullary raphe and ventromedial reticular region to pain modulation and other homeostatic functions. Annu Rev Neurosci 24: 737–777 (2001)
Neugebauer, V. Amygdala pain mechanisms. Handb Exp Pharmacol 227: 261–284 (2015)
Peirs, C, S P Williams, X Zhao, C E Walsh, J Y Gedeon, N E Cagle, A C Goldring, H Hioki, Z Liu, P S Marell, R P Seal. Dorsal Horn Circuits for Persistent Mechanical Pain. Neuron 87: 797–812 (2015)
Penn, D C, D J Povinelli. On the lack of evidence that non-human animals possess anything remotely resembling a ‘theory of mind’. Philosophical transactions of the Royal Society of London Series B, Biological sciences 362: 731–744 (2007)
Pertovaara, A. Noradrenergic pain modulation. Prog Neurobiol 80: 53–83 (2006)
Phillips, K, D J Clauw. Central pain mechanisms in chronic pain states — maybe it is all in their head. Best Pract Res Clin Rheumatol 25: 141–154 (2011)
Porreca, F, M H Ossipov, G F Gebhart. Chronic pain and medullary descending facilitation. Trends Neurosci 25: 319–325 (2002)
Roelofs, K. Freeze for action: neurobiological mechanisms in animal and human freezing. Philos Trans R Soc Lond B Biol Sci 372 (2017)
Shushruth, S. Exploring the Neural Basis of Consciousness through Anesthesia. J Neurosci 33: 1757–1758 (2013)
Tominaga, M, M J Caterina, A B Malmberg, T A Rosen, H Gilbert, K Skinner, B E Raumann, A I Basbaum, D Julius. The cloned capsaicin receptor integrates multiple pain-producing stimuli. Neuron 21: 531–543 (1998)
Usoskin, D, A Furlan, S Islam, H Abdo, P Lonnerberg, D Lou, J Hjerling-Leffler, J Haeggstrom, O Kharchenko, P V Kharchenko, S Linnarsson, P Ernfors. Unbiased classification of sensory neuron types by large-scale single-cell RNA sequencing. Nat Neurosci 18: 145–153 (2015)
Van Bockstaele, E J, E E Colago, R J Valentino. Corticotropin-releasing factor-containing axon terminals synapse onto catecholamine dendrites and may presynaptically modulate other afferents in the rostral pole of the nucleus locus coeruleus in the rat brain. J Comp Neurol 364: 523–534 (1996)
Vera-Portocarrero, L P, E T Zhang, M H Ossipov, J Y Xie, T King, J Lai, F Porreca. Descending facilitation from the rostral ventromedial medulla maintains nerve injury-induced central sensitization. Neuroscience 140: 1311–1320 (2006)
Wilson, T D, S Valdivia, A Khan, H S Ahn, A P Adke, S Martinez Gonzalez, Y K Sugimura, Y Carrasquillo. Dual and Opposing Functions of the Central Amygdala in the Modulation of Pain. Cell Rep 29: 332–346.e335 (2019)
Woolf, C J, Q Ma. Nociceptors — noxious stimulus detectors. Neuron 55: 353–364 (2007)
Zubieta, J K, Y R Smith, J A Bueller, Y Xu, M R Kilbourn, D M Jewett, C R Meyer, R A Koeppe, C S Stohler. Regional mu opioid receptor regulation of sensory and affective dimensions of pain. Science 293: 311–315 (2001)