Endorphins ("endogenous morphine") are endogenous opioid peptides that function as neurotransmitters.[1] They are produced by the pituitary gland and the hypothalamus in vertebrates during exercise,[2] excitement, pain, consumption of spicy food, love and orgasm,[3][4] and they resemble the opiates in their abilities to produce analgesia and a feeling of well-being.
The term endorphin implies a pharmacological activity (analogous to the activity of the corticosteroid category of biochemicals) as opposed to a specific chemical formulation. It consists of two parts: endo- and -orphin; these are short forms of the words endogenous and morphine, intended to mean "a morphine-like substance originating from within the body."[5]
The term endorphin rush has been adopted in popular speech to refer to feelings of exhilaration brought on by pain, danger, or other forms of stress,[2] supposedly due to the influence of endorphins. When a nerve impulse reaches the spinal cord, endorphins that prevent nerve cells from releasing more pain signals are released. Immediately after injury, endorphins allow animals to feel a sense of power and control over themselves that allows them to persist with activity for an extended time.
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Opioid neuropeptides were first discovered in 1974 by two independent groups of investigators:
β-Endorphin is released into blood from the pituitary gland and into the spinal cord and brain from hypothalamic neurons. The β-endorphin that is released into the blood cannot enter the brain in large quantities because of the blood-brain barrier, so the physiological importance of the β-endorphin that can be measured in the blood is far from clear. β-Endorphin is a cleavage product of pro-opiomelanocortin (POMC), which is also the precursor hormone for adrenocorticotrophic hormone (ACTH). The behavioural effects of β-endorphin are exerted by its actions in the brain and spinal cord, and it is presumed that the hypothalamic neurons are the major source of β-endorphin at these sites. In situations where the level of ACTH is increased (e.g., Cushing’s Syndrome), the level of endorphins also increases slightly.
β-Endorphin has the highest affinity for the μ1 opioid receptor, slightly lower affinity for the μ2 and δ opioid receptors, and low affinity for the κ1 opioid receptors. μ-Opioid receptors are the main receptor through which morphine acts. In the classical sense, μ opioid receptors are presynaptic, and inhibit neurotransmitter release; through this mechanism, they inhibit the release of the inhibitory neurotransmitter GABA, and disinhibit the dopamine pathways, causing more dopamine to be released. By hijacking this process, exogenous opioids cause inappropriate dopamine release, and lead to aberrant synaptic plasticity, which causes dependency. Opioid receptors have many other and more important roles in the brain and periphery however, modulating pain, cardiac, gastric and vascular function as well as possibly panic and satiation, and receptors are often found at postsynaptic locations as well as presynaptically.
Scientists debate whether specific activities release measurable levels of endorphins. Much of the current data comes from animal models which may not be relevant to humans. The studies that do involve humans often measure endorphin plasma levels, which do not necessarily correlate with levels in the central nervous system. Other studies use a blanket opioid antagonist (usually naloxone) to indirectly measure the release of endorphins by observing the changes that occur when any endorphin activity that might be present is blocked.
A publicized effect of endorphin production is the so-called "runner's high", which is said to occur when strenuous exercise takes a person over a threshold that activates endorphin production. Endorphins are released during long, continuous workouts, when the level of intensity is between moderate and high, and breathing is difficult. This also corresponds with the time that muscles use up their stored glycogen. During a release of endorphins, the person may be exposed to bodily harm from strenuous bodily functions after going past his or her body's physical limit. This means that runners can keep running despite pain, continuously surpassing what they once considered to be their limit. Runner's high has also been known to create feelings of euphoria and happiness.
Runner's high has been suggested to have evolutionary roots based on the theory that it helped with the survival of early humans. Runner's high allows humans to run for vast lengths without pain. Most early humans hunted and gathered for their food. This required them to cover vast distances hunting down their prey or foraging for their food. This could have caused them to develop conditions such as shin splints and stress fractures in their shin and feet bones. Without runner's high to negate the pain caused by running on bones with these conditions, early humans theoretically would not have been able to repeatedly cover these vast distances in search of their food and thus would have starved. Current African tribes make use of runner's high when conducting persistence hunting. Persistence hunting is a method of hunting in which tribesman hunt an animal and track it for many miles, normally around 10 miles, eventually killing the animal due to its vulnerability brought on by exhaustion.
In 2008, researchers in Germany reported on the mechanisms that cause the runner's high. Using PET scans combined with recently available chemicals that reveal endorphins in the brain, they were able to compare runners’ brains before and after a run.[11]
It is also suggested by many that endorphins are some of the many chemicals that contribute to runner's high; other candidates include epinephrine, serotonin, and dopamine.
Endocanabanoids are the chemical most likely responsible for causing runner's high if endorphins are proved to not cause runner's high. Endocanabanoids are the body's natural chemical that interacts with the same brain receptor responsible for causing the high associated with marijuana use. In tests by the Institute of Georgia it was shown that endocannabinoid receptors were necessary for cognitive improvements due to exercise to occur. It is also shown that the endocannabinoids are involved in the reward system of the body, controlling the rewards for both exercise and consuming dessert. Another experiment that supports the endocannabinoid theory is that when mice were bred without the endocannabinoid receptor they ran thirty to forty percent less than regular mice. The only issue with the endocannabinoid theory is that it shows motivation and reward for running more than mood change, not eliminating it from the discussion of causes of runner’s high, but does not place it in the frontrunner position for causation.
Another theory for the cause of runners high is that runner’s high is simply a trance caused by overtaxing of the brain’s information processing power. An example of this is that runner’s high has been described as pure happiness, elation, feelings of unity with one’s self and/or nature, endless peacefulness, timelessness, inner harmony, boundless energy, as well as the reduction of pain sensations. These subjective descriptions are similar to the claims of distorted perception, atypical thought patterns, diminished awareness of one’s surroundings, and intensified introspective understanding of one’s sense of identity and emotional status made by people who describe trance states. This shows that runner’s high is an actual altered state of consciousness because it shares many similar characteristics with other altered states of consciousness. The overtaxing of the brain’s information processing power creates an altered state of consciousness that is out of touch and distracted, but while this does support the theory behind runner’s high being an altered state of consciousness, it does not explain the feelings of joy and happiness that are associated with symptoms of runner's high. This eliminates it from being a primary cause of runner’s high but it still may assist in the overall cause of runner's high.
Previous research on the role of endorphins in producing runner's high questioned the mechanisms at work, their data possibly demonstrated that the "high" comes from completing a challenge rather than as a result of exertion.[12] Studies in the early 1980s cast doubt on the relationship between endorphins and the runner's high for several reasons:
Runner’s high is a phenomenon that was vital to our very survival back in primitive times, and is still crucial to the survival of some and the enjoyment in recreational running. While there are many theories as to what is the cause of the phenomenon, endorphins have the most decisive evidence to support it being the cause. Endocannabinoids are a likely cause as to the motivation behind why we run but not why runner’s high occurs. Even though the most probable individual cause of runner's high is endorphins, it is more likely a cocktail of chemicals reacting in the brain along with the overtaxing of the brain’s information processing capabilities that produces the phenomenon known as runner’s high.
Endorphins are known to play a role in depersonalization disorder. The opioid antagonists naloxone and naltrexone have both been proven to be successful in treating depersonalization [15][16]. To quote a 2001 naloxone study, "In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization."
In 2003, clinical researchers reported that profound relaxation in a float tank triggers the production of endorphins.[17] This explains the pain relief experienced during float sessions.[18]
In 1999, clinical researchers reported that inserting acupuncture needles into specific body points triggers the production of endorphins.[19][20] In another study, higher levels of endorphins were found in cerebrospinal fluid after patients underwent acupuncture.[21] In addition, naloxone appeared to block acupuncture’s pain-relieving effects.
A placental tissue of foetal origin — i.e., the syncytiotrophoblast — excretes beta-endorphins into the maternal blood system from the 3rd month of pregnancy. A recent study[22] proposes an adaptive background for this phenomenon. The authors argue that fetuses make their mothers endorphin-dependent then manipulate them to increase nutrient allocation to the placenta. Their hypothesis predicts that: (1) anatomic position of endorphin production should mirror its presumed role in foetal-maternal conflict; (2) endorphin levels should co-vary positively with nutrient carrying capacity of maternal blood system; (3) postpartum psychological symptoms (such as postpartum blues, depression, and psychosis) in humans are side-effects of this mechanism that can be interpreted as endorphin-deprivation symptoms; (4) shortly after parturition, placentophagy could play an adaptive role in decreasing the negative side-effects of foetal manipulation; (5) later, breast-feeding-induced endorphin excretion of the maternal pituitary saves mother from further deprivation symptoms. These predictions appear to be supported by empirical data.[22]
From the Greek: word endo "ενδο" meaning "within" (endogenous, Greek: ενδογενής, "proceeding from within") and morphine, from Morpheus, Greek: Μορφέας, the god of dreams in the Greek mythology, thus 'endo(genous) (mo)rphine’.
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