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Endorphins are among the brain chemicals known as neurotransmitters, which function to transmit electrical signals within the nervous system. Stress and pain are the two most common factors leading to the release of endorphins. I wanted to know if they are addictive, and found some contradicting answers:
If people can get addicted to risky sports just for the thrills they provide, they can also get addicted to painful activities where endorphins provide relief, "despite the harm to self and/or others," says Dr. Anna Lembke, chief of addiction medicine at Stanford University School of Medicine in an email interview. "For example, someone who compulsively cuts herself for the endorphin release is causing self-harm. Someone who compulsively runs, even to the point of causing musculoskeletal injury, is causing self-harm."
In contrast to the opiate drugs, however, activation of the opiate receptors by the body's endorphins does not lead to addiction or dependence.
If they are not, how can we explain the 'love' for pain in (this content might be sensitive for some of you) some people?
Addiction specialists and others who study human behavior often catageorize addiction into the two broad categories of physical dependence and psycological dependence. They are not always mutually exclusive, and they can both manifest in serious or mild cases of addiction depending on the person and a number of other factors.
What differentiates them is how they affect your physiology. A person severly addicted to alcohol or opioids can become extremely ill or even die from the withdrawl of those substances, due to the strong physical dependence their body has developed. To my knowledge, people do not experience a physical withdrawl after cessation of compulsive pain seeking behaviors. Since they didn't cite any source, we can only guess as to the intended meaning of your second source, but it's probably related to this lack of withdrawl. A quick search on PubMed shows publications referring to certain endorphins as mediating this type of addiction. Meaning that the endorphin is not addictive per se, but a compulsive or addictive behavior can be communicated to the brain in terms of a native neurochemical pathway which is otherwise a normal part of a healthy brain.
I think the lesson here is to be somewhat skeptical of online sources that don't link to peer-reviewed science. Attempts to simplify a topic for the purposes of communicating with a lay audience often result in more confusion than clarity. And if you search something on PubMed or google scholar, you'll probably find an answer in the same amount of time it took you to post your question here.
Pain is not an endorphin but p substance triggers reactions to form opioids and those are endorphins. There is a lot of research about serotonin and dopamine being highly addictive.
Here they review this and explain it a little bit
From a psychological point of view people harm them self because they want to sentence themselves, but there are very much deviations and you can not put anybody in the same pot…
UV-induced beta-endorphin production causes addiction-like symptoms in mice
Why has it been so hard to discourage people from spending time in the sun when the dangers of ultraviolet light exposure are so well recognized? A new study from Massachusetts General Hospital (MGH) investigators adds important support to the theory that ultraviolet (UV) light can actually be addictive, finding that chronic UV exposure raises circulating levels of beta-endorphin in mice and that UV-habituated mice exhibit withdrawal symptoms if beta-endorphin activity is blocked. Their report appears in the June 19 issue of Cell.
"Our study identified an organic pathway encoded in skin whereby UV radiation causes the synthesis and release of beta-endorphin and produces opiate-like effects, including addictive behavior," says David E. Fisher, MD, PhD, chair of Dermatology and director of the Cutaneous Biology Research Center (CBRC) at MGH, who led the study. "This provides a potential explanation for the 'sun seeking' behavior that may underlie the relentless rise in most forms of skin cancer."
Several studies - particularly those enrolling individuals who use indoor tanning facilities - have found evidence of addiction-like behavior in frequent tanners. For example, frequent tanners were somehow able to tell the difference between tanning beds using UV radiation and those delivering non-UV light. Other studies found that administration of an opioid blocker produced withdrawal-like symptoms in frequent tanners, implying but not proving that something had been regularly activating opioid pathways.
Part of skin's natural response to UV light is production of a protein called POMC, which is then clipped into several smaller fragments, one of which induces production of the pigment melanin. Processing of another segment of POMC leads to generation of beta-endorphin in the skin. The current study was designed to investigate whether this UV-induced beta-endorphin produces opioid-like effects such as pain relief and dependency. The study also examined whether the pathway mediating these effects is initiated by the production of endorphin in the skin.
The investigators delivered a daily dose of UV light - equivalent to the exposure of fair-skinned humans to 20 to 30 minutes of midday Florida sun - on the shaved backs of a group of mice for 6 weeks. The dose was calculated to induce tanning but not burning of the animals' skin. Within a week of the first UV exposure, the animals' blood beta-endorphin levels rose significantly, remaining elevated during the study period and gradually returning to normal after UV exposure was discontinued. Tests conducted at regular intervals during the study period showed that the UV-treated animals were less responsive to light touch or temperature changes than a control group with no UV exposure. The higher the animals' beta-endorphin levels, the less sensitive they became. But administration of naloxone, which would broadly block opioid-pathway activity, returned skin sensation back to normal in the UV-treated animals.
In UV-habituated animals, naloxone treatment also produced classic symptoms of opioid withdrawal, such as trembling, shaking and teeth chattering. And mice trained to associate the effects of naloxone with an environment they would naturally prefer - a dark box instead of a light box - invariably choose to enter the area where they had not experienced naloxone-produced symptoms. In contrast, a strain of mice in which production of POMC was selectively blocked in skin or which lacked the beta-endorphin gene altogether exhibited none of the responses or symptoms seen in normal mice after UV treatment, confirming the presence of a UV-activated opioid pathway in the skin.
"It is possible that a natural mechanism reinforcing UV-seeking behavior may have developed at certain stages of mammalian evolution through its contribution to the synthesis of vitamin D," Fisher says. "But such behavioral effects would also carry the carcinogenic risks of UV light that we now recognize. Today's alternative sources of vitamin D, such as inexpensive oral supplements, are both safer and more accurate in maintaining healthy vitamin D levels.
"Our finding that persistent UV seeking really does appear to be an addiction-related behavior suggests that reducing an individual's skin cancer risk may require actively confronting factors that influence this hazardous behavior - like the promotion of indoor tanning - instead of the more passive risk messages that have been relied on," he adds. "We also wonder whether this interaction of sun, skin and endorphins might be involved in other behaviors or disorders and whether this may represent one of the earliest behavioral responses that can be considered addictive." Fisher is the Wigglesworth Professor of Dermatology at Harvard Medical School.
The co-lead authors of the Cell paper are Gillian Fell, MD, now at Brigham and Women's Hospital, and Kathleen Robinson, PhD, MGH Dermatology and CBRC. Additional co-authors are Jianren Mao, MD, PhD, MGH Department of Anesthesia and Critical Care, and Clifford Woolf, PhD, MBBCh, Children's Hospital Boston. The study was supported by National Institutes of Health grants R01-AR043369-16 and R01-CA150226-03, and by the Melanoma Research Alliance, the US-Israel Binational Science Foundation and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation.
Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $785 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
In cavemen times, the usual sources of happiness were finding a food source or finding a mate. These are the basic needs of survival and to make sure we remember to continue doing it, our body makes us remember it. When those things happened, our body produced dopamine which engraved the feeling and memory into our head so we would keep doing it, for the survival of the species. When we get addicted to something, it uses the same concept.
The reward center in our brain is called the limbic system. It has many structures that control our emotional and behavioural responses to information it receives. Most things related to addiction, are located here.
The chemical dopamine is a neurotransmitter, which are basically dopamine is a neurotransmitter. Our brains produce over 100 different neurotransmitters and we’re discovering more and more. Neurotransmitters pass signals from neuron to neuron or to another cell it wants to activate.
There are two types of neurotransmitters, excitatory and inhibitory. Excitatory transmitters find a target cell and fill it up with chemical energy like dopamine and endorphins. Whereas inhibitory transmitters, keep their target cells still and calm like serotonin.
While facing addiction, we face problems with the excitatory transmitters, specifically dopamine. Dopamine is a chemical that forms declarative memories. It activates when something good happens and forces your body to remember the feeling so it does it more. When produces with endorphins, a chemical that helps cope with pain, it causes pleasure and people getting addicted to that.
“addiction exploits the brain’s ability to vividly remember unnatural highs and motivate itself to find more of them in the future”
Addicted to the Sun
Why has it been so hard to discourage people from spending time in the sun when the dangers of ultraviolet light exposure are so well recognized? A new study from Harvard Medical School investigators at Massachusetts General Hospital adds important support to the theory that ultraviolet (UV) light can actually be addictive.
The scientists found that chronic UV exposure raises circulating levels of beta-endorphin in mice and that UV-habituated mice exhibit withdrawal symptoms if beta-endorphin activity is blocked. Their report appears in the June 19 issue of Cell.
“Our study identified an organic pathway encoded in skin whereby UV radiation causes the synthesis and release of beta-endorphin and produces opiate-like effects, including addictive behavior,” said David E. Fisher, who led the study. He is the Wigglesworth Professor of Dermatology at HMS and Mass General. “This provides a potential explanation for the ‘sun seeking’ behavior that may underlie the relentless rise in most forms of skin cancer.”
Several studies—particularly those enrolling people who use indoor tanning facilities—have found evidence of addiction-like behavior in frequent tanners. For example, frequent tanners were somehow able to tell the difference between tanning beds using UV radiation and those delivering non-UV light.
Other studies have found that administration of an opioid blocker produced withdrawal-like symptoms in frequent tanners, implying but not proving that something had been regularly activating opioid pathways.
Part of the skin’s natural response to UV light is production of a protein called POMC, which is then clipped into several smaller fragments, one of which induces production of the pigment melanin. Processing of another segment of POMC leads to generation of beta-endorphin in the skin. The current study was designed to investigate whether this UV-induced beta-endorphin produces opioid-like effects such as pain relief and dependency. The study also examined whether the pathway mediating these effects is initiated by the production of endorphin in the skin.
The investigators delivered a daily dose of UV light—equivalent to the exposure of fair-skinned humans to 20 to 30 minutes of midday Florida sun—on the shaved backs of a group of mice for 6 weeks. The dose was calculated to induce tanning but not burning of the animals’ skin.
Within a week of the first UV exposure, levels of beta-endorphin in the animals’ blood rose significantly, remaining elevated during the study period and gradually returned to normal after UV exposure was discontinued. Tests conducted at regular intervals during the study period showed that the UV-treated animals were less responsive to light touch or temperature changes than a control group with no UV exposure. The higher the animals’ beta-endorphin levels, the less sensitive they became. But administration of naloxone, which would broadly block opioid-pathway activity, returned skin sensation back to normal in the UV-treated animals.
In UV-habituated animals, naloxone treatment also produced classic symptoms of opioid withdrawal, such as trembling, shaking and teeth chattering. And mice trained to associate the effects of naloxone with an environment they would naturally prefer—a dark box instead of a light box—invariably chose to enter the area where they had not experienced naloxone-produced symptoms. In contrast, a strain of mice in which production of POMC was selectively blocked in skin or which lacked the beta-endorphin gene altogether exhibited none of the responses or symptoms seen in normal mice after UV treatment, confirming the presence of a UV-activated opioid pathway in the skin.
“It is possible that a natural mechanism reinforcing UV-seeking behavior may have developed at certain stages of mammalian evolution through its contribution to the synthesis of vitamin D,” said Fisher, who is also chair of dermatology and director of the Cutaneous Biology Research Center at Mass General. “But such behavioral effects would also carry the carcinogenic risks of UV light that we now recognize. Today’s alternative sources of vitamin D, such as inexpensive oral supplements, are both safer and more accurate in maintaining healthy vitamin D levels.
“Our finding that persistent UV seeking really does appear to be an addiction-related behavior suggests that reducing an individual’s skin cancer risk may require actively confronting factors that influence this hazardous behavior—like the promotion of indoor tanning—instead of the more passive risk messages that have been relied on,” he added. “We also wonder whether this interaction of sun, skin and endorphins might be involved in other behaviors or disorders and whether this may represent one of the earliest behavioral responses that can be considered addictive.”
The study was supported by National Institutes of Health grants R01-AR043369-16 and R01-CA150226-03, the Melanoma Research Alliance, the US-Israel Binational Science Foundation, and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation.
Addicted To Guns? Here’s How Using A Firearm Affects Your Biology
Guns are one of the most deadly weapons known to man, with the Centers for Disease Control and Prevention reporting that about 33,736 people die from gun shots each year. While most of us understand what happens to a person who has been shot, how firearms affect the biology of the shooter is more mysterious. Here’s a short run-through of what happens to your body when you pull the trigger.
Despite their clear danger, many people enjoy firing guns in their spare time as a form of entertainment, and there may be a biological reason. When you fire a gun, your body releases hormones called endorphins, Forbes reported. These hormones promote a calm, relaxed feeling, and although they are meant to help alleviate the stress and anxiety associated with firing such a powerful weapon, they can also induce a pleasurable “high-like” sensation. These are the same hormones that are released when we have sex or use certain drugs, so it’s easy to see how some can get hooked on the feeling of using a gun.
In addition to a flood of hormones, shooting a gun can also burn calories — a surprising amount. For example, the average 130-pound shooter will burn about 148 calories per hour at the shooting range, while heavier shooters clocking in at around 205 pounds can burn as many as 233 calories an hour.
Guns also affect the brain right before you fire the gun, alpha waves in the brain are abundant in order to improve the shooter's accuracy. Along with increasing accuracy, these specific types of brain waves are also associated with creativity and alleviating depression, Psychology Today reported. In addition, shooting also stimulates the right side of the shooter’s brain in an effort to help them get the most accurate shot possible.
The Neurobiology of BDSM Sexual Practice
By now, everyone’s got an opinion about 50 Shades of Grey: It's trash it’s fun fantasy-fodder it’s misogynist it’s empowering for women it’s silly. While the 50 Shades media saturation has grown tiresome, one must admit that it’s compelled a societal discussion of sexual practices involving bondage, discipline, sadism, and masochism (BDSM) that are otherwise not broadly considered. Leaders of the BDSM community are quick to point out that 50 Shades is not an accurate representation of BDSM sexual practice where “safe, sane, and consensual” are the watchwords and that the term “BDSM” is broad, like the term “sports.” It includes people with highly divergent sexual desires and personae. Just because you like to be flogged doesn’t mean that you necessarily like to be humiliated as well.
For those outside of this group, a failure to understand the appeal of BDSM practice usually comes down to this: How can one experience pain, either the physical pain of a smack on the tush or the emotional pain of humiliation, as pleasurable? Aren’t pain and pleasure diametrically opposed?
You don’t have to be a masochistic sex enthusiast to know that pleasure and pain can be felt simultaneously: think of the pleasures of a delicious meal laden with spicy chili peppers or the blissful ache following a long-distance run. In the lexicon of cognitive neuroscience, both pleasure and pain indicate salience, that is, experience that is potentially important and thereby deserving of attention. Emotion is the currency of salience and both positive emotions like euphoria and love and negative emotions like fear and disgust signal events that we must not ignore.
How is salience built into neural pathways? We have an evolutionarily ancient and highly interconnected pleasure circuit in our brains. When neurons in a brain region called the ventral tegmental area become electrically active, thereby triggering the release of dopamine in a structure called the nucleus accumbens, this evokes the feeling of pleasure from both our vices (eating food when hungry, having an orgasm, drinking alcohol) and our virtues (meditation, learning, giving to charity).
Here are the key findings that help to explain the pleasure-pain connection. When subjects in a brain scanner received in injection into the jaw muscles that produced a protracted aching type of pain, this triggered dopamine release in the nucleus accumbens and the greatest release was seen in those subjects who rated the pain as most unpleasant. In rats, one can examine this phenomenon in greater detail. Electrical recordings from single dopamine neurons of the ventral tegmental area revealed that all of these neurons responded to the presentation of a tasty sugar-droplet, yet some of these neurons responded to a brief painful footshock with a decrease in their ongoing rate of activity while others responded with an increase. In other words, these latter dopamine-using neurons were salience detectors, releasing dopamine in response to either pleasure or pain. We also know, from different experiments, that protracted physical pain and protracted emotional pain (resulting from social rejection) can cause the release of endorphins, the brain’s own morphine-like molecules and that these endorphins can activate dopamine neurons in the ventral tegmental area. The end result is that there is an innate rewarding component to both pleasurable and painful experiences.
How then, can we account for individual differences? Why do surveys reveal that only 5 to 10 percent of people enjoy receiving pain in a sexual context? The short answer is that we don’t entirely know. Understanding how sexual kinks develop has not been a funding priority for government agencies and biomedical research charities. There are variant forms of dopamine receptor genes that attenuate the experience of pleasure and increase risk-taking and novelty-seeking behavior. However, it’s not clear that these gene variants or any others (such as those related to endorphin signaling or pain perception) are linked to the practice of sexual masochism.
Perhaps the best hypothesis for sexual masochism comes by analogy from studies of another painful practice: chili pepper consumption. If you grow up in a community where chili peppers are readily eaten, you will reject them as an infant, but by about age 5, you will almost certainly develop a taste for these painful foods. Rats and mice, by comparison, cannot be trained to choose chili peppers in their food no matter how their upbringing is manipulated by scientists. It is likely that there is a human predisposition to learn to find certain forms of pain to be rewarding. This seems to be the case when pain is survivable and doesn’t lead to permanent damage as in both masochistic sexual practice and chili pepper eating. However, it is only when that human predisposition is combined with aspects of one’s particular life experience (as influenced by cultural and religious ideas) that the brain’s neural salience circuits are modified to forge the pleasure-pain connection in a sexual context.
Endorphins and Exercise
The body produces endorphins in response to intense physical exercise.
Endorphins may play a role in the so-called "runner's high," which describes the feelings of euphoria long distance runners experience after prolonged bouts of exercise.
Endorphin release varies from person to person, which means that the same amount of exercise do not produce the same amount of endorphins for everyone.
Research suggests that exercise helps to improve mood and may even aid in the treatment of depression.
However, it's unclear whether endorphins or some other process in the brain or body is responsible for the mood-boosting effects of exercise.
Endorphins: Effects and how to increase levels
Endorphins are chemicals produced naturally by the nervous system to cope with pain or stress. They are often called “feel-good” chemicals because they can act as a pain reliever and happiness booster.
Endorphins are primarily made in the hypothalamus and pituitary glands, though they may come from other parts of the body as well. The well-known “runner’s high” that is felt after lengthy, vigorous exercise is due to an increase in endorphin levels.
The level of endorphins in the human body varies from person to person. People who have lower levels may be more likely to have depression or fibromyalgia, but more research is needed in this area.
Share on Pinterest Endorphins are chemicals that help to relieve pain or stress, and boost happiness.
Endorphins are chemicals produced by the body to relieve stress and pain. They work similarly to a class of drugs called opioids.
Opioids relieve pain and can produce a feeling of euphoria. They are sometimes prescribed for short-term use after surgery or for pain-relief.
In the 1980s, scientists were studying how and why opioids worked. They found that the body has special receptors that bind to opioids to block pain signals.
The scientists then realized that some chemicals in the body acted similarly to natural opioid medications, binding to these same receptors. These chemicals were endorphins.
The name endorphin comes from the words “endogenous,” which means “from the body,” and “morphine,” which is an opioid pain reliever.
Some of the more common opioid drugs include:
Some illegal drugs, such as heroin, are also opioids. Both legal and illegal opioid medications have a high risk of causing addiction, overdose, and death.
The National Institute on Drug Abuse state that 90 people die each day in the United States from an opioid overdose. Many of these are a result of overdosing or misusing prescription opioids.
Opioid abuse and overdose have become such a serious problem that the National Institutes of Health have declared it a crisis. Medical experts are now looking into safe and effective pain relievers without opioids.
Natural endorphins work similarly to opioid pain relievers, but their results may not be as dramatic. However, endorphins can produce a “high” that is both healthy and safe, without the risk of addiction and overdose.
TRANSITION TO ADDICTION
As we have seen, the pleasure derived from opioids’ activation of the brain’s natural reward system promotes continued drug use during the initial stages of opioid addiction. Subsequently, repeated exposure to opioid drugs induces the brain mechanisms of dependence, which leads to daily drug use to avert the unpleasant symptoms of drug withdrawal. Further prolonged use produces more long-lasting changes in the brain that may underlie the compulsive drug-seeking behavior and related adverse consequences that are the hallmarks of addiction. Recent scientific research has generated several models to explain how habitual drug use produces changes in the brain that may lead to drug addiction. In reality, the process of addiction probably involves components from each of these models, as well as other features.
Definitions of Key Terms
dopamine (DA): A neurotransmitter present in brain regions that regulate movement, emotion, motivation, and the feeling of pleasure.
GABA (gamma-amino butyric acid): A neurotransmitter in the brain whose primary function is to inhibit the firing of neurons.
locus ceruleus (LC): A region of the brain that receives and processes sensory signals from all areas of the body involved in arousal and vigilance.
noradrenaline (NA): A neurotransmitter produced in the brain and peripheral nervous system involved in arousal and regulation of blood pressure, sleep, and mood also called norepinephrine.
nucleus accumbens (NAc): A structure in the forebrain that plays an important part in dopamine release and stimulant action one of the brain’s key pleasure centers.
prefrontal cortex (PFC): The frontmost part of the brain involved in higher cognitive functions, including foresight and planning.
ventral tegmental area (VTA): The group of dopamine-containing neurons that make up a key part of the brain reward system key targets of these neurons include the nucleus accumbens and the prefrontal cortex
The 𠇌hanged Set Point” Model
The 𠇌hanged set point” model of drug addiction has several variants based on the altered neurobiology of the DA neurons in the VTA and of the NA neurons of the LC during the early phases of withdrawal and abstinence. The basic idea is that drug abuse alters a biological or physiological setting or baseline. One variant, by Koob and LeMoal (2001), is based on the idea that neurons of the mesolimbic reward pathways are naturally “set” to release enough DA in the NAc to produce a normal level of pleasure. Koob and LeMoal suggest that opioids cause addiction by initiating a vicious cycle of changing this set point such that the release of DA is reduced when normally pleasurable activities occur and opioids are not present. Similarly, a change in set point occurs in the LC, but in the opposite direction, such that NA release is increased during withdrawal, as described above. Under this model, both the positive (drug liking) and negative (drug withdrawal) aspects of drug addiction are accounted for.
A specific way that the DA neurons can become dysfunctional relates to an alteration in their baseline (“resting”) levels of electrical activity and DA release (Grace, 2000). In this second variant of the changed set point model, this resting level is the result of two factors that influence the amount of resting DA release in the NAc: cortical excitatory (glutamate) neurons that drive the VTA DA neurons to release DA, and autoreceptors (𠇋rakes”) that shut down further release when DA concentrations become excessive. Activation of opioid receptors by heroin and heroin-like drugs initially bypasses these brakes and leads to a large release of DA in the NAc. However, with repeated heroin use, the brain responds to these successive large DA releases by increasing the number and strength of the brakes on the VTA DA neurons. Eventually, these enhanced 𠇋raking” autoreceptors inhibit the neurons’ resting DA release. When this happens, the dependent addict will take even more heroin to offset the reduction of normal resting DA release. When he or she stops the heroin use, a state of DA deprivation will result, manifesting in dysphoria (pain, agitation, malaise) and other withdrawal symptoms, which can lead to a cycle of relapse to drug use.
A third variation on the set-point change emphasizes the sensitivity to environmental cues that leads to drug wanting or craving rather than just reinforcement and withdrawal (Breiter et al., 1997 Robinson and Berridge, 2000). During periods when the drug is not available to addicts, their brains can remember the drug, and desire or craving for the drug can be a major factor leading to drug use relapse. This craving may represent increased activity of the cortical excitatory (glutamate) neurotransmitters, which drive the resting activity of the DA-containing VTA neurons, as mentioned, and also drive the LC NA neurons. As the glutamate activity increases, DA will be released from the VTA, leading to drug wanting or craving, and NA will be released from the LC, leading to increased opioid withdrawal symptoms. This theory suggests that these cortical excitatory brain pathways are overactive in heroin addiction and that reducing their activity would be therapeutic. Scientists are currently researching a medication called lamotrigene and related compounds called excitatory amino acid antagonists to see whether this potential treatment strategy really can work.
Thus, several mechanisms in the LC and VTA-NAc brain pathways may be operating during addiction and relapse. The excitatory cortical pathways may produce little response in the VTA during the resting state, leading to reductions in DA. However, when the addicted individual is exposed to cues that produce craving, the glutamate pathways may get sufficiently active to raise DA and stimulate desire for a greater high. This same increase in glutamate activity will raise NA release from the LC to produce a dysphoric state predisposing to relapse and continued addiction.
Cognitive Deficits Model
The cognitive deficits model of drug addiction proposes that individuals who develop addictive disorders have abnormalities in an area of the brain called the prefrontal cortex (PFC). The PFC is important for regulation of judgment, planning, and other executive functions. To help us overcome some of our impulses for immediate gratification in favor of more important or ultimately more rewarding long-term goals, the PFC sends inhibitory signals to the VTA DA neurons of the mesolimbic reward system.
The cognitive deficits model proposes that PFC signaling to the mesolimbic reward system is compromised in individuals with addictive disorders, and as a result they have reduced ability to use judgment to restrain their impulses and are predisposed to compulsive drug-taking behaviors. Consistent with this model, stimulant drugs such as methamphetamine appear to damage the specific brain circuit—the frontostriatal loop—that carries inhibitory signals from the PFC to the mesolimbic reward system. In addition, a recent study using magnetic resonance spectroscopy showed that chronic alcohol abusers have abnormally low levels of gamma-amino butyric acid (GABA), the neurochemical that the PFC uses to signal the reward system to release less DA (Behar et al., 1999). As well, the cognitive deficits model of drug addiction could explain the clinical observation that heroin addiction is more severe in individuals with antisocial personality disorder𠅊 condition that is independently associated with PFC deficits (Raine et al., 2000).
In contrast to stimulants, heroin apparently dam-ages the PFC but not the frontostriatal loop. Therefore, individuals who become heroin addicts may have some PFC damage that is independent of their opioid abuse, either inherited genetically or caused by some other factor or event in their lives. This preexisting PFC damage predisposes these individuals to impulsivity and lack of control, and the additional PFC damage from chronic repeated heroin abuse increases the severity of these problems (Kosten, 1998).
Addiction and the Eating Disorders
Although comprehensive theories of addiction recognize the etiological importance of environmental and cognitive factors, it has been widely accepted for many years that addiction is also a brain disease and that individuals differ in their susceptibility to this condition.
Although comprehensive theories of addiction recognize the etiological importance of environmental and cognitive factors, it has been widely accepted for many years that addiction is also a brain disease and that individuals differ in their susceptibility to this condition (Leshner, 1997 Wise and Bozarth, 1987). Explanations of the eating disorders have tended to eschew biological models in favor of those that focus on psychosocial and family influences-the most prominent models arising from psychoanalytic, feminist and cultural theory. It is not surprising, therefore, that although clear parallels exist between the abuse of substances and disturbances in eating, there has been a reluctance to accept that the two may share a common etiology. It is also probable that their similarities were obscured by dramatic differences in the social profile of the stereotypic drug addict and the patient with an eating disorder-the former typically associated with male criminality and social deviance and the latter with female submissiveness and social conformity.
In the past decade, however, there has been a growing paradigmatic shift in eating disorder research, with a movement away from explanations that rely solely on psychosocial factors, to a belief that disturbances in the function of brain neurotransmitter pathways are also highly relevant (Kaye, 1999). One outcome of this change in orientation has been an emerging and increasing interest in the links between eating disorders and substance abuse disorders.
Clinical and Biological Traits
It is generally agreed that the commencement of addictive behaviors can take two motivational routes: either the seeking of positive sensations or the self-medicating of painful affective states. While current research documents a substantial lifetime comorbidity between the eating disorders and other forms of addiction, there is less agreement on the reasons for this link (Holderness et al., 1994 Wiederman and Pryor, 1996). Some researchers have suggested that a common set of personality traits predispose an individual to a range of behaviors that have the potential to become excessive (Koob and Le Moal, 1997 Leshner, 1997). Support for this idea comes from evidence that anxiety and depression are frequent premorbid characteristics both of addicts (Grant and Harford, 1995 Kessler et al., 1997) and of patients with eating disorders (Deep et al., 1995 Vitousek and Manke, 1994). Our own research has also found that among eating-disordered patients, irrespective of diagnostic category, scores on a measure of addictive personality characteristics were comparable to those reported for drug addicts and alcoholics (Davis and Claridge, 1998). Complementary to this viewpoint, an addiction to one behavior reinforces a certain style of coping pattern that leaves the individual vulnerable to developing another type of addiction (Holderness et al., 1994).
Others have suggested that the eating disorders are, themselves, a form of drug addiction since their characteristics satisfy all the clinical and biological criteria for conventional addictions such as smoking, alcoholism and cocaine abuse (Davis and Claridge, 1998 Davis et al., 1999 Marrazzi and Luby, 1986). Foremost among these is the progressively compulsive nature of the behavior, even in the face of adverse consequences to health and safety (Heyman, 1996 Robinson and Berridge, 1993). Moreover, with continual exposure, individuals typically require more of the behavior to produce the same reinforcing effect (Berridge and Robinson, 1995). They also tend to experience an obsessively increasing craving for the behavior that can persist even after a long period of abstinence. Presumably that accounts, at least in part, for the fact that addicts have a strong tendency to resume the addictive behavior after treatment and for the chronic relapsing nature of addiction (Robinson and Berridge, 1993). These characteristics find direct parallels in the core eating-disorder behaviors such as dieting, over-exercising and binge eating, all of which tend to become increasingly excessive over time. Patients also report a strong compulsion to continue these behaviors despite serious medical complications, which is reflected in their prolonged morbidity and the high rate of relapse (Herzog et al., 1999 Strober et al., 1999).
At the biological level, similarities are also evident. We know, for instance, that strenuous exercise and starvation activate the dopaminergic (DA) reward pathway of the brain (Bergh and Sodersten, 1996 Casper, 1998). The resulting biological events underlie the auto-addiction opioid theory, which proposes that a chronic eating disorder is an addiction to the body's production of endogenous opioids and therefore is identical to the physiology and psychology of substance abuse in general (Huebner, 1993 Marrazzi and Luby, 1986). In other words, starving, bingeing and exercise all serve as drug delivery devices since they increase circulating levels of -endorphins that are chemically identical to exogenous opiates, and these endorphins are as potentially addictive because of their ability to stimulate DA in the brain's mesolimbic reward centers.
Via a different route, self-starving may have other biologically rewarding properties, albeit as a negative reinforcer. For example, in certain individuals, food restriction is reported to reduce anxiety. It has been suggested this might occur because of reduced serotonin activity in those with overactivity in this neurotransmitter system (Kaye, 1999).
A key concept in current formulations about risk for addiction concerns individual differences in sensitivity to reward or the ability to experience pleasure-a concept firmly rooted in neurobiology. In recent years, theories of addiction have moved from an emphasis on physical dependence to a broader focus on motivational dependence and the importance of anhedonia and dysphoria as powerful incentives for the continuation of addictive behaviors (Di Chiara, 1999).
A large body of research has demonstrated that a relatively long-lasting anhedonic state can be induced by prolonged drug administration (Gamberino and Gold, 1999) and by exposure to chronic mild stress (Zacharko, 1994) and that this process is primarily mediated by DA receptor downregulation. Furthermore, anhedonia can also be an innate characterological trait associated with low DA availability a factor that has consistently been associated with greater risk for a variety of addictions (Volkow et al., 1999).
Recently, we proposed that this concept has great utility for understanding certain differences between patients with anorexia nervosa (AN) and patients with bulimia nervosa (BN), viz that the former display a facility for self-starving and report a decreasing interest in food, while the latter have increasing difficulty resisting food and become compulsive overeaters (Davis et al., 2000). There is no doubt that these differences are influenced by a variety of cognitive factors relating to personal identity and a need for control as well as social reinforcement. As with addiction, there is good reason to believe that biologically based motivational effects relating to capacity for reward and the regulation of affective states are also influential. Given that food is the most basic natural reinforcer, our findings that patients with AN were significantly more anhedonic than those with BN offer support for the premise that individual differences in this characteristic contribute to the avoidance and approach relationships to food found in these two groups, respectively. The cross-sectional nature of our data raises the inevitable question of whether these differences reflect premorbid-and, therefore, potentially causal-characteristics, whether the stress of starvation experienced most acutely in the patients with AN induced their anhedonic state, or both. Recently it has been suggested that differences in the ability to experience the positive-incentive value of food may be diminished in response to an extended period of food deprivation, making it easier for patients with severe anorexia to starve themselves (Pinel et al., 2000).
Summary and Conclusions
There is a strong argument that the eating disorders are a form of addiction. Clinically, the behaviors that define eating disorders and substance abuse are very similar. Similar biological mechanisms account for the compulsively progressive nature of both disorders in the case of alcohol and other drugs, from recreational use to a state of pathological dependence in AN, from casual dieting to a life-threatening refusal to eat and, in BN, the increasing inability to resist large quantities of food. There is also support for a common psychobiological vulnerability and for the notion that individuals use a variety of rewarding behaviors to self-medicate their affective disturbances depending on the specific effects of each. But why do some individuals choose nicotine, others alcohol and others food (or its absence)? Environment, sociocultural factors and personality must play an important role. For example, one who is obsessional, anxious, conforming and female is more likely to be attracted to highly sanctioned behaviors like dieting and exercise, and to the enormous rewards associated with the pursuit of thinness in our culture, than to illicit drug use. In order to understand the motivation to continue these behaviors beyond the point of body-image improvements, we must look beyond psychosocial explanations. I suggest that the great strides which have occurred in our understanding of brain mechanisms in addiction also provide excellent insight into the processes that occur in the eating disorders. As such, they also offer a useful approach to improved methods of treatment.
Bergh C, Sodersten P (1996), Anorexia nervosa, self-starvation and the reward of stress. Nat Med 2(1):21-22.
Berridge KC, Robinson TE (1995), The mind of an addicted brain: neural sensitization of "wanting" versus "liking". Current Directions Psychological Science 4:71-76.
Casper RC (1998), Behavioral activation and lack of concern, core symptoms of anorexia nervosa? Int J Eat Disord 24(4):381-393.
Davis C, Claridge G (1998), The eating disorders as addiction: a psychobiological perspective. Addict Behav 23(4):463-475.
Davis C, Woodside DB, Olmsted MP (2000), A study of anhedonia and excessive exercise in the eating disorders. Presentation at the 9th International Conference on the Eating Disorders. New York May.
Davis C, Katzman DK, Kirsh C (1999), Compulsive physical activity in adolescents with anorexia nervosa: a psychobehavioral spiral of pathology. J Nerv Ment Dis 187(6):336-342.
Deep AL, Nagy LM, Weltzin TE et al. (1995), Premorbid onset of psychopathology in long-term recovered anorexia nervosa. Int J Eat Disord 17(3):291-297.
Di Chiara G (1999), Drug addiction as dopamine-dependent associative learning disorder. Eur J Pharmacol 375(1-3):13-30.
Gamberino WC, Gold MS (1999), Neurobiology of tobacco smoking and other addictive disorders. Psychiatr Clin North Am 22(2):301-312.
Grant BF, Harford TC (1995), Comorbidity between DSM-IV alcohol use disorders and major depression: results of a national survey. Drug Alcohol Depend 39(3):197-206.
Herzog DB, Dorer DJ, Keel PK et al. (1999), Recovery and relapse in anorexia and bulimia nervosa: a 7.5 year follow-up study. J Am Acad Child Adolesc Psychiatry 38(7):829-837.
Heyman GM (1996), Resolving the contradictions of addiction. Behav Brain Sci 19(4):561-610.
Holderness CC, Brooks-Gunn J, Warren MP (1994), Comorbidity of eating disorders and substance abuse review of the literature. Int J Eat Disord 16(1):1-34.
Huebner HF (1993), Endorphins, Eating Disorders, and Other Addictive Behaviors. New York: W.W. Norton & Co.
Kaye WH (1999), The new biology of anorexia and bulimia nervosa: implications for advances in treatment. European Eating Disorders Review 7(3):157-161.
Kessler RC, Crum RM, Warner LA et al. (1997), Lifetime co-occurrence of DSM-III-R alcohol abuse and dependence with other psychiatric disorders in the National Comorbidity Survey. Arch Gen Psychiatry 54(4):313-321.
Koob GF, Le Moal M (1997), Drug abuse: hedonic homeostatic dysregulation. Science 278(5335):52-58.
Leshner AI (1997), Addiction is a brain disease, and it matters. Science 278(5335):45-47 [see comment].
Marrazzi MA, Luby ED (1986), An auto-addiction opioid model of chronic anorexia nervosa. Int J Eat Disord 5:191-208.
Pinel JPJ, Assanand S, Lehman DR (2000), Hunger, eating, and ill health. American Psychologist 55(10):1105-1116.
Robinson TE, Berridge KC (1993), The neural basis of drug craving: an incentive-sensitization theory of addiction. Brain Res Rev 18(3):247-291.
Strober M, Freeman R, Morrell W (1999), Atypical anorexia nervosa: separation from typical cases in course and outcome in a long-term prospective study. Int J Eat Disord 25(2):135-142.
Vitousek K, Manke F (1994), Personality variables and disorders in anorexia nervosa and bulimia nervosa. J Abnorm Psychol 103(1):137-147.
Volkow ND, Wang GJ, Fowler JS et al. (1999), Prediction of reinforcing responses to psychostimulants in humans by brain dopamine D2 receptor levels. Am J Psychiatry 156(9):1440-1443.
Wiederman MW, Pryor T (1996), Substance use and impulsive behaviors among adolescents with eating disorders. Addict Behav 21(2):269-272.
Wise RA, Bozarth MA (1987), A psychomotor stimulant theory of addiction. Psychol Rev 94(4):469-492.