Drug abuse and treatment for skin picking disorders

June 11, 2015

Drug abuse and treatment for skin picking disorders: How Drug Abuse Affects the Skin

The rough Road of Quitting Heroin Addiction

Drug abuse and treatment for skin picking disorders. the two conditions can destroy ones life if not addressed from the beginning

With the increasing demand for beauty globally a lot is being done to improve the quality of our skin to keep looking as youthful as possible. The worry is, even as positive efforts are being done, a lot more bad things are also being done to destroy the youthfulness and beauty of your skin. Upon discovering that there is great need to tame the problem of substance abuse which has been seen to be the primary obstacle in sustaining the beauty of your skin, doctor Akoury made a decision to create a medical center (AWAREmed Health and Wellness Resource Center) whose main objective is to transform each individual’s life through increasing awareness about health and wellness and by empowering individuals to find their own inner healing power. Dr. Akoury’s practice focuses on personalized medicine through healthy lifestyle choices that deal with primary prevention and underlying causes instead of patching up symptoms. In this facility a lot is being done to restore the lost dignities, self-confidence of many people who are struggling with drug addiction. In our previous article, we noticed that skin picking disorders are some of the consequences that come with drug addiction and especially heroin addiction. Therefore in this article, we want to look at drug addiction and treatment for skin picking disorders as a way of finding lasting solutions.

Drug abuse and treatment for skin picking disorders: The skin picking disorder

The problem of skin picking disorders are becoming very common in today’s generation due to the continuous abuse of heroin. When one is suffering from this disorder, the beauty of such a person is seriously affected owing to the effects of the heroin addiction. To deal with this condition, doctor Akoury recommends that treatment must be done to the victim for both condition (heroin addiction and the infections on the skin as a result of the same). She further says that even though treatment of addiction is very difficult and full of obstacle, the good news is that with determination, this can be done conclusively. It is therefore advisable that if you are struggling with any form of addiction you can schedule for an appointment with doctor Akoury who will professionally carry out an extensive assessment on you to evaluate your psychological soundness before taking any treatment action on you. And like I had indicated before it must be noted that this substance is very addictive and a comprehensive psychiatric assessment will always be very vital. Doctor Akoury says that under normal circumstances an initial, personalized assessment should cover the following areas:

Identification of what triggers the behavior?
Getting to know the benefits individual is getting from the behavior
Finding out if the individual have co-occurring mental health problems, like anxiety or depression
Does the individual have an alcohol or drug problem?
Does the person have a family history of mental illness?
Has the person tried any medications or therapies in the past?

Even though a lot more still needs to be done when it comes to the treatment for this condition due to the fact that at the moment the, U.S. Food and Drug Administration have not yet approved any medications specifically for the treatment of BFRBs, there are clear evidence that several drugs have been used in the past successfully to control the impulse to pick or scratch the skin and the following are some of the medications which can be essentially helpful:

Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine (Prozac) and escitalopram (Lexapro), have been approved for the treatment of depression and/or obsessive-compulsive disorder
Tricyclic antidepressants, such as amitriptyline (Elavil) and imipramine (Elavil)
Opioid antagonists, such as naltrexone (ReVia), are used to reduce the pleasurable effects of alcohol and certain narcotics
Neuroleptic medications, such as olanzapine (Zyprexa) and risperidone (Risperdal), are used to treat repetitive, compulsive behaviors

Doctor Akoury reiterates that along with medication, behavioral modification therapies like Cognitive Behavioral Therapy (CBT) and Dialectical Behavior Therapy (DBT) can help reduce the urge to self-mutilate. These therapies have also proven to be valuable in the treatment of drug addiction.

Drug abuse and treatment for skin picking disorders: Hope for Compulsive Behaviors

Skin picking and hair pulling, like drug or alcohol abuses are not conditions to be taken lightly because the consequences of not taking immediate action can be very destructive. Because we are dealing a very delicate organ, when strong substances like heroin are a bused, the effect on the skin can be very wanting. I encourage you to take the beauty restoration of your skin seriously by scheduling for an appointment with doctor Dalal Akoury today for an elaborate treatment procedure. Dr. Akoury will be waiting for your call to help you regain the life of your skin. Remember that the main objective of doctor Akoury and her team of experts is to transform each individual’s life through increasing awareness about health and wellness and by empowering individuals to find their own inner healing power. It is very interesting to note that Dr. Akoury’s practice focuses on personalized medicine through healthy lifestyle choices that deal with primary prevention and underlying causes to ensure that your health is completely restored back to normalcy so that you can live life to the fullest.

Finally dear reader when fighting addiction, it is never a one man’s job, all of us needs to pool together to defeat this problem. On her part besides offering lasting solutions to patients, doctor Akoury is also reaching out for the professionals in this discipline of addiction through offering her exclusive NER Recovery Treatment to other physicians and health care professionals through training, clinical apprenticeships, webinars and seminars. In fact this year AWAREmed Health and Wellness Resource Center is organizing the first ever Integrative Addiction Conference 2015. The conference will be held in August 23-25 at Myrtle Beach, South Carolina and the mission of this conference is to provide prevention education, awareness, options and support to patients and physicians dealing with addiction.

It is also tailored to empower physicians to be involved in determining their personal “best answer for addiction” and promoting physician/patient awareness of a natural, yet profoundly effective, addiction treatment options that result in you “thriving while surviving” during treatment and recovery. Nonetheless the Integrative Addiction Conference 2015 will cover topics such as addiction as a holistic body ecosystem derangement, the interaction between stress, survivorship, pain and addiction, the role of hormonal imbalance in the disease of addiction, the genetic and epigenetic influences on the disease of addiction, psycho neuroendocrine immune restoration essential to reverse addiction as well as new and future therapies in the horizon for addiction treatment including stem therapy for psycho neuroendocrine immune restoration. This is a must attend conference for all professionals and you can get more information by login to www.integrativeaddiction2015.com or email sharon@integrativeaddiction2015.com.

Drug abuse and treatment for skin picking disorders: How Drug Abuse Affects the Skin

Methamphetamine Use May Risk Development of Parkinson’s Disease

March 25, 2015

Methamphetamine Use May Predispose Consumers to Future Development of Parkinson’s Disease

There are several neurodegenerative disorders but it will still not be right for anybody to talk about neurodegenerative disorders without mentioning the Parkinson’s disease. This disorder is the second most common after Alzheimer’s disease and it is affecting approximately ten million people worldwide. The probability of a person suffering from this disease increases with age with most people being diagnosed after the age of 50. Early in the course of the disease, the most obvious symptoms are movement-related. These include shaking, rigidity, slowness of movement, and difficulty with walking and gait. However, the symptoms worsens as time passes by, these may include cognitive and behavioral problems with dementia commonly occurring in the advanced stages of the disease. Other symptoms include sensory, sleep, and emotional problems. PD is caused by degeneration of midbrain dopaminergic neurons that project to the striatum. The loss of striatal dopamine is responsible for the major symptoms of the disease. Although a small proportion of cases can be attributed to known genetic factors, most cases of PD are idiopathic. While the etiology of dopaminergic neuronal demise is mysterious, a combination of genetic susceptibilities, age, and environmental factors seems to play a critical role. Dopamine degeneration process in PD involves abnormal protein handling, oxidative stress, mitochondrial dysfunction, excitotoxicity, apoptotic processes, and microglial activation or neuroinflammation.

methamphetamine

Studies on animals on methamphetamine toxicity

Studies done on animals have shown that methamphetamine can cause long-term dopamine terminal damage as well as dopamine neuronal body loss. In rodents, repeated administration of methamphetamine causes a decrease in dopaminergic markers such as tyrosine hydroxylase (TH) and dopamine transporter. Accompanied by a reduction in TH activity, reduced levels of dopamine and its metabolites and decreased levels of vesicular monoamine transporter 2 (VMAT2). These effects occur primarily in the striatum but also in the cortex, thalamus, hypothalamus and hippocampus. Methamphetamine induces neurotoxicity in a dose-dependent manner as do other amphetamine-derivatives like MDMA. Although partial recovery of TH and dopamine transport fibers occurs after methamphetamine administration, methamphetamine-induced neurotoxicity is persistent. In mice, the greatest dopaminergic fiber loss is seen 24 hours after methamphetamine administration. Neurotoxic effects persist for more than seven days after methamphetamine exposure and one month after MDMA exposure. Drugs that induce PD symptoms and TH loss such as MPTP in mice also show a partial recovery with time in nonhuman monkeys and mice. The time courses and degrees of TH and dopamine transport fiber recovery after methamphetamine or after MDMA exposure are similar, suggesting terminal regrowth, as these two proteins are independently regulated. Researchers have also noted that there is partial recovery of dopamine levels in the striatum strongly suggesting that the regrown terminals are functional. However the mechanisms responsible for partial recovery are not known, but it is speculated that it might involve compensatory sprouting and branching as has been reported for regrowth following MPTP-induced damage. Dopamine terminal recovery has also been described in rhesus monkeys and velvet monkeys, although it appears to occur on a slower timescale than in mice. Methamphetamine-induced dopaminergic damage persists for more than 12 weeks in velvet monkeys and more than 3 years in rhesus monkeys, demonstrating the persistence of methamphetamine-induced brain damage.

Methamphetamine Toxicity in the Substantia Nigra

This drug doesn’t only cause fiber loss in TH but also produces dopamine cell body loss in the substantia nigra as shown in tests in mice that were treated with 3 methamphetamine injections (5 mg/kg) at 3-hour intervals. From the counts it is evident that 20 to 25% dopaminergic cell loss, measured at different time are linked to exposure to methamphetamine. The observed pattern of TH-stained neuron loss is very similar to the pattern of Nissl-stained neuron loss, indicating that neuronal loss is specific to dopaminergic neurons. Dopamine cell body loss was confirmed via staining with Fluoro-Jade, a general marker of neuronal degeneration that fluoresces after administration of known dopaminergic toxins such as 6-OHDA and MPTP. Fluoro-Jade stains scattered neurons degenerated in the substantia nigra after methamphetamine treatment. there is a possibility that the lack of complete recovery of TH fibers in the striatum is related to the loss of dopaminergic neurons in the Substantia nigra similar to what occurs in Parkinson’s disease.

methamphetamine

Increased Risk of Parkinson’s Disease in Methamphetamine Abusers

There are literatures that have linked the abuse of amphetamine to the later development of PD. In a report of a study done by Callaghan and his colleagues, there is an increase in of PD in methamphetamine users in an epidemiological investigation based on data from California statewide hospital discharge records. The researchers identified 1,863 methamphetamine users, 9,315 patients hospitalized for appendicitis as a nondrug control group, and 1,720 cocaine users as a drug control group. All subjects were aged at least 50 years, had been hospitalized in California between 1990 and 2000, and had been followed for up to 10 years after discharge. The methamphetamine user group showed an elevated incidence of PD, with a 165% higher risk for development of PD than the patients from the control group. the results have been confirmed by the same group after doing the same research but in a much broader scope; 40,000 people hospitalized for methamphetamine versus 200,000 for appendicitis and 35,000 for cocaine and a 16-year follow-up period. From these two studies it is evident that methamphetamine use increases the chances of PD development in adulthood.

Drug abuse, addiction and independence are problems that people grapple with every day. These problems need to be treated effectively through integrative medicine. Dr. Dalal Akoury (MD) is an expert at this. Call her on (843) 213-1480 for help.

Methamphetamine Use May Predispose Consumers to Future Development of Parkinson’s Disease

Striatum Methamphetamine Toxicity

March 22, 2015

Methamphetamine Toxicity in the Striatum

The striatum is a crucial part of the brain. This part of the brain plays very important roles but it can be adversely affected by the use of stimulants and other drugs of leisure. Substances such as cocaine and methamphetamine produce their primary effects inside the brain by boosting the presence of dopamine which is a neurotransmitting chemical that activates the pleasure-producing neurons contained within the limbic system. As stated above the limbic system includes the hippocampus, along with several other brain structures. According to the results of two separate studies published in 2008 in the Journal of Neuroscience and Biological Psychiatry, the presence of either cocaine or methamphetamine alters normal adult neurogenesis inside the hippocampus and damages this region’s ability replenish its neuron supply. It is no longer news that methamphetamine intoxication causes long-lasting damage to dopamine nerve endings in the striatum. However the mechanisms underlying this neurotoxicity are not yet known but oxidative stress has been linked to it.

methamphetamine

Microglia are the major antigen-presenting cells in brain and when activated, they secrete an array of factors that cause neuronal damage. Astoundingly, very little work has been directed at the study of microglial activation as part of the methamphetamine neurotoxic cascade. It has been report that methamphetamine activates microglia in a dose-related manner and along a time course that is coincident with dopamine nerve ending damage. Through tests done on mice scientists have discovered that prevention of methamphetamine toxicity by maintaining treated mice at low ambient temperature prevents drug-induced microglial activation. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) not only damages dopamine nerve endings and cell bodies but also causes extensive microglial activation in striatum as well as in the substantia nigra. Contrastingly, methamphetamine causes neither microglial activation in the substantia nigra nor dopamine cell body damage.

Dopamine transporter antagonists do not mimic the effect of methamphetamine on microglia. Hyperthermia, a prominent and dangerous clinical response to methamphetamine intoxication, has been also ruled out as the cause of microglial activation. Together, these data suggest that microglial activation represents an early step in methamphetamine-induced neurotoxicity. Other neurochemical effects resulting from methamphetamine-induced overflow of dopamine into the synapse, but which are not neurotoxic, do not play a role in this response.

Methamphetamine use on the rise despite effects

The use of methamphetamine has been on the rise despite the fact that it is a powerful stimulant drug that has adverse effects when abused as most people do. According to the UN Office on Drugs and Crime reported recently that abuse of amphetamines, including designer drugs such as methamphetamine and 3, 4-methylenedioxymethamphetamine, now exceeds that of cocaine and heroin on a global scale. This presents no sign that its use will decline any soon. Past researchers were able to establish a fact that methamphetamine causes persistent reductions of function in dopamine nerve endings of animals and humans. Methamphetamine neurotoxicity has been under intense study for over 20 years, but still there is much that still remains to be learned about how this dangerous drug causes damage to dopamine nerve endings. The theory that revolves around oxidative stress has been at the top of the speculations. Drug-induced oxidative stress is an attractive construct that can account for many of the effects of methamphetamine on the dopamine nerve ending such as inhibition of tyrosine hydroxylase activity as well as reductions in the dopamine transporter and the vesicle monoamine transporter. This may even be an early event that leads eventually to methamphetamine-induced apoptosis. However, the source of the reactant species that mediate methamphetamine-induced damage is not known.

methamphetamine

Due to their crucial roles they play in mediating the mediating damage to the nervous system, Microglia has attracted considerable attention. Immune like in many ways these interesting cells become activated by damage and then transmigrate to sites of injury where they can secrete an array of factors like cytokines, prostaglandins, nitric oxide, and superoxide that are known to have detrimental effects on neurons. However, the role of microglia in methamphetamine-induced damage to the dopamine system has received little attention. In 1994 a researcher, Bowyer and his colleagues noted for the first time that methamphetamine resulted in activation of microglia in striatum of treated rats. These investigators concluded that microglia were increased in response to nerve ending damage and were not apparently a cause of it. Recently, another research was conducted to give an in-depth analysis of the effect of methamphetamine on striatal gene expression. Numerous genes linked to microglia were activated significantly within hours of methamphetamine intoxication, suggesting the possibility that microglial activation occurs earlier in the methamphetamine toxic cascade than previously thought.

Today there are researchers who are building on the initial analysis of methamphetamine and report the pharmacological characterization of microglial activation by methamphetamine in striatum. As mentioned before, striatum is an area dense in dopamine nerve endings and is known to be targeted for damage by methamphetamine. Microglial activation coincides with the onset of methamphetamine-induced damage in striatum and the extent of this effect is related to the degree of damage to dopamine nerve endings. Numerous nontoxic effects exerted by methamphetamine, such as inhibition of the DAT, increases in synaptic levels of dopamine, activation of D1 and/or D2 DA receptors, and hyperthermia, cannot explain methamphetamine-induced microglial activation.

Finally, this is still a dark area and there is need for more literature so as to establish the mechanism of methamphetamine toxicity on the striatum. Needless to say, Drug abuse, addiction and independence are problems that people grapple with every day. These problems need to be treated effectively through integrative medicine. Dr. Dalal Akoury (MD) is an expert at this. Call her on (843) 213-1480 for help.

Methamphetamine Toxicity in the Striatum

Molecular Mechanisms of Methamphetamine Induced-Neurotoxicity

March 21, 2015

Methamphetamine is a stimulant that is also highly soluble in water and affects the CNS most. Categorically it fits in the group of synthetic drugs chemically related to amphetamine but it has more adverse effects on the Central nervous system than the parent compound. Abuse of these illegal psychostimulants has become an international public health problem, with an estimated 14 to 52 million amphetamine-type stimulant users worldwide, exceeding the total number of cocaine abusers and second only to the number of cannabis abusers. This number has continued to rise in spite of the fact that much has been done to publicize the adverse effects these amphetamine related stimulants are linked to. Meth or speed as known in stimulant use circles exists in different forms like powder, tablets and capsules. It can also be found in a purer crystalline form.

It’s dangerous why is it used?

Just like most stimulants or drugs that are known to induce euphoric feelings, methamphetamine is also taken for similar reasons for example; to induce euphoric feelings, increased sense of well-being, increase energy and to calm anxiety. Being a powerful drug its effects are felt immediately after the use but these effects can last for long hours. They may be accompanied by acute adverse effects such as increased blood pressure and heart rate, which may cause irreversible damage to blood vessels in the brain, resulting in cerebrovascular accidents, stroke, and death. Methamphetamine also produces hyperthermia, pupil dilation, flushing, tremors, trismus and bruxism, muscle tension, loss of appetite or anorexia, and loss of pleasure in food intake which further leads to deterioration of the user’s health.

methamphetamine

Effects of Methamphetamine

Being an addictive drug, after a prolonged use the users may develop tolerance. It’s most common symptoms after a prolonged use include; temporomandibular joint syndrome, dental erosion, and myofacial pain. Long-term use also produces lack of appetite, weight loss, accelerated aging, nose-bleeding problems, nonhealing wounds, tooth decay and fracture known as “Meth mouth”. Psychiatric symptoms include anxiety, depression, increased aggression, social isolation, psychosis, mood disturbances, and psychomotor dysfunction. Long periods of high consumption can cause paranoid psychosis. Other symptoms of chronic methamphetamine use may also include; deficits in attention, working memory, and decision making. Most addicts are stuck in the use of meth as a result of the withdrawal symptoms which include the following; irritability, fatigue, impaired social functioning, and intense craving for the drug. Researchers have given evidence that the negative neuropsychiatric consequences of methamphetamine abuse are due, at least in part, to drug-induced neuropathological changes in the brain. Although the exact molecular mechanisms of neuronal body loss are not known, there is evidence to suggest the coexistence of different types of cell death, including apoptosis and necrosis ; indicated by the morphology of neurons stained with hematoxylin-eosin. Growing evidence exhibits that methamphetamine and MDMA induce an increase in lipid peroxidation and DNA oxidation as well as increased levels of oxidative stress markers such as hydroxyl radical producing neurotoxicity. Methamphetamine increases expression of inducible nitric oxide synthase (nNOS)/ neuronal nitric oxide synthase (iNOS ) indicating increased synthesis of neuronal nitric oxide, which combines with superoxide radicals to form peroxynitrite which is a strong oxidant and a major neurotoxin . Induction of nNOS/iNOS by methamphetamine or MDMA constitutes part of the mechanism of methamphetamine damage, as selective inhibition or genetic inactivation of nNOS and overexpression of cupper zinc superoxide dismutase (CuZnSOD), an enzyme that catalyzes the dismutation of superoxide into oxygen and hydrogen peroxide, prevent methamphetamine neurotoxicity . Even though methamphetamine increases iNOS expression in the striatum , there is no basis for supposing the involvement of glial nitric oxide in methamphetamine-induced toxicity, but it is interesting to note that mice deficient in iNOS have increased resistance to methamphetamine-induced dopamine neuron damage.

methamphetamine

The neurotoxic effects of methamphetamine on the dopaminergic system are accompanied by activation of astroglia and microglia in the same areas being strongest in the striatum, the area with biggest toxicity. Glial cells are not activated in the nucleus accumbens, which is not much damaged . In mice, glial activation in striatum and in substantia nigra occurs shortly after methamphetamine administration, as indicated by a significant increase in Mac-1 ;a marker of reactive microglia 24 hours after methamphetamine exposure and prominent increases in GFAP ; a marker of reactive gliosis in response to injury occur within a week after treatment . The extent of these glial reactions correlates with the observed severity of neurotoxicity.

The dopaminergic system is also involved in this toxicity, as demonstrated in various mutant mice in which inactivation of dopamine transport, dopamine D1 receptors or D2 receptors affords a significant protection against methamphetamine toxicity. Administration of THC prevents dopaminergic toxicity after MDMA, a similar amphetamine derivative to methamphetamine, by CB1 receptor stimulation which is present in striatal medium spiny neurons. All these receptors are involved in different aspects of learning processes that became affected by the chronic use of methamphetamine or MDMA.

Finally, Drug abuse, addiction and independence are problems that people grapple with every day. These problems need to be treated effectively through integrative medicine. Dr. Dalal Akoury (MD) is an expert at this. Call her on (843) 213-1480 for help.

Molecular Mechanisms of Methamphetamine Induced-Neurotoxicity

Oxytocin May Remedy Drug Abuse Effects

January 13, 2015

Oxytocin May Reverse Corrosive Effects of Long-Term Drugs Abuse

A person’s social life has a great influence in his possibility of using drugs of pleasure. Most of drugs of pleasure are used in social circles and therefore it is appropriate to say that social factors play an important role in the initiation, maintenance and recovery from addictions. There is now accumulating evidence of an interaction between the neural substrates of affiliate behavior and those of drug reward, with a role for brain oxytocin systems in modulating acute and long-term drug effects.

What is oxytocin?

Oxytocin is a hormone that is made in the brain, in the hypothalamus, and it is transported to, and secreted by, the pituitary gland, which is located at the base of the brain. Chemically it is known as a nonapeptide, (because it is a peptide containing nine amino acids), and biologically, as a neuropeptide. It acts both as a hormone and as a brain neurotransmitter. Due to its roles in behavior, this hormone has been given different names such as the love hormone, cuddle hormone, bliss hormone, moral molecule and even hug hormone. Researchers say that it is released when people snuggle up or bond socially.

However this hormone seems to have many functions that can be very helpful to clinical treatment of those enslaved by drug addiction. Researchers have been able to establish a link between addiction and oxytocin and the findings are promising as new approaches can be developed on the basis of the influence of oxytocin on drug addiction to help quell drug addiction and free addicts enslaved to drug use.

Past researchers have indicated that exogenous oxytocin administration can prevent development of tolerance to ethanol and opiates, the induction of stereotyped, hyperactive behavior by stimulants, and the withdrawal symptoms associated with sudden abstinence from drugs and alcohol. In addition to this finding, stimulation of endogenous oxytocin systems is a key neurochemical substrate underlying the prosocial and empathogenic effects of party drugs such as MDMA often referred to as Ecstasy and GHB mostly known as Fantasy. According to these early research reports, brain oxytocin systems exhibit profound neuroplasticity and undergo major neuroadaptations as a result of drug exposure. Many drugs, including cocaine, opiates, alcohol, cannabis, MDMA and GHB cause long-term changes in markers of oxytocin function and this may be linked to enduring deficits in social behavior that are commonly observed in laboratory animals after going through repeated exposure to these drugs. Very recent preclinical studies have illustrated a remarkable ability of exogenously delivered oxytocin to inhibit stimulant and alcohol self-administration, to alter associated drug-induced changes in dopamine, glutamate and Fos expression in cortical and basal ganglia sites, and to prevent stress and priming-induced relapse to drug seeking. Oxytocin therefore has fascinating potential to reverse the corrosive effects of long-term drugs abuse on social behavior and to perhaps inoculate against future vulnerability to addictive disorders. However clinical studies that are examining intranasal oxytocin effects in humans with drug use disorders are still awaited but hopes are high that the results may open ways into a new dimension in fighting drug addiction by using this hormone.

Targeted as a novel treatment of Drug addiction

Over the years researchers have had speculations that oxytocin may have an effect on drug addiction and related behaviors. Clinical doctors and other researchers have got the knowledge that people who are addicted to certain drugs exhibit antisocial traits and exhibit poor decision making in the social domain. There has also been a link between high levels of oxytocin and blossoming relationships as well as stable social bonds. Due to its speculated effects on drug addiction related behavior, oxytocin has been targeted as a novel treatment for alcohol and drug abuse. This has been catapulted by the realization that the acute prosocial effects of some popular recreational drugs most likely involve stimulation of oxytocin systems and that the neural substrates of social bonding and drug reward may be intertwined.

Some drugs of pleasure like MDMA when taken affect the person in a way that he becomes more loving and close to the people around him. He also becomes more naïve as to trust those with him and even to agree with most of their arguments. In preclinical tests these prosocial behaviors have been seen in animal models, for instance in strange pairs of rats meeting for the first time, MDMA markedly reduce aggression and increase a behavior known as adjacent lying; the rats cuddle inhibiting a feeling of love and trust as always the case with human beings under the influence of this drug. MDMA and its metabolites stimulate hypothalamic oxytocin release and after this hormone has been released in high levels then the prosocial feelings are exhibited.

Many researchers have now proposed that the reason why many addicts go through drug addiction recovery programs successfully in rehabs may be because of this hormone. The addicts who are majorly summoned to anonymous meetings in the rehabs experience surge in this hormone as they relate to their fellow addicts, this is said to have therapeutic effects as they help resettle dysfunctional oxytocin pathways. In spite of it’s clearly involvement in the prosocial effects of some drugs, it is not clear whether oxytocin itself is rewarding. It is however appropriate to mention that there is still a lot that should be done on this field to avail information on how these past findings can help ease drug addiction treatment.

Oxytocin May Reverse Corrosive Effects of Long-Term Drugs Abuse

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