Opioid use disorders are characterized in part by impairments in social functioning. Previous research indicates that laboratory rats, which are frequently used as animal models of addiction-related behaviors, are capable of prosocial behavior. For example, under normal conditions, when a 'free' rat is placed in the vicinity of rat trapped in a plastic restrainer, the rat will release or 'rescue' the other rat from confinement. The present study was conducted to determine the effects of heroin on prosocial behavior in rats. For 2 weeks, rats were given the opportunity to rescue their cagemate from confinement, and the occurrence of and latency to free the confined rat was recorded. After baseline rescuing behavior was established, rats were randomly selected to self-administer heroin (0.06 mg/kg/infusion i.v.) or sucrose pellets (orally) for 14 days. Next, rats were retested for rescuing behavior once daily for 3 days, during which they were provided with a choice between freeing the trapped cagemate and continuing to self-administer their respective reinforcer. Our results indicate that rats self-administering sucrose continued to rescue their cagemate, whereas heroin rats chose to self-administer heroin and not rescue their cagemate. These findings suggest that rats with a history of heroin self-administration show deficits in prosocial behavior, consistent with specific diagnostic criteria for opioid use disorder. Behavioral paradigms providing a choice between engaging in prosocial behavior and continuing drug use may be useful in modeling and investigating the neural basis of social functioning deficits in opioid addiction.
PMID: 29726093 DOI:10.1111/adb.12633
Extinction therapy has been suggested to suppress the conditioned motivational effect of drug cues to prevent relapse. However, extinction forms a new inhibiting memory rather than erasing the original memory trace and drug memories invariably return. Perineuronal nets (PNNs) are a specialized extracellular matrix around interneurons in the brain that have been suggested to be a permissive factor that allows synaptic plasticity in the adolescent brain. The degradation of PNNs caused by chondroitinase ABC (ChABC) may generate induced juvenile-like plasticity (iPlasticity) and promote experience-dependent plasticity in the adult brain. In the present study, we investigated the effect of removing PNNs in the amygdala of rat on the extinction of drug memories. We found that extinction combined with intra-amygdala injections of ChABC (0.01 U/side) prevented the subsequent priming-induced reinstatement of morphine-induced and cocaine-induced, but not food -induced, conditioned place preference (CPP). Intra-amygdala injections of ChABC alone had no effect on the retention, retrieval, or relearning of morphine-induced CPP and storage of acquired food-induced CPP. Moreover, we found that the procedure facilitated the extinction of heroin- and cocaine-seeking behavior and prevented the spontaneous recovery and drug-induced reinstatement of heroin- and cocaine-seeking behavior. We also found that the effect of PNNs degradation combined with extinction may be mediated by the potentiation of several plasticity-related proteins in the amygdala. Altogether, our findings demonstrate that a combination of extinction training with PNNs degradation in the amygdala erases drug memories and suggest that ChABC may be an attractive candidate for the prevention of relapse.
Journal of Neuroscience, 34 (19) 6647-6658; DOI: https://doi.org/10.1523/JNEUROSCI.5390-13.2014
Ed Cara Jul 10, 2018, 4:00pm
People living with opioid addiction are increasingly using the inhalation method to get high, warns a new review published Monday in JAMA Neurology. The technique known as “chasing the dragon”, which involves heating up heroin and inhaling its fumes through a pipe, may be safer in some ways than injection, but it comes with its own set of devastating side effects, including irreversible brain damage and dementia.
The doctors behind the study, led by neurologist Ciro Ramos-Estebanez of the University Hospitals Cleveland Medical Center in Ohio, were inspired to study the topic after coming across a strange case in 2015.
A young woman suffering from opioid intoxication had fallen into a coma. The coma was caused by a build up of spinal fluid in her brain, a condition known as hydrocephalus. The woman’s spinal fluid had become trapped by chronic inflammation in the brain caused by inhaling heroin.
She ultimately recovered from her coma, though with lasting cognitive impairment, after doctors performed emergency surgery that drained the lodged spinal fluid.
It was the first case of hydrocephalus linked to inhaled heroin ever reported, and it made Ramos-Estebanez and his team eager to understand the phenomenon better
Looking at more than 30 studies and case reports, which included the cases of two other patients at their hospital, the team settled on some basic observations.
For one, while there’s sparse information on how often addicts are inhaling heroin, the little data that does exist suggests it’s the fastest growing method of use, the team found.
In countries such as Sri Lanka, Norway and India, over two-thirds of heroin users admit inhaling it regularly. In the US, injection is still the most common method, but inhalation is increasing, especially in cities and areas east of the Mississippi.
It’s also becoming more popular among teens. In 2014, the team found, 21 per cent of all inpatient hospital visits due to heroin abuse among 12- to 19-year-olds involved inhalation.
The extent of damage caused by inhaling heroin also runs along a spectrum. At its mildest, it can cause memory loss and mild but long-lasting cognitive impairment; at its worst, it can kill off and create sponge-like holes in the brain’s white matter, the bundles of connective fibre that allow brain cells to talk to one another. That can lead to seizures, problems speaking, progressively worse dementia, coma and death.
Ramos-Estebanez and his team also developed a theory as how and why this damage happens. The high temperatures used to vaporise heroin, they speculate, metabolise it into a chemical that can cross the blood-brain barrier with greater ease. And because how fast it gets to the brain, these chemicals aren’t metabolised by the body into a relatively less toxic substance. The end result is a potent high that is more directly dangerous to the brain.
“Most people who take heroin intravenously don’t develop this condition,” Ramos-Estebanez said. “You’re actually washing out the dose a bit before it gets to the brain.”
Ultimately, Ramos-Estebanez wants doctors and the public to treat inhaled heroin as an emerging public health problem. Being able to recognise its signs in opioid users earlier might just be life-saving, too: Some small studies have identified a few drugs that seem capable of preventing further brain damage if administered quickly enough.
Outside of these sites, Ramos-Estebanez wants to dispel the notion that inhaling heroin is necessarily safer than other routes, such as injection. Many people, for instance, may inhale to avoid the risk of catching bloodborne diseases through contaminated needles.
“‘Chasing the dragon’ is not as safe as portrayed. And this isn’t something some doctor is saying to scare people away, it’s reality,” Ramos-Estebanez said. “It’s a heavy cost for patients, their families and society itself.”
In addition to creating accurate criteria that doctors can use to diagnose people who have brain damage caused by inhaled heroin, Ramos-Estebanez and his team are also currently trying to establish a registry so cases can be better tracked and studied.
Males experienced around three-quarters of the total burden from alcohol use and illicit drug use in Australia in 2011. Compared to females, males experienced a greater proportion of burden due to alcohol use for most associated diseases, but most notably from Homicide and violence (27%, compared with 10% for females) and from Other unintentional injuries (23%, compared with 7.2% for females).
The burden from alcohol use and illicit drug use (calculated separately) varied according to where a person lived and their socioeconomic position. Age-standardised rates were higher in:
Email the author MD A. Benjamin Srivastava, Mark S. Gold, MD
Department of Psychiatry, Washington University School of Medicine, St Louis, MO
The opioid epidemic is the most important and most serious public health crisis today. The effects are reported in overdose deaths but are also starkly evident in declines in sense of well-being and general health coupled with increasing all-cause mortality, particularly among the middle-aged white population.1 As exceptionally well described by Rummans et al in this issue of Mayo Clinic Proceedings, the cause of the epidemic is multifactorial, including an overinterpretation of a now infamous New England Journal of Medicine letter describing addiction as a rare occurrence in hospitalized patients treated with opioids, initiatives from the Joint Commission directed toward patient satisfaction and the labeling of pain as the “5th vital sign,” the advent of extended-release oxycodone (OxyContin), an aggressive marketing campaign from Purdue Pharma L.P., and the influx of heroin and fentanyl derivatives.
To date, most initiatives directed toward fighting the opioid initiatives, and the focus of the discussion from Rummans et al, have targeted the “supply side” of the equation. These measures include restricting prescriptions, physician drug monitoring programs, and other regulatory actions. Indeed, although opioid prescriptions have decreased from peak levels, the prevalence of opioid misuse and use disorder remains extremely prevalent (nearly 5%). 4, 5 Further, fatal drug overdoses, to which opioids contribute to a considerable degree, continue to increase, with 63,000 in 2016 alone.6 Thus, although prescription supply and access are necessary and important, we need to address the problem as a whole. To this point, for example, the ease of importation and synthesis of very cheap and powerful alternatives (eg, fentanyl and heroin) and the lucrative US marketplace have contributed to the replacement pharmacy sales and diversion with widespread street-level distribution of these illicit opioids; opioid-addicted people readily switch to these illicit opioids.
A complementary and necessary approach is to target the “demand” side of opioid use, namely, implementation of preventive measures, educating physicians, requiring physician continuing education for opioid prescribing licensure, and addressing why patients use opioids in the first place. Indeed, prevention of initiation of use is the only 100% safeguard against addiction; however, millions of patients remain addicted, and they need comprehensive, rather than perfunctory, treatment. Rummans and colleagues are absolutely correct in their delineation of the unwitting consequences of a focus on pain, given that a perceived undertreatment of pain fueled the opioid epidemic in the first place. They are correct to point out how effective pain evaluation and treatment are much more than prescribing and should routinely include psychotherapy, interventional procedures, and nonopioid therapies.2 In addition, we have described the crossroads between pain and addiction as well as successful strategies to manage patients with both chronic pain syndromes and addiction.
Results: Overall, 32.2% (95% CI=29.7–34.9) of patients with a substance-induced psychosis converted to either bipolar or schizophrenia-spectrum disorders. The highest conversion rate was found for cannabis-induced psychosis, with 47.4% (95% CI=42.7–52.3) converting to either schizophrenia or bipolar disorder. Young age was associated with a higher risk of converting to schizophrenia. Self-harm after a substance-induced psychosis was significantly linked to a higher risk of converting to both schizophrenia and bipolar disorder. Half the cases of conversion to schizophrenia occurred within 3.1 years after a substance-induced psychosis, and half the cases of conversion to bipolar disorder occurred within 4.4 years.
Conclusions: Substance-induced psychosis is strongly associated with the development of severe mental illness, and a long follow-up period is needed to identify the majority of cases.
These results indicated that greater frequency of freshman year binge drinking and marijuana use is significantly related to delayed college graduation, which supports the importance of pre-college interventions targeted at decreasing heavy drinking and marijuana use. Thus, highlighting the harmful academic outcomes associated with binge drinking and marijuana use, including longer time spent in college might augment these pre-college interventions. Further, we found a significant association between delayed college graduation and decreased financial prosperity during early adulthood, which could also be integrated into incentives for college students to graduate college in 4 years.
Fixing the Addicted Brain with Electromagnets
Mark Gold MD
As experts at NIH and NIDA are calling for research and breakthrough treatments for SUDs, rTMS has been suggested to help with cravings for drugs, drug withdrawal and drug withdrawal-related sleep and depression symptoms. The long-term neurophysiological changes induced by rTMS have the potential to affect behaviors relating to drug taking, craving and relapse. In addition, rTMS is currently undergoing trials in pain management.
Chronic methamphetamine use causes neuroadaptive/pathological changes in the brain, including numerous cognitive deficits plus mood, thought and behavioral disorders, the worst of which is psychosis. Research by Wang et al, (2015) found similar patterns of delusions common in patients with schizophrenia among those with methamphetamine-induced psychoses. Moreover, when compared with schizophrenic patients, those with methamphetamine-induced psychosis present a higher prevalence of visual and tactile hallucinations but less cognitive disorganization, blunted affect and motor retardation.
Additional investigations are needed to identify biological differences between schizophrenia and methamphetamine-induced psychosis in order to develop therapeutic targets and potential medications for methamphetamine addiction and co-occurring mental illness.
Why Does This Matter?
Because of the high toxicity of meth, the debilitating effects often persist after extended periods of abstinence. As a result, the cognitive deficits (which are not easy to detect in abstinence) affect how individuals respond to treatment, which is a highly didactic and educational experience. Therefore, treatment modalities and interventions must be tailored to address the individuals’ unique cognitive and emotional deficits and co-occurring psychiatric and medical disorders.
Background Amphetamine abuse is becoming more widespread internationally. The possibility that its many cardiovascular complications are associated with a prematurely aged cardiovascular system, and indeed biological organism systemically, has not been addressed.
Methods Radial arterial pulse tonometry was performed using the SphygmoCor system (Sydney). 55 amphetamine exposed patients were compared with 107 tobacco smokers, 483 non-smokers and 68 methadone patients (total=713 patients) from 2006 to 2011. A cardiovascular-biological age (VA) was determined.
Results The age of the patient groups was 30.03±0.51–40.45±1.15 years. This was controlled for with linear regression. The sex ratio was the same in all groups. 94% of amphetamine exposed patients had used amphetamine in the previous week. When the (log) VA was regressed against the chronological age (CA) and a substance-type group in both cross-sectional and longitudinal models, models quadratic in CA were superior to linear models (both p<0.02). When log VA/CA was regressed in a mixed effects model against time, body mass index, CA and drug type, the cubic model was superior to the linear model (p=0.001). Interactions between CA, (CA)2 and (CA)3 on the one hand and exposure type were significant from p=0.0120. The effects of amphetamine exposure persisted after adjustment for all known cardiovascular risk factors (p<0.0001).
Conclusions These results show that subacute exposure to amphetamines is associated with an advancement of cardiovascular-organismal age both over age and over time, and is robust to adjustment. That this is associated with power functions of age implies a feed-forward positively reinforcing exacerbation of the underlying ageing process.
13 DECEMBER 2017 - WHO has this week endorsed a recommendation from the Expert Committee on Drug Dependence (ECDD) to include carfentanil, an analogue of the prescription opioid fentanyl, into Schedules I and IV of the 1961 UN Single Convention on Narcotic Drugs. Schedule I substances are subject to strict drug control measures. Additional control under Schedule IV imposes the strongest possible regulations on substances by prohibiting production and supply of substances except under licence for specific purposes, such as medical treatment and research. In the case of carfentanil, there is no indication for human use
Notwithstanding the $600 million federal Settlement with Purdue in 2007 — one of the largest in history with a drug company — opioid litigation has yet to financially dent the $13-billion-a-year opioid industry.
In 2016, roughly 64,000 people died from drug overdoses, and opioids accounted for nearly two-thirds of those deaths. It is difficult to comprehend the full scope and magnitude of the opioids crisis, its causes, and its consequences—for families, communities, and workplaces. But better understanding the challenges it poses is a necessary first step to informed public policy. This report gathers an unprecedented amount of data on the opioids crisis. Key findings include:
Opioid overdose deaths continue to rise at an alarming rate
Opioid-related deaths are shifting to younger demographic groups, typically white, single or divorced, and with relatively less formal education
The oversupply and abuse of legal prescription pain relievers is at the heart of the crisis
Illegally obtained opioids have rapidly become a major problem
Hospitalization for opioids abuse has also risen across geographic, demographic, and socioeconomic groups
The opioid crisis will affect the next generation for years to come
Clenbuterol is a steroid-like chemical that was initially developed to treat asthma in horses, working by relaxing the airways in the animals' lungs
This increase will lead to a variety of effects, such as:
rapid fat burning
Why is clenbuterol used?
Clenbuterol's initial use was as an asthma drug. However, bodybuilders, performance athletes, and those wanting to lose weight are now using the drug.
Clenbuterol can be used as a weight-loss aid because it can increase a person's metabolism. As well as reducing body fat and weight, it also allows the user to retain both muscle mass and body strength at the same time.
Clenbuterol became known as a celebrity diet secret because of its apparent use by celebrities and famous athletes.
Oct. 30, 2017 (HealthDay News)
Opioid addicts saved by the overdose reversal medication naloxone are still in danger following their close brush with death, a new study shows.About 10 percent of overdose patients saved with naloxone (Narcan) in Massachusetts hospitals ended up dying within a year, Harvard researchers reported.Further, half of those who died did so within one month of their rescue, the investigators found."The opioid overdose patient who sobers in the hallway, is offered a detox list, and then is discharged has a one-in-10 chance of being dead within one year, and their highest risk is within the first month," said lead researcher Dr. Scott Weiner. He is director of the Comprehensive Opioid Response and Education Program at Brigham and Women's Hospital in Boston.Patients saved with naloxone are very likely to suffer withdrawal cravings that could drive them to overdose within a matter of weeks, Weiner said."Naloxone is not the panacea solution to the crisis," Weiner said. "Patients who survive opiate overdose need to be considered extremely high risk and should receive interventions like offering buprenorphine or offering counseling and referral for treatment prior to discharge from the emergency department."
This article examines this idiosyncratic approach to the criminalisation of drug driving, highlighting its weak correlation with the important road safety objective of deterring substance-impaired driving, and the risks of both over- and under-criminalisation that it creates. It argues that public policy on the prohibition of certain drugs and the criminalisation of their use should be disentangled from public policy on impaired driving. It recommends that drug driving laws in all Australian jurisdictions should be brought back into line with drink driving laws, via legislation and testing practices that turn on substance-specific prescribed concentrations for all drugs (illicit and licit) that have the potential to impair drivers.
That the goals of improving road safety and reducing road accidents and trauma are valid and important is axiomatic. Accordingly, and alongside other measures, the detection of individuals who are driving under the influence of substances that are known to diminish driver capacity is entirely meritorious. The aim of this article is not to question the legitimacy of these objectives, but to scrutinise and produce fresh insights about the way that the criminal law is configured and deployed to this end. Specifically, it investigates whether current drug driving laws and random drug testing (RDT) practices are consistent with the evidence‐based impairment paradigm that has underpinned the success of random breath testing (RBT) and drink driving offences in transforming driving under the influence of alcohol from a common practice to a highly stigmatised criminal behaviour (Terer and Brown 2014). By producing new knowledge about the character of contemporary drug driving laws, we aim to identify reform options that will allow drug driving laws to share the combination of social acceptance, evidence‐based legitimacy and effectiveness that are widely regarded as the hallmarks of drink driving laws
These results suggest that marijuana use leads to altered neural functioning during visuospatial working memory after controlling for other prenatal and current drug use. This alteration appears to be compensated for by the recruitment of blood flow in additional brain regions. It is possible that this compensation may not be sufficient in more real-life situations where this type of processing is required and thus deficits may be observed. Awareness of these neural physiological effects of marijuana in youth is critical.
These results, although only briefly presented, extend previously reported effects of prenatal marijuana exposure on neurophysiological processing during executive functioning. These long term effects highlight the importance of optimizing the prenatal environment. The observed negative long term trans-generational effects are avoidable with knowledge transfer, education and a wider appreciation for the harmful consequences of prenatal marijuana exposure.
Background: Fentanyl is a powerful synthetic and short-acting painkiller that is 50- 100 times more potent than morphine,1 meaning that 1/10th of a gram of fentanyl is equivalent to between 5-10g of morphine*. It was first synthesized by Dr. Paul Janssen in December 19602,3 and has become one of the world’s most important and frequently used opioid analgesics, used also as a pre-medication for general anaesthetic, partly because of its rapid action and multiple routes of administration. While pharmaceutical fentanyl can be diverted for misuse, cases of fentanyl-related mortality in the US have been linked to illicitly manufactured fentanyl and a variety of fentanyl analogues.4 These newly-synthesized fentanyls are being sold as a standalone product, as a low-cost additive to increase the potency of heroin and even as counterfeit medicines.5,6,7 The overdose death rate from synthetic opioids (excluding methadone but including fentanyl and tramadol) continues to increase in the US with a 72.2% increase from 2014 to 2015, with a total of 9,580 deaths in 2015.8
15 May 2017
Over just five years, the number of new hepatitis C virus infections reported to CDC has nearly tripled, reaching a 15-year high, according to new preliminary surveillance data released by the Centers for Disease Control and Prevention (CDC).
Hepatitis C kills more Americans than any other infectious disease reported to CDC. The data indicate that nearly 20,000 Americans died from hepatitis C-related causes in 2015, and the majority of deaths were people ages 55 and older.
"By testing, curing, and preventing hepatitis C, we can protect generations of Americans from needless suffering and death," said Jonathan Mermin, M.D., director of CDC's National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention. "We must reach the hardest-hit communities with a range of prevention and treatment services that can diagnose people with hepatitis C and link them to treatment. This wide range of services can also prevent the misuse of prescription drugs and ultimately stop drug use - which can also prevent others from getting hepatitis C in the first place."
New hepatitis C virus infections are increasing most rapidly among young people, with the highest overall number of new infections among 20- to 29-year-olds. This is primarily a result of increasing injection drug use associated with America's growing opioid epidemic.
However, the majority (three-quarters) of the 3.5 million Americans already living with hepatitis C are baby boomers born from 1945 to 1965. Baby boomers are six times more likely to be infected with hepatitis C than those in other age groups and are at much greater risk of death from the virus.
While surveillance data do not accurately capture hepatitis C infection rates among infants, other recent CDC studies indicate that hepatitis C virus infections are growing among women of childbearing age - putting the youngest generation of Americans at risk. Hepatitis C treatment not only cures the vast majority of people living with the virus, but also prevents transmission to their partners and children.
(D.I Commentary – “Australia distributes 100s of thousands of clean syringes each year, without accountability what so ever, yet our BBV (Blood Borne Virus) Stats are increasing http://www.health.gov.au/sexual-health. So, is more taxpayer funded syringes making the BBV issue worse or better? Are the new STI’s that are being spread the result of ‘dirty’ or shared needles, or actually the result of unprotected sex by people who are ‘high’, ‘stoned’, ‘wasted’ on the illicit drugs that taxpayer funded ‘health’ resources (NSP’s/SSP’s) equipped them to use?”)
Cocaine traffickers attempting to launder their profits are responsible for the disappearance of millions of acres of tropical forest across large swaths of Central America, according to a report.
The study, published on Tuesday in the journal Environmental Research Letters, found that drug trafficking was responsible for up to 30% of annual deforestation in Nicaragua, Honduras and Guatemala, turning biodiverse forest into agricultural land.
The study’s lead author, Dr Steven Sesnie from the US Fish and Wildlife Service, said: “Most of the ‘narco-driven’ deforestation we identified happened in biodiverse moist forest areas, and around 30-60% of the annual loss happened within established protected areas, threatening conservation efforts to maintain forest carbon sinks, ecological services, and rural and indigenous livelihoods.”
The burden of substance abuse disorders can fall heavily on the families and friends of those who battle addictions. But society also pays a great deal through increased crime. Treatment programs can reduce those costs.
For at least two decades, we’ve known substance use and crime go hand in hand. More than half of violent offenders and one-third of property offenders say they committed crimes while under the influence of alcohol or drugs.
Researchers with the Centers for Disease Control and Prevention recently estimated that prescription opioid abuse, dependence and overdoses cost the public sector $23 billion a year, with a third of that attributable to crime. An additional $55 billion per year reflects private-sector costs attributable to productivity losses and health care expenses.
About 80,000 Americans are incarcerated for opioid-related crimes alone. The total annual economic burden of all substance use disorders — not just those involving opioids — is in the hundreds of billions of dollars.
Physicians’ prescriptions for chronic noncancer pain rose 3-fold and became the major source of opioids over the past 2 decades. This shift in practice norms was fueled by an acceptance of low-quality evidence that opioids are a relatively benign remedy for managing chronic pain. These vast opioid supplies created a risk for diversion, opioid misuse and disorder, and overdose death. A proportion of prescription opioid misusers transitioned to illicit opioids, following contraction of prescription opioid supplies, and an expanding influx of potent, low-cost heroin and fentanyl analogs. The rise in overdose deaths catalyzed formation of federal and state policies to reduce supply, augment treatment, and distribute overdose medications. The current response remains inadequate until opioid deaths decline.
April 06 2017
The use of methamphetamine or ‘ice’ in South Australia has doubled in the past four years, with the latest National Wastewater Drug Monitoring Program Report showing there were more than 500 standard doses of methamphetamine each week per 1,000 people in December 2016.
The long term effects of this steady increase in the use of methamphetamine are not yet known but research has revealed a concerning similarity between the brains of young methamphetamine users and older people who have been diagnosed with Parkinson’s disease.
To try and find some answers the Fay Fuller Foundation is investing more than $230,000 in UniSA Senior Lecturer in the School of Pharmacy and Medical Sciences, Dr Gabrielle Todd, and her colleagues’ investigations into the long-lasting effects of methamphetamine (‘ice’) on the brain regions that control movement.
“Brain scans show that the appearance of a movement-related brain region, called the substantia nigra, is abnormally bright and enlarged in methamphetamine users and in patients with Parkinson’s disease,” Dr Todd says.
“The abnormality is a well-established risk factor for Parkinson’s disease and is used to help diagnose the disease in other parts of the world so it’s very concerning to see this abnormality in young people that use methamphetamine.
“Of even greater concern, is that young methamphetamine users already show changes in the way that they move, and some of these changes resemble those that occur with Parkinson’s disease.”
Young methamphetamine users may have no idea about the long-lasting health consequences of their drug use.
“The risk is not just related to heavy methamphetamine use, we are seeing movement and brain changes in young people who may have only taken the drug as few as five times,”Dr Todd says.
“Knowledge is a powerful tool and raising awareness about the link between methamphetamine use and the way that we move may help discourage young people from using this drug.”
The project outcome will be a new evidence-based, ready-to-use health message that increases community knowledge of the long-lasting consequences of methamphetamine use, changes attitudes towards methamphetamine, and discourages use of the drug in young people. This will be achieved with a four step approach:
Step 1: Measure existing knowledge of and attitudes to the long-lasting consequences of methamphetamine use on health.
Step 2: Measure the types of movement changes that occur as a result of use of methamphetamine and how common these changes are among methamphetamine users.
Step 3: Create the new health message to inform young adults about the long-lasting consequences of methamphetamine use on movement, in collaboration with drug and alcohol treatment service providers, researchers that specialise in methamphetamine-related harm and prevention, Parkinson’s South Australia, and a marketing and communications company.
Step 4: Test the effectiveness of the new health message in improving knowledge about the long-lasting consequences of methamphetamine use.
Published: Tuesday 4 April 2017
(The Key here, is to create an environment during abstinence where the neural rebuild is attached to new and healthy reward memory creating activities – it’s not so much what you put down, rather what you take up! No Brainer D.I)
New research from The Scripps Research Institute (TSRI) suggests that the reason methamphetamine users find it so hard to quit - 88 percent of them relapse, even after rehab - is that meth takes advantage of the brain's natural learning process. The TSRI study in rodent models shows that ceasing meth use prompts new neurons to form in a brain region tied to learning and memory, suggesting that the brain is strengthening memories tied to drug-seeking behavior.
"New neuronal growth is normally thought of as a good thing, but we captured these new neurons assisting with 'bad' behaviors," said Chitra Mandyam, who led the research as an associate professor at TSRI before starting a new position at the Veterans Medical Research Foundation and the University of California, San Diego.
The scientists discovered that they could block relapse by giving animals a synthetic small molecule to stop new neurons from forming. This molecule, called Isoxazole-9 (Isx-9), also appeared to reverse abnormal neuronal growth that developed during meth use.
The new research was published in the journal Molecular Psychiatry.
Young Neurons Gone Bad
Neurons are born all the time in a process called neurogenesis. In a 2010 study, Mandyam and her colleagues at TSRI showed that increased neurogenesis is tied to a higher risk of drug relapse, but they weren't sure of the new neurons' role in the process. The researchers were especially curious about a "burst" of neurogenesis that occurs during abstinence from meth.
The new study may explain why the brain is so eager to make neurons during abstinence: meth hijacks the natural neurogenesis process.
Normally, new neurons help us learn by forming new circuits to connect rewards, like food, to reward-associated memories. For example, we learn early on that the refrigerator holds food. "In a non-drug environment, this is a healthy process," said Mandyam.
But the brain isn't good at separating healthy rewards from the dangerous high of drug use.
Using rat models of meth addiction, the researchers showed that forced abstinence prompted the development of new neurons called granule cell neurons in a brain region called the dentate gyrus, which is associated with memory formation. These new neurons drove compulsive-like drug seeking and relapse by strengthening drug-associated memories. The rats learned to associate a particular location in their environment with meth use. Returning to this location during abstinence later served as a triggering cue - prompting a recovering addict to relapse.
Rita Z. Goldstein, Ph.D., and Nora D. Volkow, M.D. Published online: October 01, 2002
OBJECTIVE: Studies of the neurobiological processes underlying drug addiction primarily have focused on limbic subcortical structures. Here the authors evaluated the role of frontal cortical structures in drug addiction.
METHOD: An integrated model of drug addiction that encompasses intoxication, bingeing, withdrawal, and craving is proposed. This model and findings from neuroimaging studies on the behavioral, cognitive, and emotional processes that are at the core of drug addiction were used to analyze the involvement of frontal structures in drug addiction.
RESULTS: The orbitofrontal cortex and the anterior cingulate gyrus, which are regions neuroanatomically connected with limbic structures, are the frontal cortical areas most frequently implicated in drug addiction. They are activated in addicted subjects during intoxication, craving, and bingeing, and they are deactivated during withdrawal. These regions are also involved in higher-order cognitive and motivational functions, such as the ability to track, update, and modulate the salience of a reinforcer as a function of context and expectation and the ability to control and inhibit prepotent responses.
CONCLUSIONS: These results imply that addiction connotes cortically regulated cognitive and emotional processes, which result in the overvaluing of drug reinforcers, the undervaluing of alternative reinforcers, and deficits in inhibitory control for drug responses. These changes in addiction, which the authors call I-RISA (impaired response inhibition and salience attribution), expand the traditional concepts of drug dependence that emphasize limbic-regulated responses to pleasure and reward.
More kids are ingesting buprenorphine, a medication usually used by addicts trying to get clean
REUTERS By Ethan Harfenist Mar 20, 2017 at 4:29 PM ET
Although buprenorphine, the main ingredient in opioid replacement medications such as Suboxone and Subutex, has helped countless addicts wean themselves off more deadly opioids, a new study has found that the medication is increasingly finding itself in the hands of children — with dangerous results.
In a new study set to publish online in the journal Pediatrics, researchers analyzed more than 188,000 calls to poison control centers made between 2005 and 2015 that dealt with child exposure to opioid substances in kids under the age of 20. Perhaps unsurprisingly, the first few years of the study saw an increase of 86 percent of opioid exposures to children. After 2009, researchers recorded a decline of almost 32 percent, barring one exception: buprenorphine. Instead, buprenorphine exposures increased from 2014 to 2015 after declining from 2011 to 2013. Additionally, children aged zero to five years accounted for almost 90 percent of buprenorphine exposures during the study.
Adapted Media Release Published: Thursday 16 March 2017
A new review published online in the scientific journal Addiction has found that dental patients with substance use disorders have more tooth decay and periodontal disease than the general population, but are less likely to receive dental care. With drug use increasing by approximately three million new users each year, this is a problem that won't disappear anytime soon.
Drug use affects oral health through direct physiological routes such as dry mouth, an increased urge for snacking, clenching and grinding of teeth, and chemical erosion from applying cocaine to teeth and gums. The lifestyle that often accompanies problematic drug use also affects oral health through high sugar diets, malnutrition, poor oral hygiene, and lack of regular professional dental care. Dental care can be further compromised by tolerance to painkillers and anaesthetics.
By Neil McKeganey
Anyone viewing the recent photographs from the North Wales Daily Post newspaper of the inside of Wrexham Bus Station here and here will be shocked to their core. So concerning are those photographs of an addict lying on the floor somewhere between being alive and dead, discarded needles, blood and a bladed weapon that the paper ought really to have carried a readers’ discretion warning.
These are the signs of a drug problem utterly out of control; publicly visible in its most gruesome respects. In response to such visible public drug use, we are now seeing calls to establish drug fix rooms in many cities throughout the UK. These are schemes that will allow addicts to inject black market drugs under some level of medical supervision. We are also seeing growing calls to provide addicts with heroin. Scratch the surface of those recommendations and you pretty soon end up at the realisation that one of the benefits of those schemes is that they make drug use less visible to a public that might rightly question why we are failing so comprehensively to tackle our drug problem, despite all of the honeyed words from highly paid experts and the hundreds of millions of pounds of public money spent following their advice.
Let us be in no doubt though, the very fact that we are even considering such schemes is a testament to our utter failure to develop effective drug prevention schemes in this country. In 2005 I was asked by the Blair government to prepare a report on what the UK drug problem might look like in 25 years’ time.
Amphetamine abuse is becoming more widespread internationally. The possibility that its many cardiovascular complications are associated with a prematurely aged cardiovascular system, and indeed biological organism systemically, has not been addressed.
Conclusions These results show that subacute exposure to amphetamines is associated with an advancement of cardiovascular-organismal age both over age and over time, and is robust to adjustment. That this is associated with power functions of age implies a feed-forward positively reinforcing exacerbation of the underlying ageing process.
Written by Ana Sandoiu Published: Thursday 2 February 2017
Misleadingly marketed as a legal and safe alternative to marijuana, synthetic cannabinoids have a variety of adverse health effects. A new review summarizes the clinical cases that have so far been linked to the use of the synthetic substances.
A new review warns that so-called synthetic marijuana is actually very different from cannabis and is potentially unsafe.
Synthetic cannabinoids (SCBs) are a type of psychotropic chemical increasingly marketed as a safe and legal alternative to marijuana.
They are either sprayed onto dried plants so that they can be smoked, or they are sold as vaporizable and inhalable liquids.
A new review from the University of Arkansas for Medical Sciences (UAMS) warns against the dangerous side effects of the compounds popularly (and misleadingly) referred to as "synthetic marijuana."
Referring to the SCBs currently sold as "K2" and "Spice," Paul L. Prather, a cellular and molecular pharmacologist at UAMS and corresponding author of the review, explains the motivation behind it:
SCBs linked to serious adverse health effects and even death
As reported in the review, some of these effects suggest that SCBs cause much more toxicity than marijuana. Toxicity has been reported across a wide range of systems, including the gastrointestinal, neurological, cardiovascular, and renal systems.
The clinical cases documented in the review include acute and long-term symptoms, such as:
Common adverse effects include prolonged and severe vomiting, anxiety, panic attacks, and irritability. Additionally, SCBs reportedly caused extreme psychosis in susceptible individuals, whereas marijuana only causes mild psychosis in those predisposed.
Furthermore, 20 deaths have been linked to SCBs between 2011 and 2014, whereas no deaths were reported among marijuana users during that time.
Finally, SCBs are likely to result in tolerance, dependence, and withdrawal.
Prescription drug abuse –A timely update
Is biological ageing accelerated in drug addiction?
Drug Policy - Changing Narrative Opinion Piece - (2nd Edition - 2016)
Chronic Methamphetamine Effects on Brain Structure and Function
A psychological perspective on addiction – Professor Robert West
Addiction is a chronic condition, learned through experience, involving repeated powerful motivation to engage in a behaviour to an extent that causes, or risks, significant unintended harm. Addiction cannot be adequately understood in terms of any one discipline, but each of the disciplines of the behavioural and social sciences, from neuroscience to anthropology, can provide valuable insights.
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