Tag Archives: addiction

What is MDMA: party drug or therapeutic agent?

MDMA in pill form (ecstasy) and powder (molly). Credit: Flickr, Kripos_NCIS.

MDMA, short for 3,4 methylenedioxymethamphetamine, is a psychoactive drug whose effects can resemble those of both stimulants and psychedelics. The drug is known to produce distortions in time and perception, enhance the enjoyment of sensory experiences, and make people feel more energized. Its defining feature is that it increases self-awareness and empathy, which together enable a feeling of connectedness that many users report.

In its tablet or capsule form, MDMA is known as Ecstasy, whereas Molly — slang for ‘molecule’ or ‘molecular’ — refers to the crystalline powder form of MDMA. However, both versions may contain a number of other drugs that can be harmful and even life-threatening. In fact, sometimes drugs sold as Ecstasy or Molly do not even contain MDMA, which is replaced by other stimulants such as methylone or ethylone. Ecstasy tablets purchased on the street are often adulterated with methamphetamine, ketamine, caffeine, ephedrine, cocaine, phencyclidine (PCP), or over-the-counter cough suppressants such as dextromethorphan.

MDMA is one of the most popular recreational drugs in the world. The drug is often associated with raves and the party scene, although recently many people in their late 30s and 40s have started using MDMA at home due to its anxiety-relieving effects. In fact, the role of MDMA in clinical practice is going through a revival thanks to recent research showing it can treat post-traumatic stress disorder (PTSD), anxiety, and addiction. In 2017, the Food and Drug Administration (FDA) granted breakthrough therapy status to MDMA-assisted psychotherapy.

MDMA was first developed by the German pharmaceutical giant Merck in 1912. Initially, MDMA was known as “Methylsafrylaminc,” a precursor compound that the company used to synthesize medications designed to control bleeding.

For decades the drug was little known until it started gaining a small following among psychiatrists in the 1970s and early 1980s who recognized its therapeutic value by making patients more communicative and open about their problems. It’s worth noting that Alexander Shulgin, an American chemist and pharmacologist affiliated with the University of San Francisco, was the linchpin of MDMA research during these early days.

Shulgin was first introduced to MDMA in 1976 by one of his students at a course he was teaching at the time at San Francisco State University. The American chemist went on to develop a new synthesis method that made it much easier to make MDMA. He then went on to introduce the chemical to psychologists in California, which then spread to hundreds of psychologists and lay therapists around the nation who found small doses of MDMA greatly aided talk therapy. Some therapists called the drug ‘Adam’ since they believed MDMA helped patients return to a more innocent, primordial state.

The CIA took note as well and experimented with MDMA, along with other hallucinogenic drugs like LSD, as part of its MK-Ultra project that sought to assess whether psychedelics could be used for ‘mind control’. Although this secret project is notorious for testing psychedelic drugs on unwitting subjects, classified reports suggest that the CIA only used MDMA on non-human subjects. These experiments produced the first known toxicology studies on MDMA — given the codename EA-1475.

It was also around this time that MDMA started becoming widely available on the street. Eventually, the DEA banned MDMA in 1985 under its ‘War on Drugs’ policy, placing it on the list of Schedule I substances — along with LSD, heroin, and marijuana — that supposedly have no currently accepted medical use and a high potential for abuse. To this day, MDMA is still classed as a Schedule I drug. Most of the MDMA in the U.S. is synthesized in clandestine labs in Canada and the Netherlands.

What are the effects of MDMA

Credit: Positivechoices.org.au.

It takes around 15 minutes for MDMA to circulate through the bloodstream and reach the brain, where it leads to psychoactive effects similar to both a stimulant and hallucinogen. These effects typically last three to six hours.

MDMA is classed as an empathogen, meaning it increases a user’s feeling of empathy and compassion towards others. The main action of MDMA in the brain is that it increases serotonin, the neurotransmitter that, among other things, is responsible for regulating prosocial behavior, empathy, and optimism.

However, too much serotonin in the brain can trigger “serotonin syndrome”, which especially happens when MDMA is taken together with other drugs such as alcohol, amphetamines, or cocaine.

Some of the most common side effects of MDMA include euphoria, feeling energetic, dilated pupils, jaw clenching and teeth grinding, excessive sweating and skin tingles, muscle aches and pains, reduced appetite, accelerated heartbeat, high blood pressure, dehydration, and heatstroke.

Overdosing on MDMA or simply taking repeated doses of the drug over a long time can cause visual and auditory hallucinations, irrational behavior, anxiety, irritability, paranoia, vomiting, high body temperature, racing heartbeat, convulsions.

After the MDMA high wears off, most users will experience a 24- to 48-hour period during which they may feel lethargic, have a low appetite, or experience a state of unease or generalized dissatisfaction with life (dysphoria, or the opposite of euphoria). Colloquially, this unpleasant period is known as “suicide Tuesday”, a reference to the fact that the crash happens after a heavy weekend of partying.

Tolerance of MDMA sets in rapidly, making users chase the euphoric effects with repeated doses. But rather than reaping the desirable effects, users who abuse MDMA and have high tolerance typically wind up experiencing more of the sympathomimetic effects, placing them at risk for cardiovascular instability, arrhythmias, and hyperthermia. Long-term abuse of MDMA can result in depression, memory and concentration problems, and liver problems.

Long-term use of MDMA can also cause dependence, although it is exceedingly rare compared with other highly addictive drugs such as cocaine or alcohol. Less than 1% of patients seeking drug treatment at clinics in Australia are for ongoing problems related to MDMA. MDMA is described as a “self-limiting” drug as the intensity of the positive effects decreases with increased use, while negative effects increase.

The spikes in blood pressure and heart rate can be dangerous for people with underlying cardiovascular problems. But perhaps the greatest risk of MDMA is that it raises body temperature, especially since its use is often accompanied by strenuous physical activity (such as dancing) in a hot environment such as a crowded venue or in the summer heat. This combination exacerbates fluid loss, which further interferes with the body’s ability to cool itself properly.

In the early 2000s, some public officials went on a crusade against ecstasy, which they nicknamed “agony”. Some warnings included that MDMA use can lead to Parkinson’s disease, a lifetime of depression, and even “holes in your brain”. Dr. John Halpern, a psychiatrist at Harvard University, thoroughly debunked these claims finding no evidence that ecstasy users have decreased cognitive performance.

The effects of MDMA can also vary because ecstasy and molly are often tainted with other substances, which have their own psychoactive effects when used alone or in combination with MDMA. Purchasing illegal substances off the street or in nightclubs is always a gamble because you can never be sure what’s inside. In 2018, a pill testing trial at a major music festival in Australia found that nearly half the pills tested were of low purity. Some 84% of people who had their pills tested thought they had bought MDMA but only 51% actually contained any MDMA. On the other end of the spectrum, pill tests in the UK and New Zealand have sometimes found up to three doses of MDMA in a single pill.

People have died as a result of taking MDMA, although the number of deaths is relatively low compared to other drugs such as heroin, alcohol, and pharmaceuticals. Most of the deaths are not directly from the drug itself but as a result of other complications or contaminants. There were 92 MDMA-related deaths in England and Wales in 2018, up from 56 the year before, and 10,000 hospitalizations for MDMA-related illness/injury in 2011 in the US.

Water intoxication and MDMA

People taking on MDMA should drink around 500ml of water an hour if they’re active and half of this amount if inactive in order to combat the dehydration effects of the drug. However, it’s easy to go overboard especially due to overheating from the venue and the effects of MDMA itself.

Unlike alcohol, MDMA is an antidiuretic, meaning it makes you retain water. When you have too much water in your body, the ratio of salts and water can be thrown off balance. Cells can start swelling with water, and the body can suffer from water intoxication, a condition called hyponatremia. Symptoms include headache, vomiting, and confusion or seizures. In some cases, water intoxication can lead to death.

MDMA-assisted therapy

Ecstasy has long been associated with rave culture, particularly electronic dance music (EDM) events. Raves refer to all-night dance parties characterized by loud music and a psychedelic atmosphere.

But more recently, MDMA is seeing a resurgence as a therapeutic drug, particularly for PTSD. There hasn’t been a new, effective drug meant to treat PTSD in nearly 20 years, but promising clinical trials performed since the previous decade have shown that MDMA might greatly enhance therapy.

The treatment protocol involves pure MDMA ingested in pill form that is not adulterated with any other substances. Moreover, the drug is always taken under the supervision of a specially-trained therapist over the course of a 12-week program. During this time, the patient will experience 2-3 daylong sessions, each lasting roughly 8 hours.

Therapists say that MDMA heightens feelings of safety and social connections, allowing patients to revisit traumatic memories and process all the terrible things they went through without triggering the same panic.

Speaking to NPR, Saj Razvi, a Colorado-based psychotherapist who was a clinical investigator in the Phase 2 trials of an MDMA study for PTSD, said that these sessions can look almost like a “bad trip”. But although they may seem nerve-wracking, MDMA-assisted therapies lead to emotional breakthroughs that otherwise “may take months or years to accomplish”.

After this phase 2 trial of MDMA-assisted therapy concluded in 2017, researchers found that 54% of the patients who took the drug improved their symptoms to the point that they no longer fit the diagnosis for PTSD, compared to 23% for the control group. What was particularly staggering was that the positive effects appeared to increase, rather than wane, over time. One year after their therapy, 68% of the participants who took MDMA no longer had PTSD.

Although MDMA is still a schedule I substance in the United States, researchers are able to perform clinical trials with the drug thanks to private sponsors such as the Multidisciplinary Association for Psychedelic Studies (MAPS). The non-profit is now working to get the FDA on board in order to include MDMA in its expanded access program, which will allow patients to use MDMA.

Besides PTSD, research has found MDMA-assisted psychotherapy considerably reduces anxiety in autistic adults and terminally-ill cancer patients, as well as prevents alcoholism relapse.

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What is fentanyl: the deadliest drug in America

Fentanyl is a synthetic opioid that is prescribed for severe, crippling pain — really bad pain since this drug is about 100 times stronger than morphine and 50 times stronger than heroin. Because it’s so strong and cheap to make, in recent years the opioid black market, which was typically dominated by heroin and prescription painkillers, has been flooded with fentanyl or fentanyl-cut products.

However, the line between medicine and poison is very thin with fentanyl. Imagine a dash of salt — if that were fentanyl, it would be enough to kill you. 

The low toxicity threshold makes it incredibly easy for people to overestimate the quantity of the substance they’re using and overdose. But most of the time people are not even aware that they are taking fentanyl as the drug is often cut into other substances to make them stronger.

According to researchers at the Centers for Disease Control and Prevention (CDC), as of 2018 fentanyl is officially the deadliest drug in the United States.

Both heroin and fentanyl are causing an opioid epidemic in the United States, but the number of deaths due to fentanyl has been rising in an alarming trend. Credit: CDC.

Official data from 2016 shows that nearly 63,000 people died of drug overdose in the United States that year. Fentanyl was involved in nearly 29% of those cases, while heroin came in second with 25% and methamphetamine was third at a rate of over 10%. What’s staggering is that in 2011, fentanyl was responsible for only 4% of overdoses. Between 2013 and 2016, overdoses from fentanyl rose 113% a year.

Since 2015, the U.S. has lost more than $2.5 trillion due to the opioid crisis.

How is fentanyl used?

Fentanyl was first developed in 1959 and is commonly used in multiple avenues of healthcare, most commonly for chronic pain management and in surgical settings under the guidance of an anesthesiologist. It is typically used in patients under great pain who are already tolerant to opioids, such as morphine.

Fentanyl pharmaceutical products come in many forms, including effervescent buccal tablets (Fentora), sublingual tablets (Abstral), sublingual sprays (Subsys), lollipops (Actiq), nasal sprays (Lazanda), skin patches (Duragesic), and injectable formulations.

But although fentanyl is prescribed in legitimate pharmaceutical varieties, most users procure illicit versions of the drug smuggled from China through the US postal service and Mexican drug cartels. Most often, smuggled fentanyl comes in the form of a white powder. Alternatively, the drug is dropped onto blotter paper, put in eye droppers and nasal sprays, or made into pills that look indistinguishable from other prescription opioids.

Part of the problem behind fentanyl being so difficult to control lies in its chemical composition, which makes it easy and cheap to reproduce by street chemists. Most of the fentanyl associated with recent overdoses is made in clandestine labs.

Many drug dealers mix fentanyl with other illicit street drugs, such as heroin, cocaine, methamphetamine, and MDMA. Fentanyl triggers an intense high for very little money, so there’s an economic incentive to use it to dope other drugs. However, if users are not made aware they are taking fentanyl, they may risk taking stronger opioids than their bodies are accustomed to, making an overdose more likely.

How does fentanyl affect the body?

Like any other opioid, fentanyl molecules bind to the body’s opioid receptors, which are mostly concentrated in areas of the brain responsible for controlling pain and emotions.

When the fentanyl binds to these receptors, it increases dopamine levels in the brain’s reward centers and produces an intense state of euphoria and relaxation.

Some of fentanyl’s effects include:

  • extreme happiness and euphoria
  • drowsiness
  • nausea
  • confusion
  • constipation
  • sedation
  • problems breathing
  • unconsciousness

Due to its extremely high potency, fentanyl is also highly addictive. Those who are addicted to the opioid and stop using it can experience severe withdrawal symptoms that begin as early as a few hours after the drug was last taken. These withdrawal symptoms include:

  • muscle and bone pain
  • sleep problems
  • diarrhea and vomiting
  • cold flashes with goosebumps
  • uncontrollable leg movements
  • severe cravings

What are common street names for fentanyl?

Fentanyl goes by many names, including Apache, China Girl, China Town, Dance Fever, Friend, TNT, Goodfellas, Great Bear, He-Man, Jackpot, King Ivory, Murder 8, and Tango & Cash.

What makes fentanyl so dangerous?

When used appropriately, fentanyl is a very effective pain mitigator for those who have grown a high tolerance to opioids, such as cancer patients who have been taking painkillers for years.

But fentanyl not only binds to receptors in the brain’s reward centers but also to those located in other areas of the brain, including those that control breathing. So although fentanyl produces a very potent high, it can also cause difficulties breathing that can potentially lead to death.

This is a problem that is caused by heroin too, as well as other opioids, but fentanyl is particularly dangerous because its chemical makeup allows it to enter opioid receptors much faster than heroin.

What’s more, fentanyl also adheres more tightly to the opioid receptor than other opioids. This means that only a small amount is enough to catalyze the molecular chain of events that initiates the opioid’s effects on the body.  

This explains why even less than a milligram of fentanyl can trigger an overdose in a user with no tolerance.

Credit: Twink Twice.

Naloxone is a medicine that can be given to a person to reverse a fentanyl overdose. Multiple naloxone doses might be necessary because of fentanyl’s potency.

Can fentanyl be stopped in the future?

According to the latest drug overdose death data from the National Institute of Drug Abuse (NIDA), 68,000 people in the United States were killed by prescription opioid painkillers and other drugs in 2018. That’s a kill rate higher than the peak annual deaths from car crashes, AIDS, or guns — combined.

On the bright side, 2018 was the first year since 1990 that drug overdoses have declined, a 5% reduction relative to 2017.

Experts in addiction and law enforcement say that the overall drop in deaths to overdoses can be pinned to tighter regulations of opioid prescriptions. In 2016, Massachusetts became the first state in the nation to pass a law that limits opioid prescriptions to 7 days. Since then, over half of all states have enacted laws that restrict the prescribing or dispensing of opioids for acute pain. 

However, while prescription opioid overdoses have fallen considerably since 2016, deaths attributed to synthetic narcotics, which includes fentanyl, are still on the rise.

Credit: Centers for Disease Control and Prevention, National Center for Health Statistics. Multiple Cause of Death 1999-2018.

From 2012 to 2018, the number of drug overdose deaths involved fentanyl or fentanyl analogs increased nearly 12-fold.

There’s no clear-cut solution to the rise of fentanyl or synthetic opioids in general. And as if fentanyl wasn’t scary enough, an analog called carfentanil is also creeping up in the illicit drug market. Carfentanil is 100 times stronger than fentanyl and is normally used as a sedative for large animals such as elephants. It’s so dangerous that some countries, the U.S. included, have described it as a ‘chemical weapon’ and have prepared contingency plans in the face of its potential use in war.  

In order to curb the opioid epidemic, both the Obama and Trump administrations have attempted to persuade Chinese authorities to crack down on the supply of fentanyl from China to the United States. These efforts seem to have paid off as China announced in April 2019 that the production, sale, and export of fentanyl and all its analogous products are prohibited, except for some authorized firms that have been granted special licenses.

However, it remains to be seen the degree to which these rules can be enforced. It’s believed there are hundreds of thousands of chemical and pharmaceutical facilities in China, which would make the challenge of enforcing fentanyl production laws formidable. What’s more, policy experts at Brookings claim that China has a history of downplaying narcotics problems, so it will be unlikely to mount counternarcotics cooperation with the United States unless it starts experiencing its own synthetic opioid epidemic. Strained U.S.-China relations add further uncertainty. 

What is kratom: an emerging alternative to opioids

Images of a kratom plant (A) and a kratom leaf (B). Credit: U.S. Drug Enforcement Administration.

Kratom (Mitragyna Speciosa) is a tropical tree in the coffee family. Found in Southeast Asia (Thailand, Indonesia, Malaysia, and Vietnam), natives have been using Kratom medicinally for thousands of years. Those who stand by kratom claim that it can improve mood, enhance concentration, relieve pain, and increase energy.

Traditionally, kratom leaves are chewed, brewed into tea, or ground to cook with food. Nowadays, kratom is either smoked or taken orally in pill form.

Most recently, kratom is being regarded as a wonder treatment to help opioid users kick their addiction. Although there is limited evidence in the scientific literature that kratom is effective at treating withdrawal caused by heroin or prescription opioid drugs, anecdotal evidence abounds.

Kratom is typically sold as a herbal extract supplement in powdered form. The plant’s leaves can also be chewed and dry kratom can be swallowed or brewed.

However, medical professionals warn that kratom users may be trading one addiction for another. Kratom can also cause serious side effects, which is why several countries have banned kratom products.

Officially, kratom is a controlled substance in Thailand, Malaysia, Australia, and some European countries. At the moment, kratom is legal in most of the United States, but it may not be for very long. In 2016, the Drug Enforcement Administration (DEA) proposed banning kratom, a proposal that is currently pending review until more research surfaces that may provide more information about the pros and cons of kratom use.

What are the effects of kratom ?

Chemical compounds in kratom interact with receptors in the brain to trigger effects similar to both opioids and stimulants.

At low doses, kratom is a stimulant that makes users feel like they have more energy. In the United States, there are now many so-called kratom bars and cafes where people ingest the drug recreationally as if it were coffee.

However, at high doses, kratom makes you sleepy, with users reporting feeling like they are in a dream-like state.

Two chemicals in kratom leaves, mitragynine and 7-α-hydroxymitragynine, interact with opioid receptors in the brain, triggering sedation, pleasure, and decreased pain. The stimulant effect is owed to mitragynine that also interacts with other receptor systems in the brain.

Additionally, kratom has over 20 alkaloids, some of which may be involved in pain-relieving action, according to a systematic review of over 35 scientific articles published prior to 2012.

The effects of kratom kick in after 5-10 minutes and last two to five hours. They can vary wildly depending on the dose and from person to person.

What are the side effects of kratom and is it safe?

Kratom is known to frequently cause nausea and constipation, as well as muscle tremors, itching, sweating, dizziness, dry mouth, seizures, hallucinations, and even liver damage. In extreme cases, kratom may trigger seizures, coma, and death. All these side effects are quite similar to opioid withdrawal.

“The acute adverse effects of kratom experienced by many users appear to be a direct result of kratom’s stimulant and opioid activities. Stimulant effects may manifest themselves in some individuals as anxiety, irritability, and increased aggression. Opioid-like effects include sedation, nausea, constipation, and itching. Again, these effects appear to be dose-dependent and to vary markedly from one individual to another. Chronic, high-dose usage has been associated with several unusual effects. Hyperpigmentation of the cheeks, tremor, anorexia, weight loss, and psychosis have been observed in individuals with long-term addiction. Reports of serious toxic effects are rare and have usually involved the use of relatively high doses of kratom (>15 g). Of particular concern, there have been several recent reports of seizures occurring in individuals who have used high doses of kratom, either alone or in combination with other drugs, such as modafinil,” wrote researchers in a study published in The Journal of the American Osteopathic Association.

As of 2019, the FDA has reported 44 deaths associated with kratom use, although most of these fatalities also involved other drugs or used kratom that was contaminated with other substances or bacteria, such as diphenhydramine (an antihistamine), alcohol, caffeine, benzodiazepines, fentanyl, and cocaine. At least one case investigated by the FDA seems to be associated with the use of pure kratom.

Between 2011 and 2017, poison control centers in the U.S. received around 1,800 calls involving kratom, some of which resulted in death. A 2019 analysis by the FDA of 30 different kratom products sold online found traces of heavy metals in some, including lead and nickel in toxic doses. “Based on these test results, the typical long-term kratom user could potentially develop heavy metal poisoning, which could include nervous system or kidney damage, anemia, high blood pressure, and/or increased risk of certain cancers,” according to the FDA report.

“We have issued numerous warnings about the serious risks associated with the use of kratom, including warnings about the contamination of kratom products with high rates of salmonella that put people using kratom products at risk, and resulted in numerous illnesses and recalls,” acting FDA Commissioner Dr. Ned Sharpless said in a statement. “Despite our warnings, companies continue to sell this dangerous product and make deceptive medical claims that are not backed by science or any reliable scientific evidence.”

Is kratom addictive?

Images of kratom products purchased at a “smoke shop” in suburban Chicago. The images show chopped leaves (A), which are typically brewed into “kratom tea”, capsules containing finely chopped leaves (B), and compressed tablets containing leaves or resin (C).

Although many turn to the drug in order to beat their opioid addiction, kratom can cause an addiction in its own right. Common withdrawal symptoms include pain, trouble sleeping, diarrhea, mood disorders, and fever.

Since kratom is still poorly studied, there is no specific medical treatment for kratom addiction.

Although many people use kratom to control withdrawal symptoms caused by opioid addiction or other addictive drugs like alcohol, there is no scientific evidence that kratom is actually effective for this purpose.

However, a survey of more than 2,700 self-reported users of the herbal supplement performed by Johns Hopkins concluded that “the psychoactive compound somewhat similar to opioids likely has a lower rate of harm than prescription opioids for treating pain, anxiety, depression and addiction.”

According to the survey, about 41% of survey responders said they took kratom to treat opioid withdrawal, and of those people who took it for opioid withdrawal, 35% reported going more than a year without taking prescription opioids or heroin.

“These findings suggest that kratom doesn’t belong in the category of a Schedule I drug, because there seems to be relatively low rate of abuse potential, and there may be medical applications to explore, including as a possible treatment for pain and opioid use disorder,” said Albert Garcia-Romeu, instructor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.

“There has been a bit of fearmongering,” he adds, “because kratom is opioidlike, and because of the toll of our current opioid epidemic.”

Is kratom legal?

In most of the United States, kratom is for the time being still legal. The Food and Drug Administration (FDA) has not approved kratom and actually voiced concerns over its use, but since it is marketed as a supplement it can be sold legally.

On August 31, 2016, the DEA published a notice that it was planning to place kratom in Schedule I, the most restrictive classification of the Controlled Substances Act. The scheduling did not occur, however, after dozens of members of Congress, as well as kratom advocates, argued that kratom’s potential medical benefits deserve more time for deliberation.

It is, however, illegal to purchase, possess, or use kratom in Alabama, Arkansas, Indiana, Rhode Island, Vermont, and Wisconsin. Other states and municipalities have classed kratom as “illegal for human consumption,” which is why you’ll find it listed as incense.

Elsewhere, kratom is classed as illegal in Israel, Japan, Thailand, Myanmar, Malaysia, Singapore, South Korea, Australia, New Zealand, Vietnam, and most European countries. This list by no means complete and every country might change how they control the use and distribution of the herbal supplement.

Kratom is easily orderable on the internet and is often sold as a green powder labeled “not for human consumption”.

Bottom line: Many users stand by the therapeutic effects of kratom with almost zealous fever. However, there are many safety concerns surrounding kratom, among them its potential for addiction and the risk of contamination with other potentially toxic substances. Kratom may have medical properties but the evidence so far is still limited, warranting further research. The FDA is rather clear about it: there is no scientific evidence that supports the use of kratom for medical purposes, nor should it be used as an alternative to prescription opioids. What’s more, kratom is not regulated so you have no guarantee that what you buy online doesn’t contain potentially toxic substances.

Although kratom is derived from a plant, consumers should not be fooled by the myth that anything natural is 100% safe. Many drugs with dangerous side effects are botanical in nature, including heroin, cocaine, and nicotine.

Schematic of deep brain stimulation procedure. Credit: Wikimedia Commons.

Chinese man receives brain implant to treat amphetamine addiction

Some addictions are so unresponsive to conventional treatment that they call for desperate measures. A man in China who has been battling with amphetamine addiction is one of the world’s first people to receive deep brain stimulation (DBS) to treat his addiction. A pacemaker-like device was surgically implanted in the man’s brain where it stimulated specific areas known to be involved in addiction.

Schematic of deep brain stimulation procedure. Credit: Wikimedia Commons.

Schematic of deep brain stimulation procedure. Credit: Wikimedia Commons.

The procedure essentially uses electrical current to target an area of the brain that controls cravings, making the patient less inclined to use drugs and crave for them. In the case of this recent trial conducted at Shanghai’s Ruijin Hospital — which is the first DBD trial for methamphetamine — researchers targetted the nucleus accumbens, a brain region thought to be directly involved in reinforcing and addictive behaviors in response to drug use.

The area is also the primary site mediating reward behavior.

In the United States, DBS has been approved to treat epilepsy and Parkinson’s disease. Previously, researchers at Oxford University used this method to produce a 50% decrease in tremors among Parkinson’s patients. In this study, DBS stimulated an area of the brain above the motor cortex, which is implicated in controlling the tremors. Scientists passed a small alternating current through the electrodes, delivering an oscillating signal which is 180 degrees out of phase with the tremor signal to cancel it out, suppressing the physical tremor. As an analogy, some of you might be familiar with noise-canceling headphones: when you turn them on, the headphones detect ambient noise and deliver a signal that cancels it out so you basically don’t hear anything besides a faint beep. DBS for addiction works in a somewhat similar way — it just targets a different brain area with a different signal.

However, despite the success of such procedures, scientists in Europe and the United States have been reluctant to use this technology for addiction, particularly as it invasive and risky.

Addiction is driven by a complex interplay of biological, social, and psychological factors, so treating it is not as easy as flipping a switch. There’s also a great deal of uncertainty about how DBS works, as well as skepticism surrounding the quality and ethics of clinical trials conducted in China. Globally, there are eight registered DBS clinical trials for drug addiction, six of which are in China. Before they turned to DBS, doctors in China surgically removed small clumps of tissue from the brains of drug addicts. According to the Associated Press, “roughly half of 1,167 patients who had their brains lesioned stayed off drugs for at least five years,” but they also suffered “mood disorders, lost memories, and altered sex drives.”

Although many argue that human experimentation with DBS for drug addiction should not be allowed, there’s a substantial societal pressure to do something about drug addiction. In 2017, more than 70,000 people died from drug overdoses in the United States, marking a twofold increase since 2007. Hundreds of thousands more are undergoing drug rehabilitation programs in drug rehab centers but for some, there aren’t any particular drug rehabilitation programs that can cure their addiction. Such was the case of ‘Yan’, the Chinese man who took part in this latest DBS trial for his amphetamine addiction. Yan lost his job, marriage, and health to his addiction but he has now reportedly stayed away from amphetamines in the six months since his surgery. “It controls your happiness, anger, grief, and joy,” the man reportedly described the device, which sounds eerily similar to the mood organ from Philip K. Dick’s landmark novel  Do Androids Dream of Electric Sheep. 

It’s too early to say whether Yan’s case is a success story — and even if it is, it’s still unclear if the advantages of DBS outweigh the many risks. A patient could die of a brain hemorrhage, emerge with seizures, garner an infection, or leave the hospital an entirely different person.

As more and more dead bodies turn out because of drug addiction, similar experimental procedures are bound to appear on US soil as well. Recently, the Food and Drug Administration (FDA) has approved a DBS trial for opioid addiction, which is due to start in early Jane at the West Virginia University Rockefeller Neuroscience Institute.

Just a few drinks can change the way memories form, eventually leading to cravings

Credit: Pixabay.

The messy thing about addiction is that it changes the brain in a lot of ways at the molecular level, making relapse easy and common. But at least we’re constantly learning new things. According to a recent study, alcohol — and very likely other addictive substances such as cocaine or opiates — hijacks a memory pathway in the brain, which can eventually lead to the cravings that underpin addiction.

“One of the things I want to understand is why drugs of abuse can produce really rewarding memories when they’re actually neurotoxins,” Karla Kaun, assistant professor of neuroscience at Brown University said in a statement. “All drugs of abuse — alcohol, opiates, cocaine, methamphetamine — have adverse side effects. They make people nauseous or they give people hangovers, so why do we find them so rewarding? Why do we remember the good things about them and not the bad? My team is trying to understand on a molecular level what drugs of abuse are doing to memories and why they’re causing cravings.”

Although they only have 100,000 neurons, versus 100 billion found in the human brain, fruit flies have much of the same molecular signals involved in the formation of reward and avoidance memories as we do. For their new study, Kaun and colleagues used genetic tools to selectively turn off key genes while training the flies where to find alcohol. By selectively tweaking genes, researchers were able to find out which proteins were required for the rewarding behavior of alcohol consumption.

One of the proteins identified by the researchers is Notch, a fundamental molecule in a signaling pathway that kicks off embryo development, brain development, and adult brain functions in humans and many other animals. Researchers say that such pathways resemble “falling dominos”, where each signal triggers the activation of other signals in a cascading effect.

Kaun’s team eventually found that one of the signaling pathways downstream of these dominos is a gene called dopamine-2-like receptor. This gene is responsible for triggering the production of a protein that enables neurons to recognize dopamine — the “feel good” neurotransmitter that plays a starring role in motivating behavior.

The pink areas are the fly's memory centers and the green dots are where the first molecular signaling "domino" Notch has been activated. Credit: Kaun Lab/Brown University.

The pink areas are the fly’s memory centers and the green dots are where the first molecular signaling “domino” Notch has been activated.
Credit: Kaun Lab/Brown University.

Previous research showed that the dopamine-2-like receptor is responsible for encoding whether a memory is pleasing or aversive. What alcohol seems to do is it hijacks this pathway so that the brain rewards alcohol consumption, despite its intoxicating effects. What essentially happens is the brain learns to enhance the formation of cues associated with alcohol, making it more likely to pursue the drug in the future.

Interestingly, alcohol did not switch the dopamine receptor on or off, or even increase or decrease the amount of protein made. Instead, the effect was much more subtle, changing the version of a protein made by a single amino acid “letter”.

“We don’t know what the biological consequences of that small change are, but one of the important findings from this study is that scientists need to look not only at which genes are being turned on and off, but which forms of each gene are getting turned on and off,” Kaun said. “We think these results are highly likely to translate to other forms of addiction, but nobody has investigated that.”

Kaun plans to continue to work by investigating similar effects triggered by opiates.

“If this works the same way in humans, one glass of wine is enough to activate the pathway, but it returns to normal within an hour,” Kaun said. “After three glasses, with an hour break in between, the pathway doesn’t return to normal after 24 hours. We think this persistence is likely what is changing the gene expression in memory circuits.

“Just something to keep in mind the next time you split a bottle of wine with a friend or spouse,” she added.

The findings appeared in the journal Neuron.

Powder meth in foil. Credit: Wikimedia Commons.

Estrogen may cause sex differences in methamphetamine addiction

Scientists know that the brain undergoes changes when it becomes addicted to methamphetamine, but little research has been done to investigate how sex-related hormones might affect that addiction. In a new study, researchers found that the brains of female rats respond differently to drugs like methamphetamine, likely mediated by estrogen. As such, addiction treatment in the future could be tailored differently for males and females.

Powder meth in foil. Credit: Wikimedia Commons.

Powder meth in foil. Credit: Wikimedia Commons.

Methamphetamine, also known as crystal meth, supercharges activity in certain areas of the brain, particularly in the prefrontal cortex. The powerful stimulant produces a high due to a surge in dopamine in the brain, but repeated exposure to the drug trains the brains to expect and crave heightened levels of the neurotransmitter. In time, methamphetamine addiction will alter the way neurons fire inside the brain, targeting synapses in the prefrontal cortex, which is the seat of decision-making and learning.

According to the National Institute of Drug Abuse in the United States, some common short-term side effects of meth use include mind and mood changes such as anxiety, euphoria, and depression. Long-term effects can include chronic fatigue, paranoid or delusional thinking and permanent psychological damage. In the United States alone, the highly addictive substance is responsible for 11,000 deaths and countless trials in drug courts. Once they’re hooked, users find it very difficult to kick their addiction.

Currently, there are no medications approved for the treatment of methamphetamine addiction, although there are drug rehabilitation programs that can provide results. Evidence suggests that bupropion — an antidepressant that is approved by the Food and Drug Administration (FDA) for the treatment of depression and for cigarette smoking cessation — might work for the treatment of meth addiction. Likewise, a drug typically used to treat alcoholism, Naltrexone, may also have promise for the treatment of addiction to methamphetamine.

As if treating meth addiction wasn’t complicated enough, this new study made by researchers at the Medical University of South Carolina suggests that there may be sex differences. The research team, led by Antonieta Lavin, an associate professor of neuroscience, examined the prefrontal cortices of both male and female rats which were either addicted or not addicted to methamphetamine. Much to everyone’s surprise, the researchers found that the synaptic response in this area was different between males and females, as well as between addicted and non-addicted animals. Specifically, female rats showed lower resting activity than male rats but then experienced a faster rise in their brain’s synaptic activity after taking the drug. This stronger response was then followed by a faster fall once the drug’s effects wore off, the authors reported in the journal eNeuro.

Sex hormones may be responsible for the observed synaptic differences — and this may also apply to humans. If this is confirmed then substance abuse disorder treatment might vary significantly between males and females in the future.

“Next, I would like to study how meth addiction changes throughout the different phases of the female cycle,” said Lavin. “This insight would help us improve treatment for women suffering from substance use disorder.”

Nicotine fluorescent.

Nicotine works inside our neurons to reinforce addiction

New research is looking into how nicotine works on a cellular level.

Nicotine fluorescent.

A biosensor targeted at a cell’s endoplasmic reticulum glows green in the presence of nicotine
Image credits Caltech / Lester laboratory.

Smoking tobacco makes you feel good because it floods the brain with nicotine. This nicotine latches onto specific receptors on the surface of neurons, producing feelings of happiness.

However, that’s not the whole story — only what we knew so far. To find out what happens after nicotine enters the cells, a  team of researchers at the California Institute of Technology has developed a protein sensor that glows in the presence of nicotine, allowing them to follow its movements inside cells and reveal more about the nature of nicotine addiction.

Inside job

The research was led by Henry Lester, Professor of Biology at Caltech. He has previously found that some nicotinic receptors (nAChRs) enter neurons and make a beeline for the endoplasmic reticulum (ER). Think of the ER as the cell’s protein assembly line. It synthesizes and packages proteins in order to be shipped to various other locations both inside and outside of the cell. Nicotinic receptors (nAChRs) are among these proteins.

After being synthesized in the ER, nicotinic receptors relocate to the cell’s surface. When nicotine molecules enter the body, they travel through the bloodstream and reach these nAChRs on the surface of neurons. Their merger triggers a chemical release as a reward — which we feel as happiness or pleasure. However, some of these nAChRs remain in the ER, inside the cell. In a way, they’re kept ‘in storage’ until they are needed.

In a bid to understand what nicotine does inside cells, Lester’s team developed a biosensor to allow them to track the substance inside cells. The biosensor is, in essence, a protein that can fold into an open or closed state, and an inactivated fluorescent protein. The first protein closing activates this fluorescent part, making it glow brightly. Because the first protein closes around nicotine, this biosensor allows the team to easily track where nicotine molecules pool up and how many of them are present in a given cell.

The team placed their biosensors on the endoplasmic reticulum and the surfaces of “mouse hippocampal neurons and human stem cell-derived dopaminergic neurons” among other types of cells in the lab, and then filmed the results. They report that nicotine entered into the endoplasmic reticulum within a few seconds of it reaching a cell’s surface. Nicotine levels observed inside the cells were also more than enough to affect nAChRs during their synthesis or as they were in transit towards the cellular membrane.

This last tidbit makes neurons more sensitive to the effects of nicotine, the team explains, enhancing the pleasure derived from a cigarette or an e-cigarette. It makes a person get a buzz more quickly and easily the more they smoke, the team adds. This is likely a key mechanism underpinning part of nicotine addiction.

The team’s efforts focused on isolated neurons in a lab setting. They plan to expand on their findings in the future, to determine whether nicotine behaves the same way in the neurons of live mice. They also plan to develop similar biosensors for other compounds, especially for opioids and antidepressants.

The paper “Determining the Pharmacokinetics of Nicotinic Drugs in the Endoplasmic Reticulum Using Biosensors” has been published in The Journal of General Physiology.

Being empathetic might put you at risk of relapsing as a coping mechanism

Empathy might be the original gateway drug, new research suggests.

Smoke.

Image via Pixabay.

Empathy smooths your way through social situations, but it might also smooth the path to drug addictions, a new paper suggests. The research, carried out at the University of Minnesota (UoM), was carried out using mice models but may carry over to humans as well.

Blue empathy

A research group led by  Dr. Jonathan Gewirtz at the UoM set out to analyze the links between empathy, stress, and drug use. The team’s hypothesis was that empathy (the awareness of another’s feelings and emotions), while very useful in social situations, can also expose one to more stress (as revealed by previous research). This stress, the team explains, can push former drug users into relapsing.

The team started by training a group of male mice to mimic drug-seeking behavior. The animals were placed in a two-sided compartment. Mice going to one side would receive a shot of saline (water and salt) solution, while those going to the other side would get a shot of morphine. Repeated over several days, the mice started associating one side with the drug.

Next, the researchers switched things up: over two weeks, mice going into either compartment would receive only saline injections. This was meant to mimic a period of sobriety. With the mice properly sobered, the team was ready to test the role of empathy in relapse. During this step, one of the sober mice witnessed another mouse in a fearful state, the team reports. This sober mouse was then immediately placed in the dual-sided compartment, and the team tracked their fear response and preference for either compartment.

These mice consistently preferred the compartment they associated with morphine. This, the team reports, suggests they were expressing drug-seeking behavior in response to witnessing another mouse going through a traumatic event. Some mice were afterward treated with oxytocin, a hormone which has been linked with social bonding among other effects. The oxytocin heightened the mice’s fear response, the team adds.

All in all, the team concludes that mice (and people too, potentially) are negatively affected by witnessing a stressful or traumatic event. This negative emotional impact is strong enough to push them to seek drugs, even after a period of sobriety. Oxytocin treatment exacerbates this response, suggesting that social bonding (and empathy, by extension) is a driving force in this behavior.

The researchers say these findings are the first to demonstrate the direct link between empathy and drug relapse, and the first to suggest that oxytocin may play a role in enhancing this response.

The findings have been presented at the 57th Annual Meeting of the American College of Neuropsychopharmacology (ACNP), held December 9-13, 2018, in Hollywood, Florida.

No Smoking.

Lab-tailored enzyme shows promise as a new and powerful treatment against tobacco addiction

New research from the Scripps Institute may pave the way to more efficient — and more enjoyable — ways of weaning off of nicotine.

No Smoking.

Image via Pixabay.

Nicotine addiction is an immensely powerful force, one that makes smokers keep smoking despite the habit’s well-documented impact on health. It’s what gets people hooked, and what makes most of those who gave up smoking relapse. Current estimations point to 60% of those who try cigarettes ending up as daily smokers, about 75% of daily smokers relapsing after quitting. However, one new, lab-tailored enzyme could help us fight against nicotine addiction by breaking most of it down before reaching the brain.

The compound was, thus far, shown to be efficient in rat models.

Nic-No-Tine

“This is a very exciting approach because it can reduce nicotine dependence without inducing cravings and other severe withdrawal symptoms, and it works in the bloodstream, not the brain, so its side effects should be minimal,” says principal investigator Olivier George, Ph.D., associate professor at Scripps Research.

The enzyme the team tested is known as NicA2-J1, and it’s a variation of a natural compound produced by Pseudomonas putida — which, interestingly, is the first patented organism in the world. This compound has previously been shown to reduce nicotine levels in the blood of mice.

And there lies the crux of the researchers’ interest in the enzyme. It breaks down nicotine before it even reaches the brain, making it very attractive as a means of fighting nicotine dependence. However, the original enzyme didn’t scrub nicotine fast enough for such a treatment strategy to work. So George’s team started by tweaking the enzyme to make it more efficient, increase its staying time in the bloodstream, and add a few other pharmacological properties.

The next step was to treat nicotine-dependent rats with the tweaked enzyme. For the first stage of the experiments, rats spent 21 hours per day, for 12 days, in a chamber where they could press a lever to receive a shot of nicotine. The rats soon understood the system, and self-administered nicotine until they became addicted to the substance. After these 12 days, the rats were only allowed access to nicotine once every 48 hours.

The rats experienced obvious withdrawal symptoms between these windows of time. They started escalating their intake while nicotine was available — a hallmark of deepening addiction — in a psychological bid to reduce discomfort caused by withdrawal.

However, not all rats fared the same. Those treated with the highest doses of NicA2-J1 (10 mg/kg) continued to pull the lever for a shot of nicotine if given the chance, but had significantly lower blood-nicotine levels compared to the rest of the animals. They also exhibited less pronounced signs of nicotine withdrawal, such as such as susceptibility to pain and aggressiveness, compared to the control group. One of the most encouraging finds is that NicA2-J1 treatment didn’t instantly trigger withdrawal symptoms, which usually happens when nicotine is blocked in a highly-dependent animal — think of quitting ‘cold-turkey’, but much more abruptly.

“It’s as if they were smoking 20 cigarettes but receiving the nicotine dose of only one or two, so that made their withdrawal process much less severe,” says study first author Marsida Kallupi.

“[W]hat’s unique about this enzyme is that it removes enough nicotine to reduce the level of dependence, but leaves enough to keep the animals from going into severe withdrawal,” George adds.

One of the most insidious effects of nicotine dependence is the continuation of use despite its adverse consequences — short-term impairment of lung function and physical fitness, alongside the longer-term risks of cancers, heart disease, or stroke. In other words, the compound is so addictive that users are compelled to seek it out no matter the cost. NicA2-J1 could also help in this regard, the team writes. When each lever-press had a 30% chance of directing an electric shock to the rats’ feet, those treated with NicA2-J1 quickly reduced their lever presses; those in the control group did not.

To model how effective the enzyme would be at fighting relapses, the team took the rats off of nicotine for 10 days straight — any smoker here will shiver at the mere thought (yes, nicotine addiction is that bad). The team gave each rat an injection of nicotine after the 10 days to restart their desire for the drug, and then restored their access to the lever. Untreated rats responded in a rather predictable way: they pressed the lever as much as they could, as fast as they could. Rats treated with NicA2-J1, in contrast, used the lever more sparingly. The same effect was seen when the team triggered relapse in all the rats using a stress-inducing compound (which was meant to mimic the way stress can cause relapse in humans).

 

[panel style=”panel-info” title=”Nicotine Addiction” footer=””]Nicotine is an extremely hard habit to kick as it fosters both physical and psychological dependence, and users develop tolerance over time. It’s an extremely addictive compound, similar to heroin and cocaine. Discontinuation of use (after dependence sets in) is particularly nasty, involving both affective (mood-related) and somatic (body-related) withdrawal symptoms, ranging from anxiety and poor mood to tremors. Withdrawal effects peak in the first few days of discontinuation but can last for upwards of several weeks. Most people don’t make it past the first few days.

“The majority of smokers would like to stop smoking, and each year about half try to quit permanently. Yet, only about 6 percent of smokers are able to quit in a given year,” reports the National Institute on Drug Abuse (NIDA).[/panel]

Since nicotine is extremely addictive, it’s hard to give up; even worse, those that do manage this feat are very prone to relapse. That, in itself, isn’t necessarily a bad thing; as the team notes in the paper’s opening line, however, “[t]obacco use disorder is the leading cause of disease and preventable death worldwide” (which is very bad). The CDC also supports this statement. NicA2-J1 shows a lot of promise as a treatment to help smokers wean off of nicotine since it prevents the substance from reaching the brain in the first place, takes the edge off of withdrawal, and makes relapses less likely to happen. The team hopes to start clinical trials with human subjects soon — but first, they’ll work on making the enzyme even more effective.

The paper “An enzymatic approach reverses nicotine dependence, decreases compulsive-like intake, and prevents relapse” has been published in the journal Science Advances.

Credit: Pixabay.

Ancient retrovirus may make some people more prone to addiction

Credit: Pixabay.

Credit: Pixabay.

Substance abuse is on the rise in the United States, claiming tens of thousands of lives each year. Despite a burgeoning rehab industry and billions of dollars dedicated to research, the underlying causes of drug dependency are still poorly understood. For instance, we don’t know what makes some people more vulnerable to addiction than others.

An international team of researchers recently published a study that suggests the answer to this question may be buried deep in our genetic fabric. According to the findings, an ancient retrovirus present in a higher proportion among people battling drug addiction may be evidence of a physical cause of addiction.

Our dark genes

Although many retroviruses went extinct hundreds of thousands or millions of years ago, they still live on in our DNA. Retroviruses infect cells and replicate by inserting their DNA into their host cell’s genome. Sometimes that cell can be a germ cell, such as a sperm or egg, so the retroviral DNA is inherited by offspring just like a normal gene. Scientists call these elements human endogenous retroviruses (HERVs).

Scientists estimate that up to eight percent of human DNA is made up of retroviral sequences.

Researchers from several institutions, including Oxford University and the National-Kapodistrian University of Athens, studied people who injected drugs in Greece and Scotland. After a basic genetic screening of the study’s participants, the researchers found that drug users were about three times more likely to have remnants of the HK2 retrovirus within a particular gene in their DNA than people who didn’t use drugs. The virus was identified in 34% of drug users tested in Glasgow, Scotland, compared to 9.5% of the local population, and in 14% of Greek patients, compared to 6% of that country’s population.

The HK2 integration is present in only 5-10% of the population, where it may affect the RASGRF2 gene, which is involved in regulating the brain’s dopamine levels. The neurotransmitter dopamine helps control the brain’s reward and pleasure centers but is also involved in addictive behavior when it’s generated in high amounts as a result of drug use.

Earlier, in 2012, scientists had linked the same gene with binge-drinking. 

“We know of clear biological roles for a small number of human endogenous retroviruses. However, there has never before been strong evidence in support of a role in human biology of an endogenous retrovirus that is unfixed, in other words not shared by all individuals in the population. Our study shows for the first time that rare variants of HK2 can affect a complex human trait. The replication of this finding in the distinct Athens and Glasgow cohorts is particularly important,” Professor Katzourakis, from the University of Oxford, who co-directed the study said in a statement.

Although they haven’t established a causal relationship, the correlation identified in the study is strong. The authors suspect that HK2 may predispose a fraction of the population to addictive behavior.

Previously, studies have found a link between HERVs and autoimmune disorders, along with other harmful effects.

“Most people think these ancient viruses are harmless. From time to time, people have shown overexpression of HK2 in cancer, but it has been difficult to distinguish cause from effect. Back in 2012, following a 20-year controversy regarding their pathogenic roles in humans, we sought to test the high-risk hypothesis that HERVs can be responsible for human disease. Our proposal was supported by the Medical Research Council, and now we have strong proof that HERVs can be pathogenic. For the first time, we are able to make a distinction between cause and effect in HERV pathogenicity,” Dr Magiorkinis, from the University of Athens, who led the study added.

The new results may represent evidence for a physical cause of addiction. If that is indeed the case, then the way drug addiction is handled both in medical practice but also in society, where it is highly stigmatized, could be severely disrupted.

Whether discussing heroin, prescription drugs, marijuana, or synthetics, American drug abuse has reached alarming levels. In 2014, the National Institute on Drug Abuse (NIDA) reported that an estimated 24.6 million Americans over the age of 12 had used an illicit drug during the last month. This accounted for 9.4% of the demographic, which is an increase from 8.3% in 2002.

Many drug users are unable to get help because of the stigma attached to their addiction. A link between a genetic trait and addiction might lead to a revolution in the way drug addiction is viewed by the public. 

The next step is to find an actual mechanism by which HK2 manipulates the dopamine system in the brain. Understanding the inner workings of this potential molecular mechanism could also allow scientists to develop better treatments for drug dependence.

“Looking into this “dark” part of the genome will unlock more genomic secrets,” said Dr. Magiorkinis.

Scientific reference: Timokratis Karamitros, Tara Hurst, Emanuele Marchi, Eirini Karamichali, Urania Georgopoulou, Andreas Mentis, Joey Riepsaame, Audrey Lin, Dimitrios Paraskevis, Angelos Hatzakis, John McLauchlan, Aris Katzourakis, Gkikas Magiorkinis. Human Endogenous Retrovirus-K HML-2 integration within RASGRF2 is associated with intravenous drug abuse and modulates transcription in a cell-line modelProceedings of the National Academy of Sciences, 2018; 201811940.

 

Alcohol addiction

Deep brain stimulation might one day treat the worst cases of alcohol addiction

Alcohol addiction

Credit: Pixabay.

Millions of people around the world are struggling with alcohol addiction, but only a small fraction stop drinking or seek treatment for their addiction. That’s because once alcohol hooks you in, it becomes extremely difficult to break free. To make matters even worse, even existing therapies are rather ineffective and bear a high rate of noncompliance —  thus, an innovative type of treatment could one day go a long way towards dealing with this issue. Writing in the journal Neurosurgical Focusresearchers at Stanford report that deep brain stimulation (DBS) — essentially, driving a mild electrical current through the brain — could treat even the most severe alcoholics.

Alcohol stimulates the release of dopamine, the ‘feel good’ neurotransmitter that is usually released during pleasurable or rewarding activities. When the brain’s reward center is overly stimulated with alcohol, a person learns to associate the psychoactive substance with positive experiences. In time, if a person drinks frequently and heavily, the brain becomes sensitized to the release of dopamine, so the enjoyment of alcohol fades. The immediate consequence is that a person needs to drink more and more in order to get the same ‘kick’.

The transition towards addiction happens when the brain becomes so used to alcohol that it compensates for the substance’s depressant effects by increasing the activity of glutamate —  the most important transmitter for normal brain function. Glumate is one of the main excitatory neurochemicals in the brain, which means alcohol will make a person more excited in the presence of alcohol — and the brain can remain in this excited state even when alcohol is absent. Ironically, a person who is hooked on alcohol — typically a depressant — needs to drink more to be less excited and feel ‘normal’.

The longer a person has been drinking, the harder it becomes to break the habit. That’s because consistent alcohol consumption rewires the brain, forcing the alcoholic into a dreadful state when there is no more alcohol in the system.  Alcohol sensitizes certain brain circuits and changes neurotransmitter levels, and it can also affect executive function, which is the part of the brain involved in decision-making that tells a person not to drink.

The effects of alcoholism on a person’s life can be devastating and, in the United States alone, the addiction is responsible for a quarter trillion dollars in health care costs per year. In 2013, 45.8 percent of liver disease deaths among Americans ages 12 and older involved alcohol.

There are various types of modern alcohol rehab treatments, but recovery rates are generally very low. Addiction recovery rates for popular 12 Step groups such as AA may be as low as 5-10%, according to Dr. Lance Dodes, the author of The Sober Truth: Debunking the Bad Science Behind 12-Step Programs and the Rehab Industry. What’s more, up to 75% of treated alcoholics relapse within 3 years.

According to a recent review of both animal and human studies, deep brain stimulation may be a far better option for treating alcohol use disorder. This type of therapy is widely used to treat Parkin’s disease and obsessive-compulsive disorder, but scientists have noticed that it can also reduce alcohol cravings.

“DBS is a minimally-invasive brain surgery,” explained senior author Casey Halpern, MD, an assistant professor of neurosurgery at Stanford. “For Parkinson’s, we place deep brain stimulators to restore normal function of the region in the brain known to be dysfunctional. Patients improve immediately when a small dose of current is delivered to this area. We anticipate a similar treatment will be possible for alcoholism. At the moment, we’re performing animal studies to optimize this potential therapy and to learn its underlying mechanism of action.”

When they’re intending to treat alcohol use disorders, researchers target the nucleus accumbens, a brain region that plays a key role in reward circuitry. Stimulating this region is linked with reduced impulsive behavior.

“The nucleus accumbens is triggered when patients anticipate a reward or prior to completing a rewarding behavior. It’s been shown to be perturbed in both addictive disorders and OCD,” said Allen Ho, MD, a Stanford neurosurgery resident working with Halpern. “By targeting this brain structure with stimulation, we hope to modulate the reward circuit in the brain to help patients resist the temptation to indulge in a binge and other addictive behaviors.”

In humans, the impact of deep brain stimulation on alcohol consumption has only been reported in a handful of patients. In one of the studies that the scientists reviewed, a 54-year-old man was struggling with severe anxiety, secondary depressive disorder, and severe alcohol dependency with daily alcohol consumption of more than 10 drinks/day. The patient had been previously hospitalized on multiple occasions for withdrawal. However, following initiation of DBS, the patient rapidly and drastically reduced his alcohol consumption, and within 1 month was consuming 1–2 drinks/day and subjectively reported having completely lost the desire to drink. The same study treated another patient, a 69-year-old man with a more than 30-year history of alcohol dependence, who drank more than 200 grams of vodka daily. He also received numerous detoxifications, withdrawal treatments, and psychopharmacological interventions that had all failed. Similar to the first patient, after DBS therapy the patient began to remarkably reduce his alcohol consumption and was completely abstinent after one year.

Treating alcohol addiction with brain surgery may sound a bit extreme but the researchers explain that the procedure is one of the safest and least invasive operations performed by neurosurgeons. Considering the devastating consequences of this type of addiction, DBS might ultimately be more than worth it.

At the moment, deep brain stimulation therapy for alcohol use disorders is not approved by the U.S. Food and Drug Administration, but that may change in the face of more positive evidence. What’s more, DBS might prove effective in treating other types of addictions, such as opioid addiction, and even obesity.

whisky

Researchers find a way to block alcohol addiction and ease withdrawal symptoms

whisky

Credit: Pixabay.

More than 15 million Americans abuse alcohol, trapped in a downward spiral where they need to ingest more alcohol in order to ease severe withdrawal symptoms. Many admit they simply can’t help themselves. But the latest findings by Scripps Research scientists could be a silver lining for numerous struggling alcoholics. Researchers found that activating a receptor in the brain of alcohol-addicted rats induced them to drink less and eased withdrawal symptoms.

The brain’s seat for alcohol

More than a decade ago, researchers who were combing through the human genome looking for genetic sequences that resemble known receptors came across a G-protein coupled receptor (GPCR) called GPR139. This class of receptors plays a key role in brain signaling, some of which have been previously linked to mental disorders, such as depression, schizophrenia, and drug-induced psychosis.

Subsequent research had shown that GPR139 is primarily found in the habenula, a brain region that mediates some forms of emotive decision-making by influencing the release of dopamine and serotonin. For instance, by inhibiting dopamine-releasing neurons, habenula activation leads to the suppression of motor behavior when an animal fails to obtain a reward or anticipates an aversive outcome. Moreover, the habenula is involved in behavioral responses to pain, stress, anxiety, sleep, and reward.

Olivier George, associate professor at Scripps Research and lead author of the new study, suspected that GPR139 might play a role in addiction, seeing how the habenula is activated during drug and alcohol withdrawal.

“We’ve been very interested in the habenula because this is the area of the brain that produces withdrawal symptoms, which an animal or human then tries to avoid by taking another drink or another dose of a drug,” said George in a statement.

Olivier George, PhD, associate professor at Scripps Research. Credit: Scripps Research.

Olivier George, PhD, associate professor at Scripps Research. Credit: Scripps Research.

In an experiment, George and colleagues gave 12 non-alcohol-dependent rats and 17 alcohol-dependent rats an experimental compound called NJ-63533054, which activates GPR139. The drug had no effect on the alcohol intake of the non-alcohol-dependent rats. However, it significantly decreased the amount of alcohol ingested by the rats addicted to alcohol. 

The JNJ-63533054 compound was particularly effective for one-subgroup of rats: those that had the highest alcohol intake and showed compulsive drinking behavior. These rats had such a severe drinking problem that they would continue to ingest alcohol even when it was adulterated with a bitter taste, which should have normally been repulsive for them. This behavior suggests that the targeted receptor is activated when the rats are drinking a lot and going through withdrawal.

[RELATED] The science of hangovers

During alcohol withdrawal, the pain threshold in rats (and humans) is generally lower. In order to confirm their findings, the researchers tracked the pain threshold of 17 rats undergoing alcohol withdrawal. When the rodents were treated with JNJ-63533054, they later had a higher threshold for pain. Yet again, the effects were strongest in the rats with the most compulsive drinking behavior.

Finally, in another experiment, the researchers delivered JNJ-63533054 directly to small areas of the brain through thin tubes. Rats ingested less alcohol when the drug was sent to the habenula, but not other brain areas. This confirmed the habenula’s role in alcohol addiction.

The experiments were performed exclusively on male rats, but the researchers suspect that the findings should carry over female rats, too. What’s more, the habenula is involved in broader types of addiction, meaning JNJ-63533054 might ease other types of addiction, besides alcohol.

“The good thing about this type of target is that is almost exclusively expressed in the brain, which limits side effects, and it seems to have no effect on individuals who are not dependent,” says George. “Those are both positive indications of the receptor being druggable.”

The findings appeared in the journal eNeuro.

What Causes Addicts to Relapse?

Addiction is a topic that is shrouded in confusion and has miffed health professionals for decades. In fact, it’s only over the last few years that we’ve started to recognize just how much of a mental health issue addiction truly is. And as this relationship has become clearer, it’s been interesting to study the role relapses play in the process of overcoming and succumbing to addiction.

What is a Relapse?

In the simplest form, a relapse is the worsening of a condition that had previously improved. In terms of drug or alcohol addiction, it’s a sudden return to a formerly abused substance after a period of abstinence.

While relapses aren’t preferred or encouraged, they’re actually quite normal. It’s common – even expected – that people overcoming an addiction will go through one or more periods of relapse before successfully giving up what they’re addicted to.

“Relapse is even considered a stage in the stages-of-change model, which predicts that people will cycle through a process of avoiding, considering quitting, taking active steps to quit and then relapsing,” writes Elizabeth Hartney, PhD. “Sometimes people will cycle through the stages several times before quitting.”

What Causes Relapses?

From a medical perspective, understanding what causes relapses is helpful in knowing how to prevent or lessen the impact of a setback. If nothing else, it provides a valuable glimpse into the mind of an addict and the challenges that exist with addiction recovery.

Let’s take a look at some of the culprits:

Cravings

It would be nice if all causes could be easily controlled, but the reality is that certain factors are largely out of the addict’s control. Cravings are one of them.

Cravings, whether physical or psychological in nature, are frequent among recovering addicts. And when you consider that most addicts suffer from underlying mental health problems, these compulsions can come and go for years at a time. Learning to curb cravings as soon as they emerge is key to long-term abstinence.

Stress

When a stressful situation arises, a person’s natural inclination is to seek self-soothing mechanisms. For a recovering addict, this often means returning to a comfortable crutch like drugs or alcohol.

Common stress factors that spark relapses include financial issues, relational problems, or health issues. Learning to deal with stress in a healthy manner is key in avoiding frequent relapses.

Lack of Sleep

Did you know that sleep plays a major role in addiction recovery (at least for alcoholics)? According to data shared by Sagebrush Treatment Centers, 60 percent of patients with baseline insomnia experience frequent/recurrent relapses, while just 30 percent of those without insomnia do. In fact, sleep disturbances are higher while abstaining from alcohol, with 25 to 60 percent of patients in early recovery reporting some issues

By dealing with sleep issues, recovering alcoholics may find it easier to avoid relapses and enjoy a more stable process.

Relationships

People often think they grow out of peer pressure, but it sticks with most people well into adulthood. Whether subtlety or overtly, social pressures can encourage addicts to return to addictive tendencies.

Re-engaging old relationships is one of the biggest challenges. While it may hurt to cut contact with close friends and family, this is often the best strategy for avoiding relapses.

Time

Time is a funny thing. Whether you like it or not, it passes. Sometimes time can be a good thing for addicts, while other times it provides a false sense of security against an addiction.

The longer an addict remains abstinent, the more comfortable they get. This causes them to let their guard down a little. As a result, they’re more likely to try something – like one glass of wine with dinner, or a single cigarette with friends. As time passes, addicts need to keep their guard up and continue making smart choices that prioritize sobriety above all else.

Responding to a Relapse

As previously mentioned, relapses are fairly normal. The key is to limit the impact a relapse has on giving up an addiction. By understanding the triggers of relapse, addicts will be more cognizant of their weaknesses and how they should organize and structure their lives to avoid falling back into old ruts.

Pot twist: Cannabis component helps fight addiction in new study

A new study published in the journal Neuropsychopharmacology has revealed that a non-psychoactive and non-addictive ingredient of the Cannabis sativa plant can help reduce the risk of relapse among cocaine and alcohol addicts. According to lead author Friedbert Weiss, non-psychoactive cannabinoids could have important medical benefits in the fight against substance addiction.

Image via Pixabay/futurefilmworks

Addiction is a powerful, vicious monster that lives inside yourself. The battle is an extremely hard one and it often carries stretches out over years and years — potentially for an entire life. Many abstinent addicts find it even harder to control themselves in drug-related settings or when they experience stress or higher levels of anxiousness. For them, it’s a true struggle to dismiss their impulses when offered an addictive drug like alcohol or cocaine.

Researchers wanted to study the effect of Cannabidiol (CBD) on drug relapse in a rat model. CBD is a non-psychoactive compound of the plant Cannabis sativa (I suppose you already know that’s weed). CBD has been considered as a treatment for neurological and psychiatric disorders, and more recently also as a treatment for drug and alcohol addiction.

“The efficacy of the cannabinoid [CBD] to reduce reinstatement in rats with both alcohol and cocaine – and, as previously reported, heroin – histories predicts therapeutic potential for addiction treatment across several classes of abused drugs,” says Weiss.

Scientists applied a gel containing CBD once per day for a week to the skin of lab rats. The rodents had a history of deliberate daily alcohol or cocaine self-administration, leading to addiction-like behavior.

Next, they performed a number of tests to observe the rats’ reaction to stressful and anxiety-provoking situations, as well as behavior tests that measured impulsivity — a psychological trait associated with drug addiction. The research team reported that CBD reduced relapse provoked by stress and drug cues. CBD also reduced anxiety and impulsivity in the rats.

The authors wrote: “CBD attenuated context-induced and stress-induced drug seeking without tolerance, sedative effects, or interference with normal motivated behavior. Following treatment termination, reinstatement remained attenuated up to ≈5 months although plasma and brain CBD levels remained detectable only for 3 days. CBD also reduced experimental anxiety and prevented the development of high impulsivity in rats with an alcohol dependence history.”

Authors hope that insight into the mechanisms by which CBD exerts these effects will be investigated in future research. They believe that the findings are proof of CBD’s potential in relapse prevention, CBD’s major benefits being its actions across several vulnerability states, and long-lasting effects with only brief treatment.

“Drug addicts enter relapse vulnerability states for multiple reasons. Therefore, effects such as these observed with CBD that concurrently ameliorate several of these are likely to be more effective in preventing relapse than treatments targeting only a single state,” Weiss concludes.

Almost 2 out of 3 people who try smoking develop a daily habit

A global study suggests that 69% of the people who tried smoking became daily smokers, even if just for a while.

Over 60% of the adult respondents answered ‘yes‘ when asked if they ever had a cigarette. Out of this whopping percent, over 2/3 started smoking daily for different periods of time. These numbers make the need to prevent teenage smoking even more pressing.

Source: Pixabay/klimkin.

Tobacco’s deceiving story

The irony lies in tobacco’s history. During a 1585 expedition, astronomer Thomas Harriot relayed that tobacco “openeth all the pores and passages of the body” so that the natives’ “bodies are notably preserved in health, and know not many grievous diseases, wherewithall we in England are often times afflicted.”

Source: Wikipedia

People genuinely believed in the therapeutical and spiritual properties of tobacco. It’s quite understandable why smoking gained such popularity worldwide. James Albert Bonsack, the American who invented the first cigarette rolling machine back in 1880, also helpeda lot in making smoking fashionable and accessible.

Bonsack’s cigarette rolling machine, as shown on U.S. patent 238,640.
Via: Wikipedia

Results of the meta-analysis encourage anti-smoking campaigns

The paper was published in the journal Nicotine & Tobacco Research and gathered data from surveys between 2000 and 2016. These surveys involved 215,000 English speakers from the UK, US, Australia and New Zeeland.

Professor Peter Hajek from Queen Mary University of London stated in a press release that it was the first time that “the remarkable hold that cigarettes can establish after a single experience has been documented from such a large set of data.”

Via Pixabay/HansMartinPaul

“In the development of any addictive behavior, the move from experimentation to daily practice is an important landmark, as it implies that a recreational activity is turning into a compulsive need. We’ve found that the conversion rate from ‘first time smoker’ to ‘daily smoker’ is surprisingly high, which helps confirm the importance of preventing cigarette experimentation in the first place”, he added.

Keeping in mind the introduction of e-cigarettes and heat-not-burn tobacco in this past few years, new questions arise. Has classical smoking come to an end? Are the new smoking alternatives actually reducing regular tobacco use?

Via Pixabay/lindsayfox

Professor Peter Hajek says: “Concerns were expressed that e-cigarettes could be as addictive as conventional cigarettes, but this has not been the case. It is striking that very few non-smokers who try e-cigarettes become daily vapers, while such a large proportion of non-smokers who try conventional cigarettes become daily smokers. The presence of nicotine is clearly not the whole story.”

All in all, this study brings good news. The UK has recorded a dramatic reduction in smoking at the moment and this corresponds with findings that only 19 percent of 11-15-year-olds have ever tried a cigarette. The world, even just for a fleeting moment, seems to be on the right tracks.

 

Drugs that cancel the buzz of alcohol are safe and efficient, meta-analysis confirms, but people don’t know about them

As many as a quarter of Americans are heavy drinkers or drink at levels that put them at risk of becoming alcoholics, but only a fraction get help. A lot of people don’t want to admit they have a drinking problem but even those who recognize they might be alcoholics seem to be unaware that there’s more to it than just attending AA meetings. For instance, there are drugs that can help a lot by inhibiting the euphoria or buzz from drinking alcohol rendering the habit essentially useless. A new meta-analysis confirms these are safe and effective.

Credit: Pixabay.

As early as 1997, studies have shown that doctors who prescribe naltrexone to treat alcohol dependence have a high success rate (70% or greater). The drug blocks the effects of opioid medication, including pain relief or feelings of well-being that can lead to opioid abuse. The opioid antagonist is so strong it can reverse a heroin overdose and bring a person back to life. Essentially, it flushes heroin molecules out of the opioid receptors in the brain and triggers instant withdrawal. But since alcohol shares opioid receptors, naltrexone works against alcohol’s effect as well. Basically, you take some of these pills, and you stop getting any buzz from drinking.

Recently, researchers from the National Institute on Alcohol Abuse and Alcoholism conducted a meta-analysis of 64 clinical trials and found naltrexone is effective and carries no significant health risks. Moreover, another drug called acamprosate was also deemed effective at helping people maintain abstinence by cutting back on some of the physical and psychological cravings for alcohol.

“In treatment for alcohol use disorders, acamprosate has been found to be slightly more efficacious in promoting abstinence and naltrexone slightly more efficacious in reducing heavy drinking and craving. Detoxification before treatment or a longer period of required abstinence before treatment is associated with larger medication effects for acamprosate and naltrexone respectively,” the researchers conclude.

You don’t need to visit a mental health doctor or addiction counselor to get any of these drugs. Any healthcare worker licensed to prescribe medication can prescribe naltrexone or acamprosate. However, few actually recommend naltrexone or acamprosate. It’s not clear why — it may be that some doctors aren’t convinced these work or are simply unaware of their efficacy against alcohol addiction. This recent meta-analysis might act as an eye opener.

This might sound like great news if you have a drinking problem or have friends that do but it’s important to note that these drugs are not miracle cures. Rather, they’re effective if used in conjunction with therapy and counseling. If used alone, results can be disappointing especially if the habit is severe.

 

Internet addiction affects over 400 million people globally, study finds

We’ve probably all experienced it at some point – you really have no reason to stay online… but you do so nonetheless. But six percent of the global population actually suffers from internet addiction (IA).

Internet addiction affects over 400 million people, study finds.

Addiction is defined as a substance or activity which is initially pleasurable, but the continued use/act of which becomes compulsive and interferes with ordinary life responsibilities, such as work, relationships, or health. Does that sound familiar? If yes, then you just might have a case of internet addiction.

“The IA prevalence rate was more than threefold higher than that of pathological gambling (0.2% to 2.1%), another impulse control disorder”, researchers explain.

Upon reading this study, you either be shocked that over 400 million people in the world are addicted to the internet, or be surprised that only six percent are. However, you have to keep in mind that only an estimated 39% of people in the world actually have access to internet, and out of them, only a fraction can afford smartphones and can be connected at all times.

“Internet addiction (IA) has emerged as a universal issue, but its international estimates vary vastly”, the paper writes.

However, what’s perhaps even more surprising is that the prevalence of internet addiction ranges from “only” 2.6% in Northern and Western Europe to a high of 10.9% in the Middle East. You’d maybe expect people from the most developed areas in the world to have a high prevalence, but this isn’t the case apparently.

However, the actual global figure may be different; researchers didn’t have any data available from Africa so the present findings may not necessarily be applicable to African nations, which have a far lower Internet penetration rate (16%) than the rest of the world.

Journal Reference.

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Addiction is a disease that first starts with dopamine overcorrection in the brain

dopamine_drgs_pills-Drug and alcohol addiction affects millions of people around the world, but despite decades worth of research and billions of dollars, our understanding of addiction is still far from being complete. Brigham Young University professor Scott Steffensen and his team have recently contributed with a few pieces in the addiction puzzle, which are of vital importance. Their work suggests that addiction starts with the brain’s attempts to correct excessive dopamine levels triggered by drugs.

“Addiction is a brain disease that could be treated like any other disease,” Steffensen said. “I wouldn’t be as motivated to do this research, or as passionate about the work, if I didn’t think a cure was possible.”

When you abuse the brain, the brain abuses back and heavily cuts on dopamine generation, even when you’re sober and needed it the most

Out of Steffenson’s lab, three research papers came out that detail the brain mechanism when dealing with addiction. The papers are about: withdrawal (The Journal of Neuroscience),  nicotine and alcohol interaction in the brain (The Journal of Pharmacology and Experimental Therapeutics), and the effects of cocaine addiction on the brain’s reward circuitry (Addiction Biology). In all of these cases the common denominator is a magic chemical: dopamine.

Dopamine is an important brain chemical in drug abuse and addiction. Many drugs affect dopamine transmission directly by either blocking or stimulating its receptors. For example, antipsychotic drugs are dopamine antagonists, whereas bromocriptine, used to treat hyperprolactinaemia and Parkinson’s disease, is a dopamine agonist. Most cases of addiction stem from drug abuse, causing an increase in brain dopamine (DA) levels, which at it’s own hand causes increased activity in the brain reward pathway – the pleasure and high feeling.

When drugs and alcohol release unnaturally high levels of dopamine in the brain’s pleasure system, oxidative stress occurs in the brain. Steffenson and his team found that the brain responds by generating a protein called BDNF (brain derived neurotrophic factor). This correcting behavior causes a suppression of dopamine generation, but continues to do so even long after a person had come off the high. So, while the brain was faced with dopamine overload during the drug’s high, afterward it is faced with dopamine deprivation. This dopamine deprivation is what causes the pains, distress and anxiety of withdrawal.

“The body attempts to compensate for unnatural levels of dopamine, but a pathological process occurs,” Steffensen said. “We think it all centers around a subset of neurons that ordinarily put the brakes on dopamine release.”

“I am optimistic that in the near future medical science will be able to reverse the brain changes in dopamine transmission that occur with drug dependence and return an ‘addict’ to a relatively normal state,” Steffensen continued. “Then the addict will be in a better position to make rational decisions regarding their behavior and will be empowered to remain drug free.”

porn-addict

There’s no such thing as porn addiction, review study says

David Ley, PhD, a clinical psychologist in practice in Albuquerque, NM, made an extensive review study of the current scientific literature discussing the idea of ‘porn addiction’. His summary is that, first of all, there’s no such thing as porn addiction, based on the currently published literature since the behavior described in this work can not be described as pathological.

porn-addictThe Diagnostic and Statistical Manual doesn’t have “porn addiction” under its classed addictions either, because of a the same lack of scientific data. Fewer than two in every five research articles (37 percent) about high frequency sexual behavior describe it as being an addiction. Only 27 percent (13 of 49) of articles on the subject contained actual data, while only one related psychophysiological study appeared in 2013.

Ley’s work argues that the scientific literature concerning the subject is extremely poor both qualitative and quantitative, accusing poor experimental designs, methodological rigor and lack of model specification of most studies surrounding it. Also, the the negative effects often discussed in porn addictions don’t seem to stand up. There was no sign that use of pornography is connected to erectile dysfunction, causes changes in the brain and it explains very little of the variance in adolescents’ behaviors.

Concerning positive effects, Ley and team found evidence that viewing pornographic images does not make it problematic de facto. It can improve attitudes towards sexuality, increase the quality of life and variety of sexual behaviors and increase pleasure in long-term relationships. It provides a legal outlet for illegal sexual behaviors or desires, and its consumption or availability has been associated with a decrease in sex offenses, especially child molestation.

“We need better methods to help people who struggle with the high frequency use of visual sexual stimuli, without pathologizing them or their use thereof,” writes Ley, who is critical about the pseudoscientific yet lucrative practices surrounding the treatment of so-called porn addiction. “Rather than helping patients who may struggle to control viewing images of a sexual nature, the ‘porn addiction’ concept instead seems to feed an industry with secondary gain from the acceptance of the idea.

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Helping a Family Member with Substance Abuse: Is Long-Term Rehab the Answer?

rehab_recoveryWatching a loved one struggle with addiction is a painful and traumatic experience. Whether the addict is a teenage child who uses methamphetamine or a grandparent who abuses prescription painkillers, it is difficult to know how and when to intervene and provide the help that they need. If the addiction progresses to the point that their life becomes disrupted, family members may want to consider placing the addict into a long-term rehabilitation program and/or facility for treatment. This article will discuss some of the signs and signals that indicate whether long-term rehabilitation may be appropriate.

Substance abuse and addiction have become a serious problem in the United States. According to data from the federal Substance Abuse and Mental Health Services Administration, over 19 million American adults (age 18 and over) had serious substance abuse issues in 2011. The majority of these abusers used substances such as marijuana/hashish, cocaine (including crack), heroin, hallucinogens, inhalants, or prescription drugs (without a prescription). Millions of families are affected by this widespread substance abuse and wrestle with the question of how to help their loved ones.

There are several signs that may indicate that a family member may need long-term rehab. The primary signal that rehab is needed is the disruption of that person’s everyday life by substance abuse. They need intervention if they can no longer get up and go to work or school, or are having difficulties such as getting fired from their job or expelled from school due to substance abuse problems.

Another sign is the loss of healthy relationships and creation of poor ones. If they abruptly break off communication with their family and begin associating with other addicts or abusers (“hanging out with the wrong crowd”), family members need to intervene to help get them back on track. Finally, if they become involved with the legal system due to an arrest for substance abuse related behavior such as possession of drugs, driving under the influence or stealing to obtain money for drugs they need to be helped through long-term rehabilitation. In many cases, placement in a long-term rehab facility can be a part of their sentence from the court.

A long-term rehabilitation facility can be very helpful in supporting a substance abuser who wants to transition to a clean lifestyle. Placing an abuser in a long-term rehab facility puts him or her into a new environment that is free of many of the temptations and distractions of their prior life that led them to be addicted. For example, if the abuser was not in school or working they had a great deal of idle time that was likely spent in an unhealthy environment with a ready supply of available drugs. That temptation is removed when they are taken to a long-term rehab facility. Another benefit of a long-term rehab facility is its structured environment and schedule. The facility will require the substance abuser to attend treatment and restructure his or her life to be able to sustain a healthy lifestyle.

The three main indicators that long-term rehab may be needed for a family member with substance abuse problems are disruption of job or school, loss of healthy relationships and involvement with the legal system. The Treatment Episode Date Set (TEDS) is a system that compiles information provided by rehab and treatment centers around the country. The most recent report highlights admissions for the years 1997 through 2007 for various drugs and alcohol abuse treatments. The total number of admissions for drug treatment reported in the United States in 2007 was approximately 1.8 million.

Only one in 10 people that abuse substances seeks and gets treatment, even so: is rehab the answer for them? Support groups like Alcohol Anonymous and other organizations centered around other substance abuse have also been found to work. Alternative therapies have also shown promise. However, these groups have been found to be less effective than long-term rehab for serious substance abusers.

Worth noting is that according to a report  published last year by the National Center on Addiction and Substance Abuse at  Columbia University “the vast majority of people in need of addiction treatment do not receive anything that approximates evidence-based care.” The report added, “Only a small fraction of individuals receive interventions or treatment consistent with scientific knowledge about what works.” The report claims most addiction treatment providers are not medical professionals and are not equipped with the knowledge, skills or credentials needed to provide the full range of evidence-based services, including medication and psychosocial therapy.

Before committing to a treatment program, substance addicts and families should   do their homework. The first step is to get an independent assessment of the need for treatment, as well as the kind of treatment needed, by an expert who is not affiliated with the program you are considering. Look for programs using research-validated techniques, like cognitive behavioral therapy, which helps addicts recognize what prompts them to use drugs or alcohol, and learn to redirect their thoughts and reactions away from the abused substance.