Author Archives: Haley

Utah Prescription Drug Abuse Statistics

In 2016, more than 40% of all U.S. opioid overdose deaths involved a prescription opioid. The most common drugs involved in these overdoses were methadone, oxycodone (e.g. OxyContin) and hydrocodone (e.g. Vicodin®). From 2000 to 2015, Utah experienced a nearly 400% spike in deaths from the misuse and abuse of prescription drugs. Utah had the seventh highest drug overdose rate in the U.S. in 2016, with 635 deaths. Of the 10 Utahns who died every week from drug overdoses in 2016, 60% were attributed to prescription opioids. The current Utah budget is about $7 million, which helps only 27% of drug abusers eligible for Medicaid. Mirroring the rest of the nation, the majority of prescription opioid deaths in Utah involved concurrent use of other drugs.

  • On average, 7,000 opioid prescriptions are filled every day in Utah.
  • Although 2015 was the first decrease in the rate of prescription opioid deaths in Utah since 2009, 24 individuals still died every month from a prescription opioid overdose.
  • Of 357 prescription drug overdose deaths in 2015, 282 were attributed to opioids.
  • Deaths from oxycodone drugs (e.g. OxyContin and Percocet) accounted for 55.0% of all prescription opioid deaths in 2015, while hydrocodone accounted for 17.7% of deaths.
  • Individuals aged 45-54 had the highest prescription opioid overdose deaths rates, with no major gender differences.
  • The highest rates of Utah ER visits for prescription opioid overdoses were in individuals aged 25-34.

Prescription Drug Overdose Deaths in Utah

In Utah, the following percentages provide a picture of the most serious co-occurring problems in individuals who died from prescription drug overdoses.

  • Substance abuse (e.g. illegal drugs, abuse of prescription medications or regular use of inhalants): 65%
  • Mental illness diagnosis: 62%
  • Physical health problems: 61%
  • History of alcohol dependence or problematic use: 16%
  • Past suicide attempt: 10%

The Path to Heroin Abuse

A study by the Kaiser Family Foundation indicates heroin overdose deaths have soared in Utah, more than tripling since 2007. In 2016, 166 Utah residents fatally overdosed on heroin compared to 127 the prior year. “When they get to a point where they can’t get prescription opioids, where they can’t afford them, then they’re turning to heroin because it’s cheaper to get,” said Jenny Johnson, Utah Department of Health (UDOH) spokeswoman. “We’re seeing a decrease in our prescription opioid deaths,” said Anna Fondario, UDOH epidemiology manager. “But in our illicit opioid deaths, we are seeing increases.”

  • In 2014-2015, about 5,000 individuals aged 12 or older in Utah used heroin in the past year, which is in line with the national average.
  • In a single-day count in 2015, 2,459 and 790 individuals received methadone and buprenorphine, respectively, in Utah opioid treatment programs as part of their substance use treatment.
  • The highest rates of Utah ER visits for heroin were in individuals aged 18-24.

Efforts to Curb Abuse

On May 31, 2018, Utah filed a lawsuit against Purdue Pharma, accusing the manufacturer of OxyContin of creating a drug epidemic in the state. In the court filing, the state claimed Purdue waged an aggressive marketing campaign for its drugs that relied on deception, exaggeration and flawed science. The lawsuit stated Purdue’s actions amounted to fraud, negligence, nuisance and a violation of state consumer sales law. In filing the lawsuit, Utah joined other attorneys general who filed their own lawsuits against Purdue, Johnson & Johnson and opioid distributor McKesson Corp. Separately, more than 700 cities and counties have sued the drug manufacturers and distributors in cases consolidated before a federal judge in Cleveland, with the first trial scheduled for March 2019.

Utah Take Back Program

Data shows nearly 60% of people in Utah prescribed an opioid in the past year had leftover medication and only 27% reported disposing it. A joint effort of the Utah Attorney General’s Office and the U.S. Drug Enforcement Administration, Utah Take Back is a day set aside to collect potentially dangerous expired, unused or unwanted prescription drugs. Last fall, more than 3,800 federal, state and local agencies collected 702,365 pounds of unused, expired, or unwanted medications at more than 5,000 collection sites across the U.S. During the 2017 event, Utah collected more than 33,000 pounds of prescription drugs to dispose of properly. Attorney General Sean D. Reyes issued this statement in April 2018:

“Prescription drug abuse and deaths related to opioids have risen to epidemic levels in Utah and across the country. Opioid addiction has ravaged rural and urban areas as well as uptown and downtown neighborhoods. It has taken far too many lives and ruined countless more. Those who suffer from addiction may be soccer moms or executives. They can be star athletes, high achieving students, popular kids or “loners.” They are our kids, grandkids and kids from the block. And whether we realize it or not, our medicine cabinets might be the very place where they are looking or have already been for their next high or pill party.”

Naloxone Distribution Saves Lives

As a result of a statewide standing order issued by the UDOH on December 8, 2016, pharmacies across the state dispensed 4,275 doses of naloxone in 2017. Naloxone is a rescue medication that can reverse the effects of an opioid overdose. Data indicate 99 naloxone overdose reversals occurred as a direct result of outreach efforts by the UDOH, local agencies and syringe exchange providers across the state. While pharmacies in rural areas of the state only comprise an estimated 30% of all participating pharmacies enrolled through the standing order, they distributed nearly 70% or 2,914 of naloxone doses in 2017.

Pharmacists and healthcare providers can play an integral role in curbing prescription opioid deaths by discussing the risks of opioids, signs of an opioid overdose and the efficacy of naloxone to reverse overdoses. In some cases, it may be more effective for medical professionals to encourage individuals to seek professional treatment for opioid addiction than when family members urge them to do so.

Muscle Relaxers & Drug Abuse

Muscle relaxers or relaxants are medications with sedative and depressant properties used to treat a wide array of musculoskeletal conditions. Typically prescribed in combination with physical therapy, the goal of these medications is to reduce skeletal muscle spasms, alleviate pain and increase mobility of impacted muscles. In addition, many of these drugs are prescribed for fibromyalgia and back pain. Studies have not demonstrated the superiority of these drugs to acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) for low back pain. Systematic reviews and meta-analyses support their use for short-term relief of acute low back pain when nonprescription drugs are poorly tolerated or ineffective. The American Pain Society and the American College of Physicians recommend using acetaminophen and NSAIDs as first-line agents for acute low back pain and reserving skeletal muscle relaxants as an alternative therapy.

Types of Muscle Relaxers

Prescription muscle relaxants are classified into two basic types. Antispasmodics are centrally acting skeletal muscle relaxants (SMRs) and antispastics are drugs that only suppress muscle spasms. Experts theorize antispasmodics help alleviate muscle spasms and associated pain through their sedative properties and/or by preventing nerves from sending pain signals to the brain. Antispastics are typically prescribed for conditions that cause muscle spasticity, including brain injuries, spinal cord injury and multiple sclerosis. Spasticity is clinically defined as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon reflexes, resulting from excitability of the stretch reflex.” In lay terms, spasticity is a problem involving excessive permanent increase in muscle tone when a person is at rest.

Muscle Relaxer Names

Perhaps you’re familiar with some of the most common and widely prescribed names of muscle relaxers, such as Valium (diazepam), Soma (carisoprodol) or Flexeril (cyclobenzaprine). These are just a few of the many muscle relaxants available by prescription. Below is a brief description of the most common muscle relaxants, categorized by type, with brand and generic names.

Antispasmodics

Soma (carisoprodol): Physical or psychological dependence is possible with potential withdrawal symptoms after discontinuation. Carisoprodol was found to be superior to diazepam for the short-term treatment of moderately severe low back pain and spasm. Carisoprodol should only be used for short periods (2-3 weeks) due to lack of evidence proving effectiveness with longer use. This drug may cause drowsiness and dizziness, and should not be used in anyone aged 65 and older.

Parafon Forte, Lorzone (chlorzoxazone): This drug acts primarily at the level of the spinal cord and subcortical areas of the brain, where it inhibits reflexes involved in skeletal muscle spasms. The side effects are similar to most muscle relaxants, with the exception of a limited number of reported cases of significant hepatotoxicity. Therefore, it is not recommended for anyone with liver problems.

Fexmid, Flexeril, Amrix (cyclobenzaprine)

This drug is the most widely studied and has been shown to be effective for muscle stiffness and pain. Structurally similar to tricyclic antidepressants, it is believed to impart analgesic effects by interfering with serotonin transmission at the spinal cord. The recommended dose of cyclobenzaprine is 5 or 10 mg three times daily for immediate release tablets or 15 or 30 mg once daily for extended release tablets. As with most drugs, it is possible to overdose on Flexeril. Combining cyclobenzaprine with opioid analgesics or antidepressant medication increases the risk of neuropsychiatric side effects such as psychosis and delirium, as well as spasmodic muscle contractions.

Skelaxin, Metaxall (metaxalone)

Typically well tolerated, this drug is a used in addition to rest, physical therapy and other measures for relief of discomfort associated with acute and painful musculoskeletal conditions. It is commonly prescribed as a muscle relaxant, although it has no direct muscle relaxant effects. Metaxalone overdose can lead to potentially deadly serotonin syndrome, as evidenced by case studies, however, both subjects ingested other medications and one intentionally attempted suicide.

Robaxin (methocarbamol)

An inexpensive and less sedating option than cyclobenzaprine or carisoprodol, this drug has shown efficacy for low back pain. In a recent study, 44% of people achieved complete low back pain relief. Robaxin methocarbamol tablets are a carbamate derivative of guaifenesin, a CNS depressant with sedative and musculoskeletal relaxant properties.

Norflex (orphenadrine)

This drug works by blocking nerve impulses or pain sensations sent to the brain. It is used together with rest and physical therapy to treat skeletal muscle conditions such as pain or injury.

Zanaflex (tizanidine)

Tizanidine is indicated for the symptomatic treatment of painful muscle spasms due to musculoskeletal disorders and at higher doses for disease-specific spasticity. It is used in adults with multiple sclerosis and spinal cord injury and in children with cerebral palsy. In combination with NSAIDs, it is superior to NSAIDs alone. A 2009 study found it was superior to aceclofenac monotherapy for the treatment of acute low back pain. It should not be used by individuals with liver disease or with the drugs fluvoxamine or ciprofloxacin.

Antispastics

Lioresal, Gablofen, Lioresal (baclofen): Baclofen is chemically related to gamma-aminobutyric acid (GABA), a naturally occurring neurotransmitter in the brain. GABA released by some nerves results in decreased activity of other nerves. It is believed the GABA-like action of baclofen blocks the activity of nerves within the part of the brain controlling the contraction and relaxation of skeletal muscles.

Dantrium (dantrolene)

This drug helps control chronic spasticity related to spinal injuries, stroke, multiple sclerosis and cerebral palsy. Dantrolene is taken as a capsule and can cause liver problems, so regular blood tests are typically required to monitor liver health. Individuals with asthma, emphysema, bronchitis or other lung diseases are more likely to experience serious side effects.

Valium (diazepam)

A benzodiazepine used to treat anxiety, muscle spasms, seizures, insomnia, epilepsy and some effects of alcohol withdrawal, Valium was introduced in 1963 and quickly gained popularity for its sedative effects. Between 1969 and 1982, Valium was the most prescribed drug in the U.S., viewed by clinicians as a worry-free panacea. In 1979, sales reached a peak with more than 2.3 billion pills sold. Diazepam has similar sedative and hypnotic effects as barbiturates, however, it is far less likely to result in lethal overdose and thought to have less abuse potential than newer benzos like Xanax. Although the peak of Valium abuse was decades ago, accounts of epidemic abuse periodically resurface and the drug continues to be sold on the black market. Valium should not be taken with any prescription opioids due to the increased risk of fatal overdose.

Side Effects of Muscle Relaxers

The side effects of muscle relaxers vary somewhat based on the medication and individual. Serious side effects include breathing problems, lightheadedness or fainting, blurred vision, confusion, nausea and urinary retention. The most common side effects of antispasmodics include:

  • Constipation
  • Drowsiness
  • Dizziness
  • Dry mouth
  • Fatigue
  • Headache
  • Nervousness
  • Reddish-purple or orange urine
  • Lowered blood pressure upon standing

The most common side effects of antispastics include:

  • Drowsiness
  • Dizziness
  • Weakness
  • Fatigue

Special Precautions

Muscle relaxants should not be combined with antihistamines, St. John’s wort or sleep medications. The excessive sedative effect when taken with other central nervous system depressants such as alcohol, opioids, benzodiazepines or barbiturates can result in respiratory depression and death. Dosing timing is important because a muscle relaxant designed to last 12 hours taken at 10 pm can cause impaired driving before 10 am. Gradual tapering off of these drugs is recommend because withdrawal symptoms such as seizures or hallucinations can occur.

Abuse of Muscle Relaxers

Muscle relaxers are prescribed on a short-term basis because they have the potential to be addictive and in that event, require specialized SOMA addiction treatment. Carisoprodol and diazepam are both classified by the U.S. Drug Enforcement Administration as Schedule IV controlled substances due to their potential for abuse and addiction, as evidenced by studies. Literature also suggests abuse potential for baclofen, methocarbamol, orphenadrine and tizanidine, although relatively few animal and human studies have been conducted.

Carisoprodol was originally thought to have a lower potential for abuse and addiction than other muscle-relaxing drugs used in the 1950s-60s. More recent evidence shows it is habit forming, especially when taken in combination with other drugs. In a person who readily metabolizes carisoprodol, large amounts result in a sedative-hypnotic effect that may lead to psychological addiction. The drug intensifies the effects of Xanax, creating a potentially lethal duo when taken together. This drug is intentionally abused to enhance the effectiveness of other drugs, with users creating “cocktails” to simulate the effects of narcotic substances including heroin. Back in 2000, the Drug Abuse Warning Network listed carisoprodol as the 20th most abused drug, ranking higher than oxycodone and methadone.

Abusing any of these muscle relaxers can increase the risk and severity of side effects and possibly lead to dependence. Only use these medications short-term as recommended, and follow all precautions. Don’t abruptly stop taking these drugs and seek professional help if you feel you have become addicted.

What Is the Role of Dopamine in Alcoholism?

Alcohol is one of the most widely used psychoactive substances in the world. Alcohol-induced changes in brain functions are key contributing factors to acute intoxication, long-term misuse and the development alcohol use disorder (AUD) or dependence. AUD is a chronic relapsing brain disease characterized by compulsive alcohol use, loss of control over alcohol intake and a negative emotional state when not drinking alcohol. Extensive research has been done on the role of dopamine in alcohol dependence, as well as other substance and behavioral addictions.

What Is Dopamine?

Dopamine is a brain chemical (neurotransmitter) released by brain cells (neurons). Often called the “feel-good” chemical, dopamine is released when people feel pleasure. Neurotransmitters transmit signals from the brain to the body by passing across small gaps (synapses) between each neuron, thereby controlling a multitude of body functions. As the primary neurotransmitter in the brain’s reward center, dopamine modulates physiological functions including food consumption, movement, sleep, learning, mood, memory, sexual behavior and attention. Unbalanced dopamine levels (low or high) are implicated in many conditions, including depression and Parkinson’s disease.

Dopamine is the primary neurotransmitter in the brain’s reward system, which is part of the limbic system. The dopamine system includes the nigrostriatal, mesolimbic and tuberoinfundibular pathways. Dopamine is mainly produced in the substantia nigra area of the brain, projected along the nigrostriatal pathways and stored in the striatum. Five subtypes of dopamine receptors have been identified and cloned. All of these function both individually and interactively as G-protein coupled receptors.

What Is the Dopamine-Alcoholism Connection?

The reward system is the target of psychoactive substances including alcohol, cocaine, amphetamine and opioids. Electrophysiological studies found acute alcohol intake can increase dopamine release in the substantia nigra and ventral tegmental area (VTA). Levels decrease during alcohol withdrawal and are restored after alcohol intake is resumed. Research also suggests the amygdala, an area of the brain in the reward circuitry, plays a central role in the alcohol-induced effects on the brain. Other studies have found alcohol can also indirectly increase dopamine levels by interacting with gamma-Aminobutyric acid (GABA) neurons and opioid receptors in the nucleus accumbens.

Alcohol and Dopamine Research

Basic studies have demonstrated optimal levels of prefrontal cortical dopamine are critical to functions such as working memory, attention, inhibitory control and risk/reward decisions. All of these are impaired in addictive disorders such as alcoholism. Decreased dopamine transmission in the mesolimbic regions, such as the VTA and medial temporal lobe, likely contributes to the psychological side effects and decreased reward sensitivity in alcohol dependent individuals.

A 2014 study used amphetamine and positron emission tomography (PET) to measure and compare cortical dopamine transmission in 21 recently abstinent alcoholics and 21 healthy controls aged 18-40. None of the subjects had any other current or past substance disorder other than nicotine. Cortical dopamine in healthy controls and alcohol dependent subjects increased by 513-798% and 0-228% respectively, following the same dose of amphetamine. This was the first study to clearly demonstrate the existence of decreased dopamine transmission in the cortex in alcoholism. Less dopamine in the prefrontal cortex, which governs executive functions, is important because it could impair an alcohol-dependent individual’s ability to learn and utilize informational/behavioral strategies critical to relapse prevention.

2016 study suggests when an alcoholic stops drinking, the brain’s ability to use dopamine changes, altering the way the reward system is wired. The study analyzed a specific type of dopamine receptor called D1 – dopamine binds to these receptors on the membranes of neuronal cells, causing neurons to become excited. Using sample postmortem brain tissue from deceased alcoholics, researchers found significantly decreased striatal D1 receptor and dopamine transporter binding sites. Fewer D1 receptors make the brain less responsive to dopamine, causing an individual to struggle in order to feel the same pleasure from alcohol others may experience. Brain tissue showed no reduction in D2 receptor sites, which bind with dopamine in order to inhibit, rather than excite neurons. The combination of these characteristics ultimately interfere with the brain’s ability to use dopamine, subsequently inhibiting the ability to feel pleasure, which potentially leads to tolerance and relapse.

The second part of the study utilized rats to determine the mechanisms leading to altered dopamine activity. Researchers tracked dopamine levels in the brains of alcohol-dependent rats after they were denied alcohol for several weeks. Dopamine levels dropped during the first six days, confirming the existing theory acute alcohol withdrawal is characterized by a hypodopaminergic state. While the availability of dopamine receptor sites and transporter sites were normal during this period, after three weeks, dopamine levels become elevated and the rats continued to exhibit signs of alcohol craving. The number of available receptor and transporter sites plummeted at this stage and the rats’ brains resembled those of the deceased alcoholic humans.

The authors concluded while acute alcohol withdrawal may be associated with a hypodopaminergic state, prolonged abstinence leads to a hyperdopaminergic state, in which dopamine levels are higher than normal. The hyperdopaminergic state is associated with increased motor activity and augmented alcohol seeking, however, both states reflect a dysfunctional reward system and may increase the risk of relapse.

Potential Alcoholism Treatment Targeting Dopamine

It has been well established the VTA plays an important role in mediating reward and reinforcement in drugs of abuse, as well as food. The important connection between the VTA and dopamine neurotransmission has been the subject of alcohol studies in animals for 30 years. Researchers hope a better understanding of the mechanisms of adaptation to alcohol after chronic use and the sequence of molecular events leading from reward-seeking to compulsive use may lead to more efficacious therapeutic interventions.

Two Swedish studies by the same research team demonstrated the potential efficacy of the dopamine stabilizer OSU6162 for the treatment of alcoholism. In the first study, half the participants were treated with OSU6162 and half with placebo for two weeks, after which both groups were exposed to potential situations that could trigger alcohol craving. The OSU6162 group experienced less alcohol craving after drinking one glass of an alcoholic beverage and less enjoyment. The group that responded best to OSU6162 consisted of individuals with the worst impulse control and the greatest risk of relapse.

In the other study, rats that voluntarily consumed alcohol for almost a year had lower levels of dopamine in their brain reward system than the alcohol-naïve control group. When the “alcohol rats” were treated with OSU6162, the substance counteracted the low concentrations of dopamine. Although far more studies are needed before this treatment can be marketed, researchers believe OSU6162 can reduce alcohol craving in alcohol-dependent individuals by returning diminished levels of dopamine in their brain reward systems to normal.

A 2018 study confirmed the efficacy of OSU6162 in improving motor impulsivity in both alcohol and alcohol-naïve rats and its possible therapeutic use for AUD. Pre-treatment with OSU6162 prior to the rats’ 10-week exposure to alcohol prevented relapse-like drinking behavior after a forced period of abstinence. The results indicate improved motor impulse control might be one mechanism underlying OSU6162’s ability to lessen alcohol-provoked behaviors.