An Illinois woman died after reportedly ingesting a synthetic substance known as "Sass", bringing yet another dangerous synthetic compound into the spotlight.
Cristina Villasana, 21, reportedly passed away on Tuesday night after taking the drug, which is a form of ecstasy made from the sassafras plant. Authorities are still trying to determine who supplied Villasana with the drug, but believe that the people who drove her to the hospital hampered the investigation by providing false information.
Safrole, which is derived from sassafras oil, has been banned from use in food by the U.S. Food and Drug Administration due to it being a cancer-causing agent. It also serves as a precursor to MDMA or ecstasy.
When sass levels in the body reach acute toxicity, some of the symptoms are similar to that of ecstasy including increased blood pressure and heart rate, sweating and a dramatic increase in body temperature. Death is typically caused either by cardiac arrests or hemorrhaging in the brain that leads to a stroke. However, the rates of death are extremely low at roughly 1 of out every 50,000 users.
Other relatively new synthetic drugs have also been causing havoc in recent months. More than two dozen high school students in Michigan were hospitalized last month after taking a synthetic cannabinoid known as Cloud 9. Also known as Hookah Relax, it is primarily sold as a liquid in eyedropper bottles. It can be smoked, drank or inhaled in a vaporizer, but is often used with e-cigarettes or "hookah pens."
Side effects of ingesting Cloud 9 include paranoia, suicidal ideation, nightmarish hallucinations, and chest pains leading to near heart attacks. In a couple of cases, high school students were admitted into psychiatric facilities after mixing the compound with prescription drugs like Xanax and Vicodin. The mixture with the prescription narcotic and the benzodiazepine led to adverse psychological reactions.
And unlike regular marijuana, the physical side effects from withdrawal can be debilitating. "She couldn't eat and couldn't sleep,” said one mother whose daughter stopped using Cloud 9. “My daughter dropped 30 pounds. There were three weeks of withdrawal from it.”
In what appears on paper to be a classic case of nepotism, Arkansas Gov. Mike Beebe announced that he will pardon his son on a felony drug charge stemming from 2003.
A spokesman for the governor confirmed that the pardon for his son, 34-year-old Kyle Beebe, will take place in the next few weeks. Kyle was charged in 2003 with possession of a controlled substance with intent to deliver, which resulted in a fine and three years of supervised probation. But Mike, who will finish out his stint as governor in the next few months, said that the recommendation is coming from the Arkansas Parole Board and was not originally pushed by him.
"I would have done it a long time ago if he'd have asked, but he took his sweet time about asking," he said. "He was embarrassed. He's still embarrassed, and frankly, I was embarrassed and his mother was embarrassed. It’s tough on the families, but hopefully the kids learn.”
However, the governor has pardoned more than 700 offenders throughout his tenure and Kyle did meet all of the requirements that would warrant one. He has avoided any issues with the law since his original charge and has demonstrated a commitment to changing his life.
"Mr. Governor, I am asking for a second chance at life. I am asking for a second chance to be the man that I know that I can be,” wrote Kyle in his pardon application. "At the time of my arrest I was living in a fantasy world, not reality. I was young and dumb. At that time in my life I felt like I was missing something and I tried to fill that emptiness by selling drugs."
Beebe isn’t the only politician to pardon a relative convicted of drug charges. Bill Clinton famously pardoned his half-brother Roger Clinton, who was convicted of dealing cocaine, on his last day in office in January 2001. Roger was arrested in 1985 and had served more than a year in prison for his crime. But after his criminal record was erased, he was charged with drunk driving and disorderly conduct in two separate incidents.
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Methamphetamine abuse played a role in Survivor singer Jimi Jamison’s death, according to the recent autopsy results.
On August 31, Jamison, 63, passed away from a stroke. He suffered from severe blockage in his coronary arteries, which ultimately led to a hemorrhagic stroke of his brain. But according to the coroner, acute methamphetamine intoxication was also a determining factor.
“Because meth was determined to be a contributor, and the circumstances leading up to the death were not suspicious, the coroner rules Jamison’s death as an accident,” according to the coroner’s report.
Jamison, who is best known for hits like Burning Heart and Is This Love, supported various charities throughout his career, including St. Jude Children’s Research Hospital and the Make-a-Wish Foundation. Jamison continued giving back up until the very end and had even performed with his band at a cancer benefit in California the night before he passed away in his Memphis home.
Jamison is survived by three children and one grandchild. “Jimi was a friend to everyone he met. He was a loving father and a grandfather and was always a person who valued people more than anything else,” Jamison’s family wrote.
Researchers at the University of Melbourne, Australia will use magnetic resonance imaging (MRI) to determine whether an individual’s neural makeup can determine if they will become addicted to nicotine.
The tests are the second stage of a study conducted by Associate Professor Rob Hester and his team, which will follow 144 individuals with varying degrees of nicotine use—occasional users, those who would qualify as dependent on the drug, and non-users—for the next five years to see if there are differences at the neural level that could indicate whether a person could be “predestined” for addiction. The subjects will be placed in a functional magnetic resonance imaging machine and asked to complete tasks that will determine their ability to deliberately stop and start behaviors, such as pushing a button until asked to stop.
“It turns out that these types of tasks tap into the ability for self-control that is of interest to us when researching addiction,” said Hester. “They also correlate very well with the problems that people have in the real world.”
Their initial tests have suggested that a loss of neurological sensitivity—essentially, becoming numb to the idea of negative consequences—may provide the key factor in determining susceptibility to addiction. Occasional smokers, whom the research has shown to exhibit a poorer sense of self-control and a heightened sensitivity to reward, may have come to believe that the short-term relief of a cigarette carries less freight than the benefits of abstinence or reduced risk to smoking-related diseases.
Hester hopes that his study will provide a more definitive picture of the impact of this reduced sensitivity on dependent behavior. By doing so, it could provide more concrete evidence to assist in public health efforts to reduce smoking.
“Nicotine dependence is the single biggest cause of preventable death in Australia,” he notes. Smoking is a key factor in most of the top 10 leading causes of death in the United States, including heart disease, cancer, chronic lower respiratory disease and diabetes.
Changing the way that a gene in the brain region operates may offer the key to reducing addictive cravings and depression.
That is the finding in a recent study conducted at the Icahn School of Medicine at Mount Sinai and published in the journal Nature Neuroscience. The study focuses on changes wrought on human genes by transcription factors; proteins that bind to specific DNA sequences and influence the function of individual genes.
These transcription factors can be altered by exposure to chemicals or stress that will, in turn, produce a response that can make the genes more susceptible to stress or addiction. In the study, the research team introduced synthetic transcription factors called Zinc Finger Proteins (ZFPs) into a single gene, FosB, in the nucleus accumbens—a region of the brain closely associated with other centers that maintain the production of dopamine and the reduction of serotonin—of mice test subjects.
When FosB is encouraged to express, the individual experiences a greater sensitivity to drug interaction and less resilience to stressors. The FosB-ZFPs caused chemical modifications that produced the opposite effect: the mice appeared to be more resilient to stress and less susceptible to cocaine dependency.
The study authors indicate that their research is the first step in developing not only therapeutics to positively affect the diseases of depression and addiction, but also other genetic-based conditions. “The use of engineered transcription factors has broad implications outside of neuroscience, because gene regulation underlies many diseases, including most forms of cancer,” said the study’s lead author, Elizabeth A. Heller, PhD.