Hope everyone’s summer is going well! :)
This blog will be a tad dry for the next two weeks as I prep for and then go on vacation. I’ll be back August 10th and posting will resume soon thereafter.
Study shows depression in younger women linked to higher risk of death from heart disease
An Emory University study, published June 19th in the Journal of the American Heart Association, shows women age 55 and younger are twice as likely to suffer a heart attack, die or require artery-opening procedures if they are moderately or severely depressed.
The research, funded by the National Institutes of Health and the Emory Heart & Vascular Center, also showed that women in this age group are at greater risk than men and older women to suffer from depression — possibly a “hidden” risk factor that helps explain why more women die after a heart attack.
“Women in this age group are also more likely to have depression, so this may be one of the ‘hidden’ risk factors that can help explain why women die at a disproportionately higher rate than men after a heart attack,” says study author Amit J. Shah, MD, assistant professor of epidemiology, Rollins School of Public Health (RSPH), and assistant professor of medicine (cardiology), Emory University School of Medicine (SOM).
"Although the risks and benefits of routine screening for depression are still unclear, our study suggests that young women may benefit from special consideration," says senior study author Viola Vaccarino, MD, PhD, professor and Wilton Looney Chair of Epidemiology at RSPH and professor of medicine, Emory University SOM. “Unfortunately, this group has largely been understudied before.”
LSUHSC contributes to work identifying new DNA regions associated with schizophrenia
"Nancy Buccola, MSN, APRN, PMHCNS-BC, CNE, Assistant Professor of Clinical Nursing at LSU Health Sciences Center New Orleans School of Nursing, contributed samples used in a study reporting new locations of genetic material associated with schizophrenia and also suggesting a possible link between the immune system and schizophrenia. The study, “Biological insights from 108 schizophrenia-associated genetic loci,” was published online July 22, 2014 in Nature, available at http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13595.html.
Buccola collected samples as part of the Molecular Genetics of Schizophrenia (MGS) study. A large international collaboration, called the Schizophrenia Working Group of the Psychiatric Genomics Consortium, combined these previously collected samples with published or unpublished genome-wide association study genotypes into a single, systematic analysis. To the Consortium’s knowledge this is the largest molecular genetic study of schizophrenia ever conducted.”
Ok, this is long. really long. Like an hour long. But so so very good. Learn what we’ve learned through BFRB research so far, and why TLC is going big with the BPM Research Program. Also, maybe you’ll see why we are Jon Grant super-fans. Check out www.trich.org/research for more info
Hayes, S. C., Levin, M. E., Plumb-Vilardaga, J., Villatte, J. L., & Pistorello, J. (2013). Acceptance and commitment therapy and contextual behavioral science: Examining the progress of a distinctive model of behavioral and cognitive therapy. Behavior Therapy, 44(2), 180-198.
ANON. PART 2- My question is, since anecdotes are not science, what happens to a sad kid who won’t leave the couch without a cocktail of antidepressants? What’s the alternative? What are those in the field of psychology working on to take their place?Is there evidence of harm from antidepressants, despite lack of evidence for their effectiveness? (Or does it go both ways?) I’m really fascinated by this subject (and really open-minded,) and would love more information! Thanks for your time!ANON 3- Sorry for the rambling question. I don’t know if it even makes sense. I’m just convinced that my brother was able to complete high school thanks to both his own strength and a boost out of the fog of major depression. Is that possible? Also, if the drugs are not the best, do we have a sense of what to do in extreme cases? Are there alternatives at this point?I’m sorry to hear about your struggles, and I’m happy to hear there has been some relief (from what it sounds). Let’s go with bullet points for this one!
- I can’t say much about a kid who won’t leave the couch without a cocktail of antidepressants because, of course, that’s a very broad situation. It’s sort of like asking, “how do you treat cancer?” A broad answer might suffice, but there’s not much specific you can give aside from “probably chemotherapy.” Same thing here. I can say I would consider more intensive behavioral therapy, but I can’t say much beyond that; I don’t know this kid and I don’t know the variables at play.
- We already have alternatives to pharmaceuticals, and behavioral therapy would be one. People suggest that combining the two is most effective, but that’s actually not accurate in long-term studies. Some also suggest that pharmaceuticals are required for what people call treatment-resistant depression (TRD), but that also has not received sufficient research.
- There is some evidence that SSRIs can be incredibly harmful for adolescents and young adults, specifically in the realm of increased suicidality. The FDA, which is typically incredibly medication-friendly, has even placed a black box warning on them for adolescents/young adults (at least historically - I’m not sure if that was lifted in recent years as I think of it now?)
- Anything in an individual case is possible (within reason; I doubt someone will start flying after taking antidepressants). In science we are concerned with variance, or the extent to which individuals differ from one another, and what accounts for that variance. So we might take a group of people who take antidepressants and a group of people who take placebo and see that there is not much difference between these groups (i.e., little variance between them). But this is a group statistic. Of course it could be the case that certain individuals differ greatly from one another, meaning it’s more than possible that one individual taking an antidepressant does significantly better than another individual taking placebos. The notion that antidepressants lack effectiveness is based on a group trend. So yes, your brother’s case is absolutely possible, but the problem is without adequate study of your brother we can’t be certain what caused the change (e.g., placebo or antidepressant?), just that some sort of change occurred during the time of medication. But, is that important? If your brother is doing better, then congratulations to him all the same!
- Your last question is kind of similar to the other one in the sense that I can’t really offer specifics. You can have two individuals who qualify as “extreme” cases and they can be (and often are) different in key aspects.
Hope that helps a bit! Let me know if you have any other questions, it’s no bother at all!
Regardless of whether it’s genuine or a “made-for-TV moment,” Clendening’s story prompts a poignant point: The disorder is not one-size-fits-all….
Incredible article from HuffPost
Teenage Latinas are more likely to commit suicide than other teen girls. Spread awareness and let’s break this statistic.
Webinar: The EASA Center of Excellence is pleased to announce the upcoming launch of the webinar series, Early Psychosis Intervention for Teens and Young Adults: New and Empowering Approaches…
PTSD is more common among military veterans.
Funded by a $1 million award from the Keck Foundation, biomedical researchers at UCSB will strive to find out who could be more vulnerable to addiction
We’ve all heard the term “addictive personality,” and many of us know individuals who are consistently more likely to take the extra drink or pill that puts them over the edge. But the specific balance of neurochemicals in the brain that spurs him or her to overdo it is still something of a mystery.
“There’s not really a lot we know about specific molecules that are linked to vulnerability to addiction,” said Tod Kippin, a neuroscientist at UC Santa Barbara who studies cocaine addiction. In a general sense, it is understood that animals — humans included — take substances to derive that pleasurable rush of dopamine, the neurochemical linked with the reward center of the brain. But, according to Kippin, that dopamine rush underlies virtually any type of reward animals seek, including the kinds of urges we need to have in order to survive or propagate, such as food, sex or water. Therefore, therapies that deal with that reward system have not been particularly successful in treating addiction.
However, thanks to a collaboration between UCSB researchers Kippin; Tom Soh, professor of mechanical engineering and of materials; and Kevin Plaxco, professor of chemistry and biochemistry — and funding from a $1 million grant from the W. M. Keck Foundation — the neurochemistry of addiction could become a lot less mysterious and a lot more specific. Their study, “Continuous, Real-Time Measurement of Psychoactive Molecules in the Brain,” could, in time, lead to more effective therapies for those who are particularly inclined toward addictive behaviors.
“The main purpose is to try to identify individuals that would be vulnerable to drug addiction based on their initial neurochemistry,” said Kippin. “The idea is that if we can identify phenotypes — observable characteristics — that are vulnerable to addiction and then understand how drugs change the neurochemistry related to that phenotype, we’ll be in a better position to develop therapeutics to help people with that addiction.”
To identify these addiction-prone neurochemical profiles, the researchers will rely on technology they recently developed, a biosensor that can track the concentration of specific molecules in vivo, in real time. One early incarnation of this device was called MEDIC (Microfluidic Electrochemical Detector for In vivo Concentrations). Through artificial DNA strands called aptamers, MEDIC could indicate the concentration of target molecules in the bloodstream.
“Specifically, the DNA molecules are modified so that when they bind their specific target molecule they begin to transfer electrons to an underlying electrode, producing an easily measurable current,” said Plaxco. Prior to the Keck award, the team had shown that this technology could be used to measure specific drugs continuously and in real time in blood drawn from a subject via a catheter. With Keck funding, “the team is hoping to make the leap to measurements performed directly in vivo. That is, directly in the brains of test subjects,” said Plaxco.
For this study, the technology would be modified for use in the brain tissue of awake, ambulatory animals, whose neurochemical profiles would be measured continuously and in real time. The subjects would then be allowed to self-dose with cocaine, while the levels of the drug in their brain are monitored. Also monitored are concomitant changes in the animal’s neurochemistry or drug-seeking (or other) behaviors.
“The key aspect of it is understanding the timing of the neurochemical release,” said Kippin. “What are the changes in neurochemistry that causes the animals to take the drug versus those that immediately follow consumption of the drug?”
Among techniques for achieving this goal, a single existing technology allows scientists to monitor more than one target molecule at a time (e.g., a drug, a metabolite, and a neurotransmitter). However, Kippin noted, it provides an average of one data point about every 20 minutes, which is far slower than the time course of drug-taking behaviors and much less than the sub-second timescale over which the brain responds to drugs. With the implantable biosensor the team has proposed, it would be possible not only to track how the concentration of neurochemicals shift in relation to addictive behavior in real time, but also to simultaneously monitor the concentrations of several different molecules.
“One of our hypotheses about what makes someone vulnerable to addiction is the metabolism of a drug to other active molecules so that they may end up with a more powerful, more rewarding pharmacological state than someone with a different metabolic profile,” Kippin said. “It’s not enough to understand the levels of the compound that is administered; we have to understand all the other compounds that are produced and how they’re working together.”
The implantable biosensor technology also has the potential to go beyond cocaine and shed light on addictions to other substances such as methamphetamines or alcohol. It also could explore behavioral impulses behind obesity, or investigate how memory works, which could lead to further understanding of diseases such as Alzheimers.
Cognitive-behavioral therapy (CBT) has been shown to greatly reduce anxiety levels in schoolchildren ages nine to 10 years old, according to new research from…
Recent published research in the Journal of Clinical Investigation demonstrates how changes in dopamine signaling and dopamine transporter function are linked to neurological and psychiatric diseases, including early-onset Parkinsonism and attention deficit hyperactivity disorder (ADHD).
"The present findings should provide a critical basis for further exploration of how dopamine dysfunction and altered dopamine transporter function contribute to brain disorders" said Michelle Sahai, a postdoctoral associate at the Weill Cornell Medical College of Cornell University, adding "it also contributes to research efforts developing new ways to help the millions of people suffering."
Sahai is also studying the effects of cocaine, a widely abused substance with psychostimulant effects that targets the dopamine transporter. She and her colleagues expect to release these specific findings within the next year.
Dopamine is a neurotransmitter that plays an important role in our cognitive, emotional, and behavioral functioning. When activated from outside stimuli, nerve cells in the brain release dopamine, causing a chain reaction that releases even more of this chemical messenger.
To ensure that this doesn’t result in an infinite loop of dopamine production, a protein called the dopamine transporter reabsorbs the dopamine back into the cell to terminate the process. As dopamine binds to its transporter, it is returned to the nerve cells for future use.
However, cocaine and other drugs like amphetamine, completely hijack this well-balanced system.
"When cocaine enters the bloodstream, it does not allow dopamine to bind to its transporter, which results in a rapid increase in dopamine levels," Sahai explained.
The competitive binding and subsequent excess dopamine is what causes euphoria, increased energy, and alertness. It also contributes to drug abuse and addiction.
To further understand the effects of drug abuse, Sahai and other researchers in the Harel Weinstein Lab at Cornell are delving into drug interactions on a molecular level.
Using supercomputer resources, she is able to observe the binding of dopamine and various drugs to a 3D model of the dopamine transporter on a molecular level. According to Sahai, the work requires very long simulations in terms of microseconds and seconds to understand how drugs interact with the transporters.
Through the Extreme Science and Engineering Discovery Environment (XSEDE), a virtual cyberinfrastructure that provides researchers access to computing resources, Sahai performs these simulations on Stampede, the world’s 7th fastest supercomputer, at the Texas Advanced Computing Center (TACC).
"XSEDE-allocated resources are fundamental to helping us understand of how drugs work. There’s no way we could perform these simulations on the machines we have in house. Through TACC as an XSEDE service provider, we can also expect an exponential increase in computational results, and good customer service and feedback."
Ultimately, Sahai’s research will contribute to an existing body of work that is attempting to develop a cocaine binding inhibitor without suppressing the dopamine transporter.
"If we can understand how drugs bind to the dopamine transporter, then we can better understand drug abuse and add information on what’s really important in designing therapeutic strategies to combat addiction," Sahai said.
A Common Link in the Research
While Sahai is still working to understand drug abuse, her simulations of the dopamine transporter have contributed to published research on Parkinson’s disease and other neurological disorders.
In a collaborative study with the University of Copenhagen, Copenhagen University Hospital, and other research groups in the U.S. and Europe, researchers revealed the first known link between de novo mutations in the dopamine transporter and Parkinsonism in adults.
The study found that mutations can produce typical effects including debilitating tremors, major loss of motor control, and depression. The study also provides additional support for the idea that dopamine transporter mutations are a risk factor for attention deficit hyperactivity disorder (ADHD).
After identifying the dopamine transporter as the mutated gene linked to Parkinson’s, researchers once again turned to the Harel Weinstein Lab due to its long-standing interest and investment in studying the human dopamine transporter.
Sahai’s simulations using XSEDE and TACC’s Stampede supercomputer supported clinical trials by offering greater insight into how the dopamine transporter is involved in neurological disorders.
"This research is very important to me," Sahai said. "I was able to look at the structure of the dopamine transporter on behalf of experimentalists and understand how irregularities in this protein are harming an actual person, instead of just looking at something isolated on a computer screen."
While there is currently no cure for Parkinson’s disease, a deeper understanding of the specific mechanisms behind it will help the seven to ten million people afflicted with the disease.
"Like my work on drug abuse, the end goal is thinking about how we can help people. And it all comes back to drug design," Sahai said.