Duke Research Blog

Following the people and events that make up the research community at Duke.

Category: Lecture Page 1 of 15

How the Flu Vaccine Fails

Influenza is ubiquitous. Every fall, we line up to get our flu shots with the hope that we will be protected from the virus that infects 10 to 20 percent of people worldwide each year. But some years, the vaccine is less effective than others.

Every year, CDC scientists engineer a new flu virus. By examining phylogenetic relationships, which are based on shared common ancestry and relatedness, researchers identify virus strains to target with a vaccine for the following flu season.

Sometimes, they do a good job predicting which strains will flourish in the upcoming flu season; other times, they pick wrong.

Pekosz’s work has identified why certain flu seasons saw less effective vaccines.

Andrew Pekosz, PhD, is a researcher at Johns Hopkins who examines why we fail to predict strains to target with vaccines. In particular, he examines years when the vaccine was ineffective and the viruses that were most prevalent to identify properties of these strains.

A virus consists of RNA enclosed in a membrane. Vaccines function by targeting membrane proteins that facilitate movement of the viral genome into host cells that it is infecting. For the flu virus, this protein is hemagglutinin (HA). An additional membrane protein called neuraminidase (NA) allows the virus to release itself from a cell it has infected and prevents it from returning to infected cells.  

The flu vaccine targets proteins on the membrane of the RNA virus. Image courtesy of scienceanimations.com.

Studying the viruses that flourished in the 2014-2015 and 2016-2017 flu seasons, Pekosz and his team have identified mutations to these surface proteins that allowed certain strains to evade the vaccine.

In the 2014-2015 season, a mutation in the HA receptor conferred an advantage to the virus, but only in the presence of the antibodies present in the vaccine. In the absence of these antibodies, this mutation was actually detrimental to the virus’s fitness. The strain was present in low numbers in the beginning of the flu season, but the selective pressure of the vaccine pushed it to become the dominant strain by the end.

The 2016-2017 flu season saw a similar pattern of mutation, but in the NA protein. The part of the virus membrane where the antibody binds, or the epitope, was covered in the mutated viral strain. Since the antibodies produced in response to the vaccine could not effectively identify the virus, the vaccine was ineffective for these mutated strains.

With the speed at which the flu virus evolves, and the fact that numerous strains can be active in any given flu season, engineering an effective vaccine is daunting. Pekosz’s findings on how these vaccines have previously failed will likely prove invaluable at combating such a persistent and common public health concern.

The Costs of Mental Effort

Every day, we are faced with countless decisions regarding cognitive control, or the process of inhibiting automatic or habitual responses in order to perform better at a task.

Amitai Shenhav, PhD, of Brown University, and his lab are working on understanding the factors that influence this decision making process. Having a higher level cognitive control is what allows us to complete hard tasks like a math problem or a dense reading, so we may expect that the optimal practice is to exert a high level of control at all times.

Shenhav’s lab explores motivation and decision making related to cognitive control.

Experimental performance shows this is not the case: people tend to choose easier over hard tasks, require more money to complete harder tasks, and exert more mental effort as the reward value increases. These behaviors all suggest that the subjects’ automatic state is not to be at the highest possible level of control.

Shenhav’s research has centered around why we see variation in level of control. Because cognitive control is a costly process, there must be a limit to how much we can exert. These costs can be understood as tradeoffs between level of control and other brain functions and consequences of negative affective changes related to difficult tasks, like stress.

To understand how people make decisions about cognitive control in real time, Shenhav has developed an algorithm called the Expected Value of Control (EVC) model, which focuses on how individuals weigh the costs and benefits of increasing control.

Employing this model has helped Shenhav and his colleagues identify situations in which people are likely to choose to invest a lot of cognitive control. In one study, by varying whether the reward was paired only with a correct response or was given randomly, Shenhav simulated variability in efficacy of control. They found that people learn fairly quickly whether increasing their efforts will increase the likelihood of earning the reward and adjust their control accordingly: people are more likely to invest more effort when they learn that there is a correlation between their own effort and the likelihood of reward than when rewards are distributed independent of performance.

Another study explored how we adjust our strategies following difficult tasks. Experiments with cognitive control often rely on paradigms like the Stroop task, where subjects are asked to identify a target cue (color) while being presented with a distractor (incongruency of the word with its text color). Shenhav found that when subjects face a difficult trial or make a mistake, they adjust by decreasing attention to the distractor.

The Stroop task is a classic experimental design for understanding cognitive control. Successful completion of Stroop task 3 requires overriding your reflex to read the word in cases where the text and its color are mismatched.

A final interesting finding from Shenhav’s work tells us that part of the value of hard work may be in the work itself: people value rewards following a task in a way that scales to the effort they put into the task.

Bias in Brain Research

Despite apparent progress in achieving gender equality, sexism continues to be pervasive — and scientists aren’t immune.  

In a cyber talk delivered to the Duke Institute for Brain Sciences, professor Cordelia Fine of the University of Melbourne highlighted compelling evidence that neuroscientific research is yet another culprit of gender bias.

Fine says the persistent idea of gender essentialism contributes to this stagnation. Gender essentialism describes the idea that men and women are fundamentally different, specifically at a neurological level. This “men are from Mars, women are from Venus” attitude has spread from pop culture into experimental design and interpretation.

However, studies that look for sex differences in male and female behavior tend to show more similarities than differences. One study looked at 106 meta-analyses about psychological differences between men and women. The researchers found that in areas as diverse as temperament, communication styles, and interests, gender had a small effect, representing statistically small differences between the sexes.

Looking at fMRI data casts further doubt on how pronounced gender differences really are. A meta-analysis of fMRI studies investigating functional differences between men and women found a large reporting bias. Studies finding brain differences across genders were overrepresented compared to those finding similarities.

Of those small sex differences found in the central nervous system, Fine points out how difficult it is to determine their functional significance. One study found no difference between men and women in self-reported emotional experience, but found via fMRI that men exhibited more processing in the prefrontal cortex, or the executive center of the brain, than women. Although subjective experience of emotion was the same between men and women, the researchers reported that men are more cognitive, while women are more emotional.

Fine argues that conclusions like this are biased by gender essentialism. In a study she co-authored, Fine found that gender essentialism correlates with stronger belief in gender stereotypes, that gender roles are fixed, and that the current understanding of gender does not need to change.

When scientists allow preconceived notions about gender to bias their interpretation of results, our collective understanding suffers. The best way to overcome these biases is to ensure we are continuing to bring more and more diverse voices to the table, Fine said.

Fine spoke last month as part of the Society for Neuroscience Virtual Conference, “Mitigating Implicit Bias: Tools for the Neuroscientist.” The Duke Institute for Brain Sciences (@DukeBrain) made the conference available to the Duke community.  

Post by undergraduate blogger Sarah Haurin
Post by undergraduate blogger Sarah Haurin

The Importance of Moms

Emily Bray, Ph.D., might have the best job ever. Since earning her bachelor’s at Duke in 2012, she has been researching cognitive development in puppies, which basically means she’s spent the last seven years playing with dogs. If that’s not success, I don’t know what is.

Last Friday marked the 10th birthday of Duke’s Canine Cognition Center, and the 210th birthday of Charles Darwin. To celebrate, Brian Hare, Ph.D., invited former student Bray back to campus to share her latest research with a new generation of Duke undergraduates. The room was riveted — both by her compelling findings and by the darling photos of labs and golden retrievers that accompanied each slide.

Dr. Emily Bray shows photos of her study participants

During her Ph.D. program at the University of Pennsylvania, Bray worked with Robert Seyfarth, Dorothy Cheney, and James Serpell to investigate the effects of mothering on puppy development. For her dissertation, she studied a population of dog moms and their puppies at The Seeing Eye, Inc. The Seeing Eye is one of the oldest and largest guide dog schools in the U.S. They have been successfully raising and training service dogs for the blind since 1929, but like most things, it is still an imperfect science. Approximately half of the puppies bred at The Seeing Eye fail out of program. A dog that completes service training at The Seeing Eye represents two years of intensive training and care, and investing so much time and money into a dog that might eventually fail is problematic. Being able to predict the outcomes of puppies would save a lot of wasted time and energy, and Emily Bray has been doing just this.

What makes a good dog mom? (Photo from Dirk Vorderstraße, from Wikimedia Commons)

Through her work at The Seeing Eye, Bray found that, similar to humans, dogs have several types of mothering styles. She discovered that dog moms tend to fall somewhere on the spectrum from low to high maternal involvement. Some of the moms were very involved with their puppies, and seldom left their side. These hovering moms had high levels of cortisol, and became quite stressed when separated briefly from a puppy. They coddled their children, and often nursed from a laying down position, doing everything they could to make life easy for their babies. On the other side of the spectrum, Bray also observed moms that displayed much more relaxed mothering. They often took personal time, and let their puppies fend for themselves. They were more likely to nurse while sitting or standing up, which made their children work harder to feed. They were less stressed when separated from a puppy, and also just had generally lower levels of cortisol. Sound like bad parenting? Believe it or not, this tough love actually resulted in more successful puppies.

Duke’s very own assistance dogs in training!

As the puppies matured, Bray conducted a series of cognitive and temperament tests to determine if maternal style was associated with a certain way of thinking in the puppies. Turns out, dogs who experienced high maternal care actually performed much worse on the tests than dogs who were shown tough love when they were young. At The Seeing Eye graduation, it was also determined that high maternal care and ventral nursing was associated with failure. Puppies that were over-mothered were more likely to fail as service dogs.

Her theory is that tough love raises more resilient puppies. When mom is always around, the puppies don’t get the chance to experience small stressors and learn how to deal with challenge. The more relaxed moms actually did their kids a favor by not being so overbearing, and allowed for much more independent development.

Bray is now doing post-doctoral research at the University of Arizona, where she is working with Canine Companions for Independence (CCI) to determine if maternal style has similar effects on the outcomes of dogs that will be trained to assist people with a wide range of disabilities. She is also now doing cognition and temperament tests on moms pre-pregnancy to determine if maternal behavior can be predicted before the dogs have puppies. Knowing this could be a game changer, as this information could be used for selective breeding of better moms.

Me snuggling Ashton, one of the Puppy Kindergarten dogs

If you got the chance to hang out with puppies Ashton, Aiden, or Dune last semester, you have an idea of how awesome Bray’s day-to-day work is. These pups were bred at CCI, and sent to Duke to be enrolled in Duke Puppy Kindergarten, a new program on campus run through Duke’s Canine Cognition Center. Which of these three will make it to graduation? I’ve got money on Ashton, but I guess we’ll have to wait and see.

The bottom line according to Bray? “Mothering matters, but in moderation.”

Nature vs. Nurture and Addiction

Epigenetics involves modifications to DNA that do not change its sequence but only affect which genes are active, or expressed. Photo courtesy of whatisepigenetics.com

The progressive understanding of addiction as a disease rather than a choice has opened the door to better treatment and research, but there are aspects of addiction that make it uniquely difficult to treat.

One exceptional characteristic of addiction is its persistence even in the absence of drug use: during periods of abstinence, symptoms get worse over time, and response to the drug increases.

Researcher Elizabeth Heller, PhD, of the University of Pennsylvania Epigenetics Institute, is interested in understanding why we observe this persistence in symptoms even after drug use, the initial cause of the addiction, is stopped. Heller, who spoke at a Jan. 18 biochemistry seminar, believes the answer lies in epigenetic regulation.

Elizabeth Heller is interested in how changes in gene expression can explain the chronic nature of addiction.

Epigenetic regulation represents the nurture part of “nature vs. nurture.” Without changing the actual sequence of DNA, we have mechanisms in our body to control how and when cells express certain genes. These mechanisms are influenced by changes in our environment, and the process of influencing gene expression without altering the basic genetic code is called epigenetics.

Heller believes that we can understand the persistent nature of the symptoms of drugs of abuse even during abstinence by considering epigenetic changes caused by the drugs themselves.

To investigate the role of epigenetics in addiction, specifically cocaine addiction, Heller and her team have developed a series of tools to bind to DNA and influence expression of the molecules that play a role in epigenetic regulation, which are called transcription factors. They identified the FosB gene, which has been previously implicated as a regulator of drug addiction, as a site for these changes.

Increased expression of the FosB gene has been shown to increase sensitivity to cocaine, meaning individuals expressing this gene respond more than those not expressing it. Heller found that cocaine users show decreased levels of the protein responsible for inhibiting expression of FosB. This suggests cocaine use itself is depleting the protein that could help regulate and attenuate response to cocaine, making it more addictive.

Another gene, Nr4a1, is important in dopamine signaling, the reward pathway that is “hijacked” by drugs of abuse.  This gene has been shown to attenuate reward response to cocaine in mice. Mice who underwent epigenetic changes to suppress Nr4a1 showed increased reward response to cocaine. A drug that is currently used in cancer treatment has been shown to suppress Nr4a1 and, consequently, Heller has shown it can reduce cocaine reward behavior in mice.

The identification of genes like FosB and Nr4a1 and evidence that changes in gene expression are even greater in periods of abstinence than during drug use. These may be exciting leaps in our understanding of addiction, and ultimately finding treatments best-suited to such a unique and devastating disease.   

Post by undergraduate blogger Sarah Haurin

Post by undergraduate blogger Sarah Haurin

Sean Carroll on the Evolution of Snake Venom

What’s in a snake bite?

According to University of Wisconsin-Madison evolutionary biologist Sean Carroll who visited Duke and Durham last week, a snake bite contains a full index of clues.

In his recent research, Carroll has been studying the adaptations of novelties in animal form, such as snake venom. Rattlesnakes, he explains, are the picture of novelty. With traits such as a limbless body, fangs, infrared pits, patterned skin, venom, and the iconic rattle, they represent an amazing incarnation of evolution at work.

Rattlesnakes: the picture of novelty (Photo from USGS)

Snake venoms contain a complex mixture of proteins. This mixture can differ in several ways, but the most interesting difference to Carroll is the presence or absence of neurotoxins. Neurotoxic venom has proven to be a very useful trait, because neurotoxins destroy the nervous tissue of prey, effectively paralyzing the animal’s respiratory system.

Some of today’s rattlesnake species have neurotoxic venom, but some don’t. So how did this happen? That’s what Carroll was wondering too.

Some genes within genomes, such as HOX genes, evolve very slowly from their original position among the chromosomes, and see very few changes in the sequence in millions of years.

But snake venom Pla2 genes are quite the opposite. In recent history, there has been a massive expansion of these genes in the snake genome, Carroll said. When animals evolve new functions or forms, the question always arises: are these changes the result of brand new genes or old genes taking on new functions?

Another important consideration is the concept of regulatory versus structural genes. Regulatory genes control the activity of other genes, such as structural genes, and because of this, duplicates of regulatory genes are generally not going to be a favorable adaptation. In contrast, structural gene activity doesn’t affect other genes, and duplicates are often a positive change. This means it is easier for a new structural gene to evolve than a regulatory one. Carroll explained.

Evolutionary Biologist Sean Carroll (Photo from seanbcarroll.com)

Carroll examined neurotoxic and non-neurotoxic snakes living in overlapping environments. His research showed that the most recent common ancestor of these species was a snake with neurotoxic venom. When comparing the genetic code of neurotoxic snakes to non-neurotoxic ones, he found that the two differed by the presence or absence of 16 genes in the metalloproteinase gene complex. He said this meant that non-neurotoxic venom could not evolve from neurotoxic venom.

So what is the mechanism behind this change? What could be the evolutionary explanation?

When Carroll’s lab compared another pair of neurotoxic and non-neurotoxic species in a different region of the US, they found that the two species differed in exactly the same way, with the same set of genes deleted as had been observed in the first discovery. With this new information, Carroll realized that the differences must have occurred through the mechanism of hybridization, or the interbreeding of neurotoxic and non-neurotoxic species.

Carroll’s lab is now doing the structural work to study if the genes that result in neurotoxic and  non-neurotoxic protein complexes are old genes carrying out new functions or entirely new genes. They are using venom gland organoids to look into the regulatory processes of these genes.

In addition to his research studying the evolution of novelties, Carroll teaches molecular biology and genetics at Madison and has devoted a large portion of his career to  storytelling and science education.

Drug Homing Method Helps Rethink Parkinson’s

The brain is the body’s most complex organ, and consequently the least understood. In fact, researchers like Michael Tadross, MD, PhD, wonder if the current research methods employed by neuroscientists are telling us as much as we think.

Michael Tadross is using novel approaches to tease out the causes of neuropsychiatric diseases at a cellular level.

Current methods such as gene editing and pharmacology can reveal how certain genes and drugs affect the cells in a given area of the brain, but they’re limited in that they don’t account for differences among different cell types. With his research, Tadross has tried to target specific cell types to better understand mechanisms that cause neuropsychiatric disorders.

To do this, Tadross developed a method to ensure a drug injected into a region of the brain will only affect specific cell types. Tadross genetically engineered the cell type of interest so that a special receptor protein, called HaloTag, is expressed at the cell membrane. Additionally, the drug of interest is altered so that it is tethered to the molecule that binds with the HaloTag receptor. By connecting the drug to the Halo-Tag ligand, and engineering only the cell type of interest to express the specific Halo-Tag receptor, Tadross effectively limited the cells affected by the drug to just one type. He calls this method “Drugs Acutely Restricted by Tethering,” or DART.

Tadross has been using the DART method to better understand the mechanisms underlying Parkinson’s disease. Parkinson’s is a neurological disease that affects a region of the brain called the striatum, causing tremors, slow movement, and rigid muscles, among other motor deficits.

Only cells expressing the HaloTag receptor can bind to the AMPA-repressing drug, ensuring virtually perfect cell-type specificity.

Patients with Parkinson’s show decreased levels of the neurotransmitter dopamine in the striatum. Consequently, treatments that involve restoring dopamine levels improve symptoms. For these reasons, Parkinson’s has long been regarded as a disease caused by a deficit in dopamine.

With his technique, Tadross is challenging this assumption. In addition to death of dopaminergic neurons, Parkinson’s is associated with an increase of the strength of synapses, or connections, between neurons that express AMPA receptors, which are the most common excitatory receptors in the brain.

In order to simulate the effects of Parkinson’s, Tadross and his team induced the death of dopaminergic neurons in the striatum of mice. As expected, the mice displayed significant motor impairments consistent with Parkinson’s. However, in addition to inducing the death of these neurons, Tadross engineered the AMPA-expressing cells to produce the Halo-Tag protein.

Tadross then treated the mice striatum with a common AMPA receptor blocker tethered to the Halo-Tag ligand. Amazingly, blocking the activity of these AMPA-expressing neurons, even in the absence of the dopaminergic neurons, reversed the effects of Parkinson’s so that the previously affected mice moved normally.

Tadross’s findings with the Parkinson’s mice exemplifies how little we know about cause and effect in the brain. The key to designing effective treatments for neuropsychiatric diseases, and possibly other diseases outside the nervous system, may be in teasing out the relationship of specific types of cells to symptoms and targeting the disease that way.

The ingenious work of researchers like Tadross will undoubtedly help bring us closer to understanding how the brain truly works.

Post by undergraduate blogger Sarah Haurin

Post by undergraduate blogger Sarah Haurin

 

Falling Out of Love With Science and Our Civic Duties

Last Friday, I attended Falling Out of Love with Science, a lunch function during which Milan Yager,executive director of the American Institute for Medical and Biological Engineering, discussed why those of us interested in scientific research should care about the actions of prominent politicians, especially those that relate to the underfunding of scientific research.

Milan Yager of AIMBE

Milan Yager is the executive director of the American Institute for Medical and Biological Engineering.

Before attending Yager’s talk, I guess I didn’t quite realize how much of innovation was enabled by government funding. Many revolutionary discoveries are made possible through the NIH (https://www.nih.gov) that we don’t even realize we use on a daily basis.

However, as I came to realize, public support for research funding is jeopardized by the propagation of fake news defeating the need for concrete scientific research, hence propelling research under-funding. Over time, funding for the NIH and other government research funding has declined, which has slowed American innovation.

What I enjoyed most about his talk however, was the unexpected motivational turn that it took at the end. He discussed how we, as young researchers invested in finding our personal truths through science, needed to use our voices to stand up against the proliferation of myths in politics in favor of concrete facts.

NIH funding trends

Here’s a curve we definitely want to bend: NIH research funding has flattened and fallen.

Though this can be done in different ways, Yager made sure to point out how essential it is for Americans to vote, citing a statistic that points out that 20 percent of Americans don’t vote because they are “simply too lazy.” (Learn how to register to vote in North Carolina.)

He also encouraged us to send letters to our senators, rally for what we believed in, and not give up on our goals in the face of adversity — something that he called “sitting at the table.” Yager points out that if you don’t “sit at the table,” then your issue won’t get the necessary exposure needed for it to be fixed.

What can we, as Duke students, take away from what Yager had to say? Mainly this: Duke is a research institution that is partially made capable by government funding; for our capacity for research to be continued to be fully realized, we must use our voices to make sure that the propagation of ‘fake news’ does not cut funding for factual research.

This is mainly achieved by voting– those who perpetuate false “facts” in order to remain in power must be replaced with those who realize the importance of scientific research.

Perhaps, for society to fall back in love with science, we need to fall out of love with the myths propagated by tribal politics.

Post by Rebecca Williamson

Aging and Decision-Making

Who makes riskier decisions, the young or the old? And what matters more in our decisions as we age — friends, health or money? The answers might surprise you.

Kendra Seaman works at the Center for the Study of Aging and Human Development and is interested in decision-making across the lifespan.

Duke postdoctoral fellow Kendra Seaman, Ph.D. uses mathematical models and brain imaging to understand how decision-making changes as we age. In a talk to a group of cognitive neuroscientists at Duke, Seamen explained that we have good reason to be concerned with how older people make decisions.

Statistically, older people in the U.S. have more money, and additionally more expenditures, specifically in healthcare. And by 2030, 20 percent of the US population will be over the age of 65.

One key component to decision-making is subjective value, which is a measure of the importance a reward or outcome has to a specific person at a specific point in time. Seaman used a reward of $20 as an example: it would have a much higher subjective value for a broke college student than for a wealthy retiree. Seaman discussed three factors that influence subjective value: reward, cost, and discount rate, or the determination of the value of future rewards.

Brain imaging research has found that subjective value is represented similarly in the medial prefrontal cortex (MPFC) across all ages. Despite this common network, Seaman and her colleagues have found significant differences in decision-making in older individuals.

The first difference comes in the form of reward. Older individuals are likely to be more invested in the outcome of a task if the reward is social or health-related rather than monetary. Consequently, they are more likely to want these health and social rewards  sooner and with higher certainty than younger individuals are. Understanding the salience of these rewards is crucial to designing future experiments to identify decision-making differences in older adults.

A preference for positive skew becomes more pronounced with age.

Older individuals also differ in their preferences for something called “skewed risks.” In these tasks, positive skew means a high probability of a small loss and a low probability of a large gain, such as buying a lottery ticket. Negative skew means a low probability of a large loss and a high probability of a small gain, such as undergoing a common medical procedure that has a low chance of harmful complications.

Older people tend to prefer positive skew to a greater degree than younger people, and this bias toward positive skew becomes more pronounced with age.

Understanding these tendencies could be vital in understanding why older people fall victim to fraud and decide to undergo risky medical procedures, and additionally be better equipped to motivate an aging population to remain involved in physical and mental activities.

Post by undergraduate blogger Sarah Haurin

Post by undergraduate blogger Sarah Haurin

Combatting the Opioid Epidemic

The opioid epidemic needs to be combatted in and out of the clinic.

In the U.S. 115 people die from opioids every day. The number of opioid overdoses increased fivefold from 1999 to 2016. While increased funding for resources like Narcan has helped — the opioid overdose-reversing drug now carried by emergency responders in cities throughout the country — changes to standard healthcare practices are still sorely needed.

Ashwin A Patkar, MD, medical director of the Duke Addictions Program, spoke to the Duke Center on Addiction and Behavior Change about how opioid addiction is treated.

The weaknesses of the current treatment standards first appear in diagnosis. Heroin and cocaine are currently being contaminated by distributors with fentanyl, an opioid that is 25 to 50 times more potent than heroin and cheaper than either of these drugs. Despite fentanyl’s prevalence in these street drugs, the standard form and interview for addiction patients does not include asking about or testing for the substance.

Patkar has found that 30 percent of opioid addiction patients have fentanyl in their urine and do not disclose it to the doctor. Rather than resulting from the patients’ dishonesty, Patkar believes, in most cases, patients are taking fentanyl without knowing that the drugs they are taking are contaminated.

Because of its potency, fentanyl causes overdoses that may require more Narcan than a standard heroin overdose. Understanding the prevalence of Narcan in patients is vital both for public health and educating patients so they can be adequately prepared.

Patkar also pointed out that, despite a lot of research supporting medication-assisted therapy, only 21 percent of addiction treatment facilities in the U.S. offer this type of treatment. Instead, most facilities rely on detoxification, which has high rates of relapse (greater than 85 percent within a year after detox) and comes with its own drawbacks. Detox lowers the patient’s tolerance to the drug, but care providers often neglect to tell the patients this, resulting in a rate of overdose that is three times higher than before detox.

Another common treatment for opioid addiction involves using methadone, a controlled substance that helps alleviate symptoms from opioid withdrawal. Because retention rate is high and cost of production is low, methadone poses a strong financial incentive. However, methadone itself is addictive, and overdose is possible.

Patkar points to a resource developed by Julie Bruneau as a reference for the Canadian standard of care for opioid abuse disorder. Rather than recommending detox or methadone as a first line of treatment, Bruneau and her team recommend buprenorphine , and naltrexone as a medication to support abstinence after treatment with buprenorphine.

Buprenorphine is a drug with a similar function as methadone, but with better and safer clinical outcomes. Buprenorphine does not create the same euphoric effect as methadone, and rates of overdose are six times less than in those prescribed methadone.

In addition to prescribing the right medicine, clinicians need to encourage patients to stick with treatment longer. Despite buprenorphine having good outcomes, patients who stop taking it after only 4 to 12 weeks, even with tapering directed by a doctor, exhibit only an 18 percent rate of successful abstinence.

Patkar closed his talk by reminding the audience that opioid addiction is a brain disease. In order to see a real change in the number of people dying from opioids, we need to focus on treating addiction as a disease; no one would question extended medication-based treatment of diseases like diabetes or heart disease, and the same should be said about addiction. Healthcare providers have a responsibility to treat addiction based on available research and best practices, and patients with opioid addiction deserve a standard of care the same as anyone else.

Post by undergraduate blogger Sarah Haurin

Post by undergraduate blogger Sarah Haurin

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