How DNA Testing Botched My Family’s Heritage, and Probably Yours, Too

Original Article

My grandfather was caramel-skinned with black eyes and thick, dark hair, and until he discovered that he was adopted, he had no reason to suspect that he was not the son of two poor Mexicans as he’d always been told. When he found his adoption papers, according to family lore, he pestered the nuns at the Dallas orphanage where he had lived as an infant for the name of his birth mother. Name in hand, at 10 years old, he hopped a bus to Pennsylvania, met his birth mother, and found out that he was actually Syrian.

At least that’s what we thought until my Aunt Cat mailed a tube of her spit in to AncestryDNA.

The author’s grandparents in Dallas on their wedding day. Image Courtesy the author

Genetic testing suggested that my aunt’s genetic makeup was only a tiny bit Middle Eastern—16 percent, not the 50 percent you might expect if your father was a full-blooded Syrian, as my grandfather believed himself to be. The rest of her Ancestry breakdown provided some explanation, but mostly more confusion. While we typically think of the Caucasus as countries on the Black and Caspian seas like Turkey and Armenia, Ancestry’s test also said it includes Syria. According to Ancestry, the Caucasus accounted for another 15 percent of my Aunt Cat’s DNA. What about the other 20 percent? One line-item stood out as something my aunt hadn’t expected, based on what she knew about either of her parents: She was 30 percent Italian-Greek. My mother’s test revealed similar results.

This caused a minor family scandal. My grandfather’s mother was born in Pennsylvania, but she had lived in an insular Syrian community that never really assimilated. She became pregnant as a teen by her father’s best friend. The assumption had always been that he was Syrian, too. If we weren’t who we thought we were, well, then, who were we?

“I guess we never knew the name of Dad’s father,” my aunt told me, bemused. Suddenly it seemed as though all along we had been missing a gigantic puzzle piece of information about our family tree. At least, my aunt quipped, this was a solid explanation for why she loved pasta.

It’s right there in the fine print of any consumer DNA test, if you bother to read it: DNA testing can come with identity-disrupting surprises, be it an unexpected relative, genetic condition, or, in our case, heritage. But something about this particular surprise didn’t feel quite right.

My Aunt Cat is our family’s amateur genealogist, and she has logged hundreds of hours both on Ancestry.com and in my grandmother’s attic, piecing together the story of our family tree. She’s found countless third, fourth, and fifth cousins with ties to Syria, but no one from either Italy or Greece. In her twenties, she even visited my grandfather’s biological mother and aunt. She recalled them passing around a hookah, yelling in Arabic, and expressing repulsion at the American-style cold cut platter served at a community function. Given how segregated the family was, it seemed like a stretch, she told me, to imagine that anyone had ever had so much as a friendly conversation with an Italian.

I suspected the error might lay not in my family narrative, but in the DNA test itself. So I decided to conduct an experiment. I mailed my own spit samples to AncestryDNA, as well as to 23andMe and National Geographic. For each test I got back, the story of my genetic heritage was different—in some cases, wildly so.

The author’s DNA test results from AncestryDNA.

My AncestryDNA test revealed that I, too, had geographic roots in the Middle East, the Caucasus, and Southern Europe, along with the expected big dose of Scandinavian from my very Norwegian father. Weirdly, though, my percentages of Middle Eastern and Caucasus were almost as high as my mom and aunt’s, though you would expect them to be closer to half.

It got more confusing from there. My test through National Geographic (which partners with the DNA sequencing company Helix for its test) gave me even more links to the Middle East, with 16 percent of my DNA from Asia Minor, 6 percent from the Persian Gulf and 9 percent something called “Jewish Diaspora.” Unlike AncestryDNA, National Geographic’s test assigns your heritage to broad regions instead of modern nation-states. But I could infer that, according to National Geographic, I was less Scandinavian based on my percentage of Northwestern European. I was also more Southern European and, for fun, now had a good chunk of Eastern European thrown in there, too.

The author’s DNA test results from National Geographic.

23andMe’s ancestry results were the most confounding of all. It found that I was only 3 percent Scandanavian, a number that, based on my recent family history, I know is flatly wrong. It also found I was only 5.5 percent Middle Eastern and a whopping 62.6 percent Northwestern European. And no Eastern European at all.

The author’s DNA test results from 23andMe.

 I also uploaded my 23andMe data to GenCove, a small ancestry-test startup founded by scientists. Based on the exact same data that 23andMe had crunched, GenCove reported that 8 percent of my DNA was from the Indian subcontinent. 23andMe had found I had no South Asian DNA at all.

The author’s DNA test results from GenCove, using 23andMe data.

Four tests, four very different answers about where my DNA comes from—including some results that contradicted family history I felt confident was fact. What gives?

There are a few different factors at play here.

Genetics is inherently a comparative science: Data about your genes is determined by comparing them to the genes of other people.

As Adam Rutherford, a British geneticist and author of the excellent book “A Brief History of Everyone Who Ever Lived,” explained to me, we’ve got a fundamental misunderstanding of what an ancestry DNA test even does.

“They’re not telling you where your DNA comes from in the past,” he told me, “They’re telling you where on Earth your DNA is from today.”

Ancestry, for example, had determined that my Aunt Cat was 30 percent Italian by comparing her genes to other people in its database of more than six million people, and finding presumably that her genes had a lot of things in common with the present-day people of Italy.

Heritage DNA tests are more accurate for some groups of people than others, depending how many people with similar DNA to yours have already taken their test. Ancestry and 23andMe have actually bothpublished papers about how their statistical modeling works.

As Ancestry puts it: “When considering AncestryDNA estimates of genetic ethnicity it is important to remember that our estimates are, in fact, estimates. The estimates are variable and depend on the method applied, the reference panel used, and the other customer samples included during estimation.”

That the data sets are primarily made up of paying customers also skews demographics. If there’s only a small number of Middle Eastern DNA samples that your DNA has been matched against, it’s less likely you’ll get a strong Middle Eastern match.

“Different companies have different reference data sets and different algorithms, hence the variance in results,” a spokesman from 23andMe told me. “Middle Eastern reference populations are not as well represented as European, an industry-wide challenge.”

As a person of Syrian descent, the British genealogist Debbie Kennett told me, my test was simply not going to be as accurate as fellow Americans whose relatives skew more European. “The tests are mainly geared for an American audience, and they tend to not have a lot of Middle Eastern ancestry,” she said.

Likewise, Kennett said, because relatively few English people have taken tests from American companies like Ancestry or 23andMe, residents of the U.K. are likely to find less useful results.

“A lot of English people come up with a low percentage of British. My dad was only 8 percent British and most of his ancestors as far back as I can trace came back from Great Britain,” she told me. “People in America come up with much higher percentage of British, often.”

Another anecdote that stuck with me came from my friend Alexis Madrigal. Initially, he said, his Mexican family came up as Arab North African, which was surprising. As 23andMe refined its test and its data set grew, it also refined the results: Now, he was descended from Jewish people from Southern Europe. The number of Madrigals in central Spain had long led the family to suspect that their migratory path to Mexico had at some point passed through this region. As more people took the test, the picture of where his family was “from” changed. The Canadian bioethicist Timothy Caulfield shared a similar story. At first a DNA test revealed he was entirely Irish, but as the data set changed, he gradually became less Irish.

When we talk about “ancestry,” we also don’t always mean the same thing. Ancestry just implies people you’re descended from. But when? In America, we often mean whenever our relatives came to the U.S. On my dad’s side, I expected to see a lot of Scandinavian, because just a few generations ago my great grandparents came from Norway to North Dakota. On my mom’s side, my grandmother has a relative that came to America on the Mayflower. Both are what come to mind when I think of my “ancestors,” but they are separated by several generations and hundreds of years in time. Rutherford pointed out that if we went 5oo years back, my ancestors were probably from all over Europe.

“You and I are probably fifth cousins,” he said.

Where your ancestors are from depends on what period in time you’re talking about. Why don’t I instead say I’m 50 percent North Dakotan and 50 percent Texan?

Tests also differ from one another because they’re simply looking at different things. The results of ancestry tests aren’t based on a reading of your whole genome. The vast majority of every human’s DNA is identical to any other human’s. Ancestry tests look at SNPs, the places on your genome where an individual letter tends to differ between people and give us insight into characteristics like disease, ancestry, and physical appearance. When an SNP occurs within a gene, then, in science-speak, that gene has more than one allele, or alternate forms of a gene that exist in the exact same place on a chromosome. To make matters more confusing, some tests look at mitochondrial and Y chromosome DNA, while others don’t.

The CEO of GenCove, the company where I had uploaded my 23andMe data to get drastically different results, told me that even though he expects a fair amount of variability between algorithms, even he was surprised at how differently his company and 23andMe had interpreted my DNA data. He asked me to also upload my Ancestry data, and ran both data sets again after GenCove’s algorithm had been updated. The results were all over the map.

“To be honest I’m a little confused about what’s going on,” CEO Joseph Pickrell told me.

Each testing company is looking at different alleles from different parts of the genome, and using different algorithms to crunch that data. (You can see a list of how company tests differ here.) It’s worth mentioning that genetics is also probabilistic: just because you have the gene, doesn’t mean you have the trait.

“One British company identified an allele in me that gave me ginger hair, and 23andMe didn’t,” said Rutherford. “That’s a simple case where they just used different alleles. That’s relatively simple to explain.”

And sometimes, the algorithms might just get it wrong. Rutherford told me his 23andMe test came back with a tiny amount of Native American DNA. The finding actually linked up with one anecdote from his family lore, about a relative of his father’s that was a Native American tribesman and horse jumper in a British traveling circus.

“As a geneticist, I am absolutely convinced that they’re not related,” he told me. “It’s just statistical noise that happens to coincide with this cool story.” Statistically, it’s unlikely that such tiny amount of Native American DNA would have been enough to show up on Rutherford’s test.

A big problem is that many of us have a basic misunderstanding of what exactly we’re reading when Ancestry or 23andMe or National Geographic sends us colorful infographics about how British or Irish or Scandinavian we are. It’s not that the science is bad. It’s that it’s inherently imperfect, an estimation based on how much our DNA matches up with people in other places around the world, in a world where people have been mixing and matching and getting it on since the beginning of human history.

“You’re creating different algorithms and you’re using different data sets as your reference points, so it makes sense that you’re going to get some different responses,” the Harvard geneticist Robert Green explained to me, as I tried to make sense of my own DNA data. “It’s not that one’s wrong and one’s right. It’s that there isn’t an agreed-upon approach to pick the right number of markers and combine them mathematically. Everyone is sort of just making it up as they go along.”

At the continental level, said Kennett, ancestry testing is useful. It can tell you pretty reliably whether you are African or Asian or European. It can also reliably identify close familial relatives, as distant as third or fourth cousins. Otherwise, Kennett said, “take it with a large pinch of salt.”

Nearly everyone I interviewed for this story said that, taken with the right mindset, ancestry DNA testing can be fun. As more people take DNA tests and company data sets grow, the results from those tests will also become more detailed and accurate. Anecdotally, I saw this in my own results. Ancestry has the biggest DNA database, and its interpretation of my DNA was also most in-line with what I expected.

“The more people that take tests, the better the experience for all of us,” an Ancestry spokesman told me. “Your DNA does not change, our science does.”

But consumer genetic testing companies have also fueled the misunderstanding of their products, suggesting that those colorful results reveal something profound about what makes you, you.

Take this AncestryDNA ad about Kyle Merker, who, the ads explains, grew up German, wearing a lederhosen and performing traditional German dances. Then an AncestryDNA test revealed he was actually Scottish and Irish. He bought a kilt.

Ancestry.com is suggesting—quite heavy-handedly—that your DNA can define your identity. A few changes to those As, Gs, Ts, and Cs, and all of the sudden you’re river dancing.

“Your culture is not your genes,” said Caulfield. “But the message these companies send is somehow where your genes are from matters. That’s not necessarily constructive. The role of genes in who we are is very complex. If anything, as genetic research moves forward we’re learning that it’s even more complex than we thought.”

In truth, your specific ancestors actually have relatively little impact on your DNA. Some 99.99 percent of your DNA is identical to every other human’s. We’re mostly just all the same. But instead of embracing our genetic similarities, we cling to those differences as symbols of what makes us unique. Consumer DNA testing tends to reinforce that—even though the difference that one test reveals might not even exist in another.

“These companies are asking people to pay for something that is at best trivial and at worst astrology,” said Rutherford. “The biggest lesson we can teach people is that DNA is probabilistic and not deterministic.”

Your DNA is only part of what determines who you are, even if the analysis of it is correct. Plenty of people love pasta, with or without Italian DNA.

If the messaging of consumer DNA companies more accurately reflected the science, though, it might be a lot less compelling: Spit in a tube and find out where on the planet it’s statistically probable that you share ancestry with today.

Learning he was Syrian did not seem to impact my grandfather’s identity as a Mexican man. And how could it? His life story was the story of so many children of immigrants. His father, Manuel, had swum the Rio Grande from Mexico to America in hopes of a better future. He worked as a waiter, and my great-grandmother as a seamstress. At age 10, my grandfather was sent to work at a Coca-Cola bottling plant to help the family make ends meet. He lost a finger. Eventually, he met my blonde-haired, blue-eyed grandmother and moved to California, hoping to raise their children somewhere it would matter less that one of their parents spoke Spanish as a first language.

But me, I don’t even look the part. I’m fair with blue eyes. As a kid, I remember wincing when my friend’s mom made xenophobic comments directed at Mexicans, never suspecting her daughter’s fair friend had some Mexican ties, even if they were not by blood but by heart. As an adult, I learned Arabic and perfected my tamale-making, all in search of some sort of an identity fit. When my grandfather was dying, I struggled with the relationship between DNA and cultural identity. I wondered what would become of my Mexican heritage, once my last living link to it was gone.

In the end, I finally found the same wisdom my grandfather never seemed to question. Sometimes your heritage doesn’t have anything at all to do with your genetics—and I didn’t even have to spit in a test tube to figure it out.

New Antibody Attacks 99% of HIV Strains

Original Article

By James Gallagher

HIVImage copyright SPL

Scientists have engineered an antibody that attacks 99% of HIV strains and can prevent infection in primates.

It is built to attack three critical parts of the virus – making it harder for HIV to resist its effects.

The work is a collaboration between the US National Institutes of Health and the pharmaceutical company Sanofi.

The International Aids Society said it was an “exciting breakthrough”. Human trials will start in 2018 to see if it can prevent or treat infection.

Our bodies struggle to fight HIV because of the virus’ incredible ability to mutate and change its appearance.

These varieties of HIV – or strains – in a single patient are comparable to those of influenza during a worldwide flu season.

So the immune system finds itself in a fight against an insurmountable number of strains of HIV.

Super-antibodies

But after years of infection, a small number of patients develop powerful weapons called “broadly neutralising antibodies” that attack something fundamental to HIV and can kill large swathes of HIV strains.

Researchers have been trying to use broadly neutralising antibodies as a way to treat HIV, or prevent infection in the first place.

The study, published in the journal Science, combines three such antibodies into an even more powerful “tri-specific antibody”.

Dr Gary Nabel, the chief scientific officer at Sanofi and one of the report authors, told the BBC News website: “They are more potent and have greater breadth than any single naturally occurring antibody that’s been discovered.”

The best naturally occurring antibodies will target 90% of HIV strains.

“We’re getting 99% coverage, and getting coverage at very low concentrations of the antibody,” said Dr Nabel.

Experiments on 24 monkeys showed none of those given the tri-specific antibody developed an infection when they were later injected with the virus.

Dr Nabel said: “It was quite an impressive degree of protection.”

The work included scientists at Harvard Medical School, The Scripps Research Institute, and the Massachusetts Institute of Technology.

‘Exciting’

Clinical trials to test the antibody in people will start next year.

Prof Linda-Gail Bekker, the president of the International Aids Society, told the BBC: “This paper reports an exciting breakthrough.

“These super-engineered antibodies seem to go beyond the natural and could have more applications than we have imagined to date.

“It’s early days yet, and as a scientist I look forward to seeing the first trials get off the ground in 2018.

“As a doctor in Africa, I feel the urgency to confirm these findings in humans as soon as possible.”

Dr Anthony Fauci, the director of the US National Institute of Allergy and Infectious Diseases, said it was an intriguing approach.

He added: “Combinations of antibodies that each bind to a distinct site on HIV may best overcome the defences of the virus in the effort to achieve effective antibody-based treatment and prevention.”

Poliovirus Kills Off Cancer Cells Stops Tumor Regrowth

Original Article

By Ana Sandoiu

Researchers from Duke University in Durham, NC, may have discovered a new way of killing off cancer cells.

The team was jointly led by Dr. Matthias Gromeier, a professor in the Department of Neurosurgery, and Prof. Smita Nair, who is an immunologist in the Department of Surgery.

The new research – which is published in the journal Science Translational Medicine – shows how a modified poliovirus enables the body to use its own resources to fight off cancer. The modified virus bears the name of recombinant oncolytic poliovirus (PVS-RIPO).

PVS-RIPO has been in clinical trials since 2011 and preliminary results have offered hope to patients with one of the most aggressive forms of brain tumor: recurrent glioblastoma. So, the researchers set out to investigate more deeply how exactly PVS-RIPO works.

Explaining the rationale behind their research endeavor, Dr. Gromeier says, “Knowing the steps that occur to generate an immune response will enable us to rationally decide whether and what other therapies make sense in combination with poliovirus to improve patient survival.”

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Poliovirus attacks tumors, inhibits regrowth

The researchers examined the behavior of the poliovirus in two human cell lines: melanomaand triple-negative breast cancer. They observed that the poliovirus attaches itself to cancerous cells. These cells have an excess of the CD155 protein, which acts as a receptor for the poliovirus.

Then, the poliovirus starts to attack the malignant cells, triggering the release of antigens from the tumorAntigens are toxic substances that the body does not recognize, therefore setting off an immune attack against them.

So, when the tumor cells release antigens, this alerts the body’s immune system to start attacking. At the same time, the poliovirus infects the dendritic cells and macrophages.

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Dendritic cells are cells whose role it is to process antigens and “present” them to T cells, which are a type of immune cell. Macrophages are another type of immune cell – namely, large white blood cells whose main role is to rid our bodies of debris and toxic substances.

The cell culture results – which the researchers then verified in mouse models – showed that once PVS-RIPO infects the dendritic cells, these cells “tell” T cells to start the immune attack.

Once started, this process seems to be continuously successful. The cancer cells continue to be vulnerable to the immune system’s attack over a longer period of time, which appears to stop the tumor from regrowing.

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As Prof. Nair explains, “Not only is poliovirus killing tumor cells, it is also infecting the antigen-presenting cells, which allows them to function in such a way that they can now raise a T cell response that can recognize and infiltrate a tumor.”

“This is an encouraging finding, because it means the poliovirus stimulates an innate inflammatory response.”

Prof. Smita Nair

Speaking to Medical News Today about the clinical implications of the findings and the scientists’ directions for future research, Dr. Gromeier said, “Our findings provide clear rationales for moving forward with clinical trials in breast cancer, prostate cancer, and malignant melanoma.”

“This includes novel combination treatments that we will pursue,” he added.

More specifically, he explains, because the study revealed that after treatment with the poliovirus “immune checkpoints are increased on immune cells,” a future strategy the researchers plan to explore is “[oncolytic] poliovirus combined with immune checkpoint blockade.”

Studies of Pregnant Mice Highlight Link Between Immune Response and Autism

Original Article

A century ago, a largely forgotten, worldwide epidemic that would kill nearly a million people was beginning to take hold. Labelled as sleepy sickness — or more properly encephalitis lethargica — the disease caused a number of bizarre mental and physical symptoms and frequently left people in a catatonic state, sometimes for decades. (Oliver Sacks described his successful treatment of some of them in 1969, in the book Awakenings.) The cause has never been officially pinned down, but the most common suggestion is that some kind of infectious agent triggered an autoimmune response, which targeted and inflamed part of the brain.

The role of the immune system in mental disorders is subject to much important research at the moment. The onset of conditions from depression and psychosis to obsessive–compulsive disorder has been linked to the abrupt changes in biology and physiology that occur when the body responds to infection, especially in childhood. And some researchers have traced the possible chain of events back a generation. Studies have highlighted that pregnant women could react to infection in a way that influences their baby’s developing brain, which could lead to cognitive and neurodevelopmental problems in the child.

One consequence of this ‘maternal immune activation’ (MIA) in some women could be to increase the risk of autism in their children. And two papers published online this week in Nature (S. Kim et alNaturehttp://dx.doi.org/10.1038/nature23910; 2017 and Y. S. Yim et al. Naturehttp://dx.doi.org/10.1038/nature23909; 2017) use animal models to examine how this might happen, as well as suggest some possible strategies to reduce the risk.

Kim et al. looked at the impact of MIA on the brains and behaviour of mice. They found that pregnant female animals exposed to circumstances similar to a viral infection have offspring that are more likely to show atypical behaviour, and they unpick some of the cellular and molecular mechanisms responsible. Some of their results confirm what scientists already suspected: pregnancy changes the female mouse’s immune response, specifically, by turning on the production of a protein called interleukin-17a. But the authors also conducted further experiments that give clues about the mechanisms at work.

“It’s tempting to draw parallels with mechanisms that might increase the risk of autism in some people.”

The types of bacteria in the mouse’s gut seem to be important. When the scientists used antibiotics to wipe out common gut microorganisms called segmented filamentous bacteria in female mice, this seemed to protect the animals’ babies from the impact of the simulated infection. The offspring of mice given the antibiotic treatment did not show the unusual behaviours, such as reduced sociability and repetitive actions. Segmented filamentous bacteria are known to encourage cells to produce more interleukin-17a, and an accompanying News & Views article (C. M. Powell Nature http://dx.doi.org/10.1038/nature24139; 2017) discusses one obvious implication: some pregnant women could use diet or drugs to manipulate their gut micro­biome to reduce the risk of harm to their baby if an infection triggers their immune response. Much science still needs to be done before such a course could be recommended — not least further research to confirm and build on these results.

Yim et al. analysed the developing brain of mice born to mothers who showed MIA. They traced the abnormalities to a region called the dysgranular zone of the primary somato-sensory cortex (S1DZ). The authors genetically engineered the mice so that neurons in this region could be activated by light, and they showed that activation of S1DZ induced the same telltale atypical behaviours, even in mice that were born to mothers with no MIA.

It’s unusual to be able to demonstrate such a direct link between the activities of brain regions and specific behaviours — although plenty of work on mental disorders makes a strong theoretical case for linking particular conditions to over- and under-active brain zones and circuitry.

Encephalitis lethargica, for example, has been linked to changes in the deep regions of the basal ganglia, and the disease produces symptoms that are similar to those often seen in autism, including stereotyped and repetitive behaviours. Yim et al.’s study shows that the S1DZ region projects to one of those deep brain regions — the striatum — and that this connection helps to trigger repetitive actions in the animals. But S1DZ also connects to a separate, distinct, region in the cortex, and this is what seems to drive the changes in sociability.

Taking the two studies together, it’s tempting to draw parallels with mechanisms that might increase the risk of autism in some people and explain some of its symptoms. Scientists and others should be cautious about doing so — much can change when results from animal models are applied to human biology. But the studies do offer some intriguing leads.

Researchers Reverse the Negative Effects Of Adolescent Marijuana Use

Original Article

Researchers at Western University have found a way to use pharmaceuticals to reverse the negative psychiatric effects of THC, the psychoactive chemical found in marijuana. Chronic adolescent marijuana use has previously been linked to the development of psychiatric diseases, such as schizophrenia, in adulthood. But until now, researchers were unsure of what exactly was happening in the brain to cause this to occur.

“What is important about this study is that not only have we identified a specific mechanism in the prefrontal cortex for some of the mental health risks associated with adolescent  use, but we have also identified a mechanism to reverse those risks,” said Steven Laviolette, professor at Western’s Schulich School of Medicine & Dentistry.

In a study published online today in Scientific Reports the researchers demonstrate that adolescent THC exposure modulates the activity of a neurotransmitter called GABA in the  region of the brain. The team, led by Laviolette and post-doctoral fellow Justine Renard, looked specifically at GABA because of its previously shown clinical association with .

“GABA is an  and plays a crucial role in regulating the excitatory activity in the frontal cortex, so if you have less GABA, your neuronal systems become hyperactive leading to behavioural changes consistent with schizophrenia,” said Renard.

The study showed that the reduction of GABA as a result of THC exposure in adolescence caused the neurons in adulthood to not only be hyperactive in this part of the brain, but also to be out of synch with each other, demonstrated by abnormal oscillations called ‘gamma’ waves. This loss of GABA in the cortex caused a corresponding hyperactive state in the brain’s dopamine system, which is commonly observed in schizophrenia.

By using drugs to activate GABA in a rat model of schizophrenia, the team was able to reverse the neuronal and behavioural effects of the THC and eliminate the schizophrenia-like symptoms.

Laviolette says this finding is especially important given the impending legalization of marijuana in Canada. “What this could mean is that if you are going to be using marijuana, in a recreational or medicinal way, you can potentially combine it with compounds that boost GABA to block the negative effects of THC.”

The research team says the next steps will examine how combinations of cannabinoid chemicals with compounds that can boost the brains GABA system may serve as more effective and safer treatments for a variety of  disorders, such as addiction, depression and anxiety.