Alzheimer’s Prevention Starts with Marijuana, According to British Journal


A paper published by the British Journal of Pharmacology suggests that the chemical compounds in marijuana likely prevent the onset of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and age-related dementia.

Alzheimer's Disease includes reduced brain activity and function (red areas above), the result of years of accumulated damage. THC and CBD in marijuana seem to prevent this damage.

Alzheimer’s Disease includes reduced brain activity and function (red areas above), the result of years of accumulated damage. THC and CBD in marijuana seem to prevent this damage.

Chronic brain inflammation, oxidative stress, and intra-cellular dysfunction are the primary reasons why people develop these debilitating neurological diseases. The study found that both THC and CBD (the primary chemical compounds found in marijuana) positively affect nerve cell function in consumers, significantly reducing these harmful neurological conditions.

THC and CBD (called cannabinoids) tap into a primal, chemical signaling system in cells called “the endocannabinoid system.” The paper shows cannabinoids dampen inflammation, protect cells from oxidative damage, and promote cell health on a number of levels.

This paper echoes claims made in January by Gary Wenk, professor of neuroscience, immunology, and medical genetics at Ohio State University, that “if you do anything, such as smoke a bunch of marijuana in your 20s and 30s, you may wipe out all of the inflammation in your brain and then things start over again. And you simply die of old age before inflammation becomes an issue for you,”

The implications of marijuana’s medicinal effects on our brains are monumental, from not just a health perspective, but a financial one as well, for more than five million Americans with Alzheimer’s. One in three seniors will die with Alzheimer’s or another form of dementia, and Alzheimer’s is the sixth leading cause of death in the nation, costing the country about $203 billion in 2013.

Why Hasn’t Big Pharma Developed Mass Market Marijuana?


Significant obstacles discourage pharma companies from devoting the power needed to develop a patentable drug to take the plant’s place.

In the 1980s, scientists working for Pfizer set their sights on developing a drug for the pharmaceutical giant that would relieve hypertension and help save the lives of those suffering from angina. After years of tireless research by some of the best scientific minds money could buy, Pfizer created the chemical compound sildenafi l citrate in 1989. The company poured more money, time and talent into putting its new drug through clinical trials, only to discover sildenafi l citrate wasn’t very effective in treating heart problems. However, men taking the would-be heart medication reported increased erections, and Pfizer decided to spin the drug’s side effect into its main purpose. On March 27, 1998, the FDA approved sildenafi l citrate for public consumption under the brand name Viagra. Sale of the little blue pill swelled Pfizer’s bottom line, with the company reporting more than $2 billion in revenue in 2012, almost 15 years after the medicine’s market debut. The story of Viagra stands as one of the biggest successes in the history of commercial pharmaceuticals. With companies marketing drugs directly to consumers promising cures for almost anything, an increasingly destigmatized cannabis seems a likely target for the industry’s next game-changing medicine

But while the state-by-state legalization of medical (and recreational) cannabis has led to prescription-wielding patients availing themselves to strains of Purple Kush and Skywalker OG, significant obstacles discourage pharmaceutical companies from devoting the money and manpower needed to develop a marketable, patentable drug to take the plant’s place. Cannabis sits on the federal government’s list of Schedule I drugs—substances the government has deemed to have no medicinal value. For those tasked with creating new pharmaceuticals, this makes the already-laborious process of research and clinical trials even more arduous. The FDA, DEA and U.S. Public Health Service have to approve the release of cannabis to outside parties, and every bit of the plant has to be accounted for and secured, adding to the headache for those wanting to rake in a profit from pot. Even if a company created a drug, protecting the fruits of its labor with a patent is a dubious prospect at best. “You can’t take a plant and patent it,” Kenneth Kaitin, director of the Center for Drug Development at Tufts University, told Healthline in April 2015. “You’d have to have some sort of a process for isolating the active compound. But once you get away from product patents, the patent strength starts to diminish. Patents are progressively less and less of a protection because it’s a lot easier to reproduce a compound using a slightly different process.”

A few pharmaceutical companies outside of the United States have dipped their toes into turning cannabis into a product customers could find on the shelves of drugstores, most notably the British-based biofirm GW Pharmaceuticals. GW grows its cannabis in the U.K., where the legal restrictions have less of a stranglehold on researchers, and is in the processes of creating medicines based on that crop. Currently, the company’s cannabis extract mouth spray Sativex is in the final clinical trials in the U.S. for cancer-related pain. Sativex received a patent from the United States Patent and Trademark Office in 2013, in part thanks to the federal government not officially considering it cannabis (even though the spray contains both THC and CBD). If approved and marketed, Sativex would follow in the footsteps of Marinol, a pill containing THC that doctors have prescribed to AIDS and cancer patients suffering from loss of appetite, which the FDA approved in 1985. But getting Sativex into the hands (and mouths) of patients is still years away, and the broader market for medicinal marijuana products lies untapped. Whether anyone will brave the inhospitable business climate and hazy legality of cannabis to create the next Viagra remains a mystery.

In the 1980s, scientists working for Pfizer set their sights on developing a drug for the pharmaceutical giant that would relieve hypertension and help save the lives of those suffering from angina. After years of tireless research by some of the best scientific minds money could buy, Pfizer created the chemical compound sildenafi l citrate in 1989. The company poured more money, time and talent into putting its new drug through clinical trials, only to discover sildenafi l citrate wasn’t very effective in treating heart problems. However, men taking the would-be heart medication reported increased erections, and Pfizer decided to spin the drug’s side effect into its main purpose. On March 27, 1998, the FDA approved sildenafi l citrate for public consumption under the brand name Viagra. Sale of the little blue pill swelled Pfizer’s bottom line, with the company reporting more than $2 billion in revenue in 2012, almost 15 years after the medicine’s market debut. The story of Viagra stands as one of the biggest successes in the history of commercial pharmaceuticals. With companies marketing drugs directly to consumers promising cures for almost anything, an increasingly destigmatized cannabis seems a likely target for the industry’s next game-changing medicine.

weed-2016

A few pharmaceutical companies outside of the United States have dipped their toes into turning cannabis into a product customers could find on the shelves of drugstores, most notably the British-based biofirm GW Pharmaceuticals. GW grows its cannabis in the U.K., where the legal restrictions have less of a stranglehold on researchers, and is in the processes of creating medicines based on that crop. Currently, the company’s cannabis extract mouth spray Sativex is in the final clinical trials in the U.S. for cancer-related pain. Sativex received a patent from the United States Patent and Trademark Office in 2013, in part thanks to the federal government not officially considering it cannabis (even though the spray contains both THC and CBD). If approved and marketed, Sativex would follow in the footsteps of Marinol, a pill containing THC that doctors have prescribed to AIDS and cancer patients suffering from loss of appetite, which the FDA approved in 1985. But getting Sativex into the hands (and mouths) of patients is still years away, and the broader market for medicinal marijuana products lies untapped. Whether anyone will brave the inhospitable business climate and hazy legality of cannabis to create the next Viagra remains a mystery.

 

Researchers Find the 1st Possible Negative Side Effect of Marijuana Use in Adults.


Article Image

Man smoking a joint.

The stigma against marijuana in the US has been eroding for decades. But over the last ten years, use has skyrocketed. Since 2002, the number of Americans using the drug has almost doubled, according to a recent survey. In 2001, 4.1% said they had smoked marijuana within the past year. By 2014, 9.5% had done so. The number of patients using it to control the symptoms of an illness or disorder has risen substantially as well. Since it has been found far less dangerous that alcohol and other intoxicants, cannabis is quickly becoming the drug of choice for many Americans. New laws have allowed for medical marijuana in over half the states and recreational marijuana in about a half dozen.

Cannabis is also the most commonly used illicit drug in the world, according to the WHO. While opponents to liberalization often talk about it as a gateway drug, there is little evidence of this. In fact, scant data exists alleging that marijuana causes any damage whatsoever, if used in moderation, once the brain has stopped developing. But for chronic users, a new study imposes a harsh warning.

Researchers at Amen Clinics Inc. of California have found evidence that chronic use may increase the risk of Alzheimer’s. This is because it restricts blood flow to the regions of the brain where the condition takes root. Co-author Dr. Elisabeth Jorandby and colleagues recruited participants with marijuana use disorder. Around nine percent of users get addicted to cannabis. That’s a relatively low number.

Cannabis or marijuana use disorder is defined as using the drug chronically, even when it is clearly causing significant cognitive impairment. The symptoms may be mild, moderate, or severe, depending on the particular case. Chronic use is considered daily or near daily use. Those who habitually consume are more susceptible to psychiatric disorders.

Medical marijuana is available in 28 states in the US today. Seven states now allow the recreational kind, and many more cities across the nation have decriminalized pot.

In this study, published in the Journal of Alzheimer’s Disease, 982 current or former chronic users and 92 healthy controls underwent brain scans to evaluate blood flow there. Those diagnosed with cannabis use disorder showed a significant reduction in brain blood flow in almost every region. The hippocampus, which is where Alzheimer’s originates, saw the largest reduction. This is the area responsible for learning and memory.

Few previous studies have evaluated blood flow inside the brain as an effect of chronic marijuana use, researcher’s said. This was measured using single photon emission computed tomography (SPECT). Participants had their brains scanned while performing a task and while at rest. Reduced brain blood flow would cause less oxygen to travel to neurons, which could lead to tissue damage.

Blood flow was especially restricted in the right hippocampus. Researchers believe marijuana may affect memory formation due to this effect. The study suggests consistent marijuana use causes damage to the brain. Possible effects include memory formation disruption. Other studies have suggested that restricted blood flow to the hippocampus can increase the risk of Alzheimer’s.

More research will have to be conducted to corroborate this claim. But it’s reasonable that someone who only lights up occasionally won’t have such an issue. This study conflicts with a 2014 preclinical trial, also published in the Journal of Alzheimer’s Disease. There, tiny doses of marijuana’s active ingredient, delta 9-tetrahydrocannabinol (THC) had neuroprotective qualities. It helped ward off Alzheimer’s by destroying beta amyloid proteins which are what cause the disease. So in the end, it may be an issue of dosage. A little is okay, but too much is damaging. But only more studies can tell us for sure.

Marijuana compound removes toxic Alzheimer’s protein from the brain.


An active compound in marijuana called tetrahydrocannabinol (THC) has been found to promote the removal of toxic clumps of amyloid beta protein in the brain, which are thought to kickstart the progression of Alzheimer’s disease.

The finding supports the results of previous studies that found evidence of the protective effects of cannabinoids, including THC, on patients with neurodegenerative disease.

marijs_1024

“Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer’s, we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells,” says one of the team, David Schubert from the Salk Institute for Biological Studies in California.

Schubert and his colleagues tested the effects of THC on human neurons grown in the lab that mimic the effects of Alzheimer’s disease.

If you’re not familiar with this special little compound, it’s not only responsible for the majority of marijuana’s psychological effects – including the high – thanks to its natural pain-relieving properties, it’s also been touted as an effective treatment for the symptoms of everything from HIV and chemotherapy to chronic pain, post traumatic stress disorder, and stroke.

In fact, THC appears to be such an amazing medical agent, researchers are working on breeding genetically modified yeast that can produce it way more efficiently than it would be to make synthetic versions.

The compound works by passing from the lungs to the bloodstream, where it attaches to two types of receptors, cannabinoid receptor (CB) 1 and 2, which are found on cell surfaces all over the body.

In the brain, these receptors are most concentrated in neurons associated with pleasure, memory, thinking, coordination and time perception, and usually bind with a class of lipid molecules called endocannabinoids that are produced by the body during physical activity to promote cell-to-cell signalling in the brain.

But THC can also bind to them in much the same way, and when they do, they start messing with your brain’s ability to communicate with itself. The can be a good and a bad thing, because while you might forget something important or suddenly be incapable of swinging a baseball bat, you’ll probably feel amazing, and want to eat all the snacks

Over the years, research has suggested that by binding to these receptors, THC could be having another effect on ageing brains, because it appears to helps the body clear out the toxic accumulations – or ‘plaques’ – of amyloid beta.

No one’s entirely sure what causes Alzheimer’s disease, but it’s thought to result from a build-up of two types of lesions: amyloid plaques and neurofibrillary tangles.

Amyloid plaques sit between the neurons as dense clusters of beta-amyloid molecules – a sticky type of protein that easily clumps together – and neurofibrillary tangles are caused by defective tau proteins that clump up into a thick, insoluble mass in the neurons.

It’s not clear why these lesions begin to appear in the brain, but studies have linked inflammation in the brain tissue to the proliferation of plaques and neurofibrillary tangles. So if we can find something that eases brain inflammation while at the same time encourages the body to clear out these lesions, we could be on the way to finding the first effective treatment for Alzheimer’s ever.

Back in 2006, researchers at the Scripps Research Institute found that THC inhibits the formation of amyloid plaques by blocking the enzyme in the brain that produces them, and now Schubert and his team have demonstrated that it can also eliminate a dangerous inflammatory response from the nerve cells, ensuring their survival.

“Inflammation within the brain is a major component of the damage associated with Alzheimer’s disease, but it has always been assumed that this response was coming from immune-like cells in the brain, not the nerve cells themselves,” says one of the team, Antonio Currais.

“When we were able to identify the molecular basis of the inflammatory response to amyloid beta, it became clear that THC-like compounds that the nerve cells make themselves may be involved in protecting the cells from dying.”

It’s exciting stuff, but it’s so far only been demonstrated in neurons in the lab, so the next step will be for Schubert and his team to observe the link between THC and reduced inflammation and plaque build-up in a clinical trial. And they’ve reportedly already found a drug candidate called J147 that appears to have the same effects as THC, so this might be the way they can test the effects of THC without the government getting in the way.

It’s Official: Solar Is Becoming World’s Cheapest Form of New Electricity


For the first time, solar power is becoming the cheapest form of electricity production in the world, according to new statistics from Bloomberg New Energy Finance (BNEF) released Thursday.

While unsubsidized solar has occasionally done better than coal and gas in individual projects, 2016 marked the first time that the renewable energy source has out-performed fossil fuels on a large scale—and new solar projects are also turning out to be cheaper than new wind power projects, BNEF reports in its new analysis, Climatescope.

The cost of solar in 58 developing nations dropped to about a third of 2010 levels, with China in particular adding a record number of solar projects. And as the Independent notes, solar “has proved a godsend for remote islands such as Ta’u, part of America Samoa, in the South Pacific.”

In fact, Ta’u has been able to abandon the use of fossil fuels altogether and power itself almost entirely on renewable energy.

“Solar investment has gone from nothing—literally nothing—like five years ago to quite a lot,” said Ethan Zindler, head of BNEF’s U.S. policy analysis.

Disclosed capex for onshore wind and PV projects in 58 non-OECD countries.Bloomberg New Energy Finance

BNEF chairman Michael Liebreich also told investors this week that “[r]enewables are robustly entering the era of undercutting” fossil fuel prices.

Unsurprisingly, developing countries are at the forefront of this advancement, having invested in clean energy economies to stave off the catastrophic effects of climate change at a greater rate than wealthy nations.

“[F]or populations still relying on expensive kerosene generators, or who have no electricity at all, and for those living in the dangerous smog of thickly populated cities,” Bloomberg reports, “the shift to renewables and increasingly to solar can’t come soon enough.”

School replaces detention with meditation and goes an entire year with no suspensions


Baltimore’s Robert W. Coleman Elementary School has taken an interesting step in the way they handle trouble-making kids.  Any time a kid goes too far, they’re sent to the “Mindful Moment Room” where they undergo breathing exercises and talk through it with a councilor to reflect on what they did.

Strict parents and educators might want to reconsider their approach.

The room is decorated with bright colors, plush purple pillows to sit on, and lamps, making it stand out in contrast to a bland detention hall.

Since the program  has been initiated, the school has reported zero suspensions.

Sometimes when I get mad I just breathe deep… I just, like I picture me being in a certain place I like, and I just thought I could overcome everybody and then I just stop being mad…I think of being a bigger person and doing something maybe a wise man would do… I think of something that a stronger, a mentally stronger person would do.

If a kid’s good, but still wants to participate, they’re able to join an after-school program called Holistic Me, where they can learn mindfulness and yoga .

If kids misbehave at school, they get punished—it’s a system we’ve all come to accept as normal. But now, Baltimore’s Robert W. Coleman Elementary School is trying to change the system by replacing detention with meditation.

Students who act out in class are sent to the “Mindful Moment Room” to calm down with breathing exercises that help them reflect on their mistakes. This space is was decorated with bright colors, plush purple pillows to sit on, and lamps. It’s about as far from forcing kids to sit quietly in an empty classroom with their peers as you could get.

Of course, misbehaving isn’t the only way for students to get involved with meditation. In partnership with the Holistic Life Foundation, the elementary school also hosts an after-school program called Holistic Me to teach its students mindfulness and yoga.

Apparently, the school has already seen a change in attitudes, which has caused other nearby schools to adopt the program, too. According to Upworthy, Robert W. Coleman Elementary didn’t issue a single suspension last year. On the Holistic Life Foundation’s testimonial page, students say the program has helped them focus during tests, avoid fighting with their peers, and even to keep calm around their parents.

Here’s how one 5th grader explains it:

Sometimes when I get mad I just breathe deep… I just, like I picture me being in a certain place I like, and I just thought I could overcome everybody and then I just stop being mad…I think of being a bigger person and doing something maybe a wise man would do… I think of something that a stronger, a mentally stronger person would do.

JEREMY ENGLAND, THE MAN WHO MAY ONE-UP DARWIN


Because this guy could change the way we think about evolution — and faith.

 On a sunny afternoon, at a bustling cafe less than a mile from Stanford University’s campus, near Palo Alto, and more than 5,000 miles from his home, an assistant professor from MIT is telling me about science. Very advanced science. His name is Jeremy England, and at 33, he’s already being called the next Charles Darwin.

Say what?

In town to give a lecture, the Harvard grad and Rhodes scholar speaks quickly, his voice rising a few pitches in tone, his long-fingered hands making sudden jerks when he’s excited. He’s skinny, with a long face, scraggly beard and carelessly groomed mop of sandy brown hair — what you might expect from a theoretical physicist. But then there’s the street-style Adidas on his feet and the kippah atop his head. And the fact that this scientist also talks a lot about God.

EVERY 30 YEARS OR SO WE EXPERIENCE THESE GIGANTIC STEPS FORWARD. …AND THIS MIGHT BE IT.

Carl Franck, a Cornell physics professor

The 101 version of his big idea is this: Under the right conditions, a random group of atoms will self-organize, unbidden, to more effectively use energy. Over time and with just the right amount of, say, sunlight, a cluster of atoms could come remarkably close to what we call life. In fact, here’s a thought: Some things we consider inanimate actually may already be “alive.” It all depends on how we define life, something England’s work might prompt us to reconsider. “People think of the origin of life as being a rare process,” says Vijay Pande, a Stanford chemistry professor. “Jeremy’s proposal makes life a consequence of physical laws, not something random.”

England’s idea may sound strange, even incredible, but it’s drawn the attention of an impressive posse of high-level academics. After all, while Darwinism may explain evolution and the complex world we live in today, it doesn’t account for the onset of intelligent beings. England’s insistence on probing for the step that preceded all of our current assumptions about life is what makes him stand out, says Carl Franck, a Cornell physics professor, who’s been following England’s work closely. “Every 30 years or so we experience these gigantic steps forward,” Franck says. “We’re due for one. And this might be it.”

And all from a modern Orthodox Jew with fancy sneakers.

****

Before England became a religious man — he prays three times a day — he was a scientist. From the time he could read, he devoured books on subjects from philosophy to music to fantasy. By 9 he was plowing his way through Stephen Hawking’s opus, A Brief History of Time . “He couldn’t comprehend it, but he tried really hard,” says his father, Richard England, an economics professor at the University of New Hampshire. Yes, Dad is an economics professor and Mom a public school teacher, and the couple took their two children to museums and to visit the Harvard campus, just a few hours from their small seacoast town. But the elder England contends his son’s upbringing doesn’t begin to explain his intellectual curiosity.

Or England’s long timeline of asking big questions. Over drinks some years ago, a childhood friend reminded him of a time that young Jeremy turned to him out of nowhere and reflected: “You know, Adam, if the dinosaurs can go extinct, then so can we.” England was 3 then. For his part, England says it wasn’t until he hit about 7 that he felt a sense of anxiety about “not knowing enough.” That anxiety would compel him through an almost comical list of academic bastions — Harvard, Oxford, Stanford and Princeton, and now, a 3-year-old teaching gig at MIT.

Still, God wasn’t a big player for England during most of his early life. While his mom is Jewish — his dad was raised Lutheran but never felt strongly about passing on his Protestant ties — there wasn’t a lot of religious talk while he was growing up. The Englands would share a festive meal for Passover and light candles for Hanukkah, but the family didn’t keep a Bible in the home. His mother, England says, was born in Poland in 1947 to a family ravaged by the Holocaust. Much of her extended family — including her grandparents — were killed by the Nazis, and in the wake of such destruction, England says, Judaism brought up negative, painful feelings for her; she distanced herself.

It seems ironic, then, that anti-Semitism would eventually push England to the faith he says his mother spurned. While studying at Oxford in the early 2000s, he faced his first anti-Israel sentiment from classmates — which got him, in expected fashion, reading books and picking people’s brains to figure out where he stood on the issue. And in 2005, he visited Israel for the first time — where he “fell in love.” Studying the Torah provided an opportunity for intellectual engagement that he says was “unlike anything I had ever experienced in terms of subtlety and grandeur of scope.”

Back in Palo Alto, between meeting with Berkeley professors and Stanford students, England reboots his computer to show me a simulation he’s been working on, meanwhile explaining that his lab is less test tubes and white coats than blackboards and computers screens. Jet-setting across the country to talk about his theories isn’t England’s usual routine. That, he says, looks more like dirty diapers, brainstorming atop a yoga ball with his infant son, working with students and plugging data into formulas.

England didn’t begin with number-crunching, though. During his postdoc research on embryonic development, he kept coming back to the question: What qualifies something as alive or not? He later superimposed an analytical rigor to that question, publishing an equation in 2013 about how much energy is required for self-replication to take place. For England, that investigation was only the beginning. “I couldn’t stop thinking about it,” he says, his normally deep voice rising until eventually cracking. “It was so frustrating.” Over the next year, he worked on a second paper, which is under peer review now. This one took his past findings and used them to explain theoretically how, under certain physical circumstances, life could emerge from nonlife.

In the most basic terms, Darwinism and the idea of natural selection tell us that well-adapted organisms evolve in order to survive and better reproduce in their environment. England doesn’t dispute this reasoning, but he argues that it’s too vague. For instance, he says, blue whales and phytoplankton thrive in the same environmental conditions — the ocean — but they do so by vastly different means. That’s because that while they’re both made of the same basic building blocks, strings of DNA are arranged differently in each organism.

Now take England’s simulation of an opera singer who holds a crystal glass and sings at a certain pitch. Instead of shattering, England predicts that over time, the atoms will rearrange themselves to better absorb the energy the singer’s voice projects, essentially protecting the glass’s livelihood. So how’s a glass distinct from, say, a plankton-type organism that rearranges it self over several generations? Does that make glass a living organism?

These are pretty things to ponder. Unfortunately, England’s work hasn’t yet provided any answers, leaving the professor in a kind of speculative state as he doggedly tries to put numbers to it all. “He hasn’t put enough cards on the table yet,” Franck says. “He’ll need to make more testable predictions.” So it remains to be seen where England will land in the end. Other scientists have made similar claims about energy dissipation in the context of non-equilibrium thermodynamics, but none has found a definitive means for applying this science to the origin of life.

So what does God have to do with all this? In his quest for answers, England, of course, finds himself at the center of the classic struggle between science and spirituality. While Christianity and Darwinism are generally opposed, Judaism doesn’t take issue with the science of life. The Rabbinical Council of America even takes the stance that “evolutionary theory, properly understood, is not incompatible with belief in a Divine Creator.”

For his part, England believes science can give us explanations and predictions, but it can never tell us what we should do with that information. That’s where, he says, the religious teachings come in. Indeed, the man who’s one-upping Darwin has spent the past 10 years painstakingly combing through the Torah, interpreting it word by word much the way he ponders the meaning of life. His conclusion? Common translations are lacking. Take the term “creation.” England suggests we understand it not as the literal making of the Earth but rather as giving Earth a name. All throughout the Bible, he says, there are examples of terms that could be interpreted differently from what we’ve come to accept as standard.

That even applies to some of the good book’s most famous players, like Joseph, the ancient biblical interpreter of dreams, who rose to become the most powerful man in Egypt after the pharaoh. Maybe, England suggests, he wasn’t a fortune-teller. Maybe he was a scientist.

Canadian Doctors Can Now Legally Prescribe Heroin To Patients With Opioid Addiction


While activists and healthcare professionals continue to fight for the legalization of marijuana, or at least its rescheduling, prescription heroin is now legal in all of Canada as a way to manage addiction.

The quiet approval by the Canadian government is already in effect and have made the dealings of Crosstown, a clinic that has a heroin-maintenance program, completely legal and regulated. The clinic is the first of its kind to have this type of program in North America, but it follows the structure of other clinics in some European nations.

The use of medical-grade heroin is only allowed for patients who have a severe addiction to opioids and have not responded to other traditional treatments. Canada’s health department, Health Canada, said this of the decision:

“A number of countries have allowed doctors to use diacetylmorphine-assisted treatment to support the small percentage of patients with opioid dependence who have not responded to other treatment options. There is also a significant body of scientific evidence supporting its use.”

Diacetylmorphine is the name for pharmaceutical-grade heroin and health practitioners and medical facilities can now apply to use the substance in their facility. Physicians will have to apply to Health Canada to be allowed to use the heroin, and nurses will have to inject the drug into the patient 2-3 times per day.

Opponents of the new law have pointed out that treating addicts in this way will not help their condition because the objective isn’t to ween them off over time; instead, it’s to keep addicts controlled when all else fails and physicians believe that the patient can’t be helped.

While it’s easy to oppose the treatment, proponents are typically the healthcare professionals that actually treat these patients and understand what they’re working with. Scott MacDonald, the lead physician at the Crosstown Clinic, has been treating patients since 2005 and his clinic sees 52 patients regularly, operating a court-ordered exemption before the law was passed. MacDonald says some of the people he sees have been addicted to heroin for over 50 years and that traditional treatments have failed numerous times on them.

 

Other positives for the treatment include patients appearing to be healthier, and their participation in the program significantly decreases their involvement in criminal activities, as they no longer need to get their fix somewhere else.

Still, in general heroin treatments are just as addicting as the drug itself. An anonymous person spoke on Wednesday about being on methadone on Humans of New York and said,

“It doesn’t get you high like heroin, but it takes away the urges. But it’s like liquid handcuffs because the withdrawals are just as bad. If I stop for twenty-four hours, it feels like fire in my bones. And they only give you one dose at a time. So I get to the clinic every morning at 6am, and there are already one hundred people in line.”

On Prime Minister Justin Trudeau’s agenda is to also make marijuana legal by next year; he already has a special team to determine how it will be regulated, sold, and taxed. Marijuana has also proven to be an effective treatment in opioid addiction.

Neurometabolic Disorders Could Contribute to Depression


Impairments in the production of neurotransmitters may lead to depression in some patients, preliminary results show, opening new avenues for research..

Deficiencies in key compounds that help the body make neurotransmitters may contribute to the intractability of depression in some people.

In 2002, psychiatrist Lisa Pan, a depression and suicide prevention researcher at the University of Pittsburgh Medical Center (UPMC), met Kyle, a 19-year-old suffering from depression (name altered to preserve confidentiality). He was among the estimated 15 percent of depression patients in the U.S. for whom treatments such as antidepressants or therapy do not help. He “had been through every available treatment” including electroconvulsive therapy, but nothing worked, Pan recalls. “At one time, he was on 17 medications simultaneously.” The teenager had attempted suicide, and doctors determined that he was at risk for similar episodes. The next step for him would be state hospitalization.

Having exhausted conventional treatment options, Pan went off script. She enlisted a colleague at UPMC, geneticist David Finegold, to run tests on Kyle’s neurometabolic system, which supplies nutrients necessary to maintain neurons with a healthy supply of neurotransmitters. The tests revealed that Kyle underproduced tetrahydrobiopterin (BH4), a necessary cofactor for enzymes involved in making serotonin, dopamine, and other compounds that modulate emotions and mood. Pan gave him sapropterin, a synthetic form of BH4, to bring his system back into balance. “It took some time, but he got better,” she says. Kyle left the hospital and went on to graduate from college.

“We felt like we might be onto something,” Pan says. She began exploring the possibility that metabolic imbalances affected others for whom standard depression treatment had failed. She and her colleagues conducted an array of blood, urine, and cerebrospinal fluid tests in 33 such individuals, each of whom had shown negligible response to at least three different maximum-dose depression medications administered for six weeks or more. Ranging from teenagers to middle-age adults, the group included some who also suffered post-traumatic stress disorder (PTSD), anxiety, or attention deficit hyperactivity disorder (ADHD).

When the tests came back, about a third of the patients showed a deficiency in the levels of folate in their spinal fluid, another key compound for producing a variety of neurotransmitters. Taking a folate supplement to correct this imbalance improved patients’ depression symptoms, lowering their scores on a questionnaire for suicidal thinking and another for mental and physical signs of depression. And Pan says that as each patient continued to take the supplement, their symptoms continued to improve (Am J Psych, appiajp201615111500, 2016).

Since the publication of these results, “we have gotten hundreds of phone calls from people just asking for help,” she says. As Pan returns these calls, she explains that her findings are preliminary. Her study documents relatively few individual treatment outcomes and is not a formal clinical trial. As the study continues and expands to include more patients, Pan and her colleagues will work to identify the cause of folate deficiency and to investigate whether folate supplementation could become a standard treatment. But these results suggest that treating an underlying neurometabolic imbalance can alleviate depression at least in some cases, which should open a door to new research. Receiving the influx of phone calls “makes me want to work more,” Pan says.

Characterizing depression in broad strokes is almost impossible, cautions David Brent, a former advisor to Pan and coauthor on the study. “There are a lot of people who look the same that probably have very different causes” of depression. Other psychological conditions, including PTSD and anxiety, frequently coincide with and complicate the disorder. “We’re really just at the beginning of extricating” these interacting factors, Pan says, and at this stage, developing solutions that can be standardized for treating many people is difficult.

Even so, Finegold notes that preliminary studies like this one have a way of offering hope to people who have not found a successful depression treatment. He, too, receives phone calls from people living with depression, and some express their gratitude simply to know that new aspects of the problem are being explored.

One avenue of Pan’s further exploration is to search for genetic markers associated with neurometabolic imbalances. Ideally, genetic testing could be used alongside traditional clinical evaluations to provide physicians with as much patient information as possible, says coauthor David Peters, a geneticist at UPMC. Testing spinal fluid is invasive and time-consuming; a quick DNA swab is much more practical, and Peters says incorporating genetic testing is a “very exciting prospect.”

Every six months or so, Pan checks in with Kyle. Having graduated college, he now works in environmental science, and the only medication he takes is sapropterin. In a statement he authorized her to share, Kyle says, “It’s safe to say that I owe my life to the successful diagnosis.”

Research could lead to blood test to detect Creutzfeldt-Jakob disease


CJD research
Prion proteins are visualized with immunostaining in this tissue sample from a tonsil biopsy in from a patient variant CJD. 

The detection of prions in the blood of patients with variant Creutzfeldt-Jakob disease (vCJD) could lead to a noninvasive diagnosis prior to symptoms and a way to identify prion contamination of the donated blood supply, according to researchers at McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth).

The results of the research, led by senior author Claudio Soto, MD, professor in the Department of Neurology and the director of the George and Cynthia Mitchell Center for Alzheimer’s disease and Related Brain Disorders at UTHealth, are published in Science Translational Medicine. First author of the paper is Luis Concha-Marambio, senior research assistant in the Department of Neurology at McGovern Medical School.

CJD research

Claudio Soto, PhD, in his lab at McGovern Medical School at UTHealth.

“Our findings, which need to be confirmed in further studies, suggest that our method of detection could be useful for the noninvasive diagnosis of this disease in pre-symptomatic individuals,” Soto said. “Early diagnosis would allow any potential therapy to be given before substantial brain damage has occurred. In the case of the blood supply, availability of a procedure to efficiently detect small quantities of the infectious agent would allow removal of blood units contaminated with prions, so that new cases can be minimized substantially.”

Human prion diseases are infectious and invariably fatal neurodegenerative diseases. They include sporadic Creutzfeldt-Jakob disease (sCJD), the most common form, and variant Creutzfeldt-Jakob disease, which is caused by the transmission of bovine spongiform encephalopathy—commonly known as mad cow disease—from infected cattle to humans.

Since 1990, 178 people in the United Kingdom have died from vCJD, according to the National CJD Research & Surveillance Unit at the University of Edinburgh. The disease has claimed an additional 49 people worldwide, including four United States residents, according to the European Centre for Disease Prevention and Control. In a handful of cases, the disease was spread through the donated blood supply.

The disease can lay silent in the body for decades as damage slowly builds in the brain from the misfolded infectious proteins called prions. On average, people infected with vCJD die two years after the development of the first symptoms, which can include psychiatric alterations such as depression, anxiety and hallucinations that progress to more severe dementia, muscle contractions and loss of coordination.

Soto’s team analyzed blood samples from 14 cases of vCJD and 153 controls, which included patients affected by sCJD and other neurodegenerative or neurological disorders as well as healthy subjects. To detect the prions, the team used a protein misfolding cyclic amplification assay, invented in Soto’s lab, which mimics the prion replication process in vitro that occurs in prion disease.

The results showed that prions could be detected with 100 percent sensitivity and specificity in blood samples from vCJD patients.

The new study builds on years of research by Soto’s team, whose detection of prions in urine was published in the New England Journal of Medicine in August 2014. In June of this year, Soto received $11 million (USD) from the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health (U.S.), to study the pathogenesis, transmission and detection of prion diseases including chronic wasting disease in deer.

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