We are living in an era of a viral pandemic, COVID-19, in which viral particles are spread through the air from one person to another. Numerous scientific studies show that if most people even simple cloth face masks while near each other, this dramatically reduced the viral particles in the air, and increases safety. The effect of wearing masks is so effective that in areas where people follow social distancing & mask rules, the incidence of COVID is shrinking.
However, there has been a growing resistance to wearing a mask, fueled by conspiracy theories, pseudoscience, and Russian social media troll farms deliberately spreading misinformation. It now appears that millions of Americans believe that wearing a face mask is unhealthy.
Many of us have met individuals who claimed that face masks either “block oxygen from getting in” or “make us breathe carbon monoxide.” Both claims are literally impossible, yet widely believed. So if we have a student make such a claim then how can we turn this into a teachable moment?
Addressing the “air can’t get through the mask” claim
Conspiracy theorists try to have it both ways: They claim that the virus particles are so small that they can get through the mask (and supposedly, therefore would make us sick) yet also claim that the oxygen molecules are too large to pass through the mask, so we (supposedly) get low oxygen and brain damage.
The obvious problem is that the virus particle is over 250 times larger than an oxygen molecule! The covid molecule is 0.125 microns while an O2 molecule is only 0.0005 microns.
Also, to be clear, single viral particles don’t make people sick. The disease is only spread if people inhale multiple exhalation water-virus droplets, each drop let being thousands of times larger than a viral particle, and each drop containing at least many hundreds of viral particles each. And these drops are what the masks are pretty good at filtering.
First off, even without a virus, your body automatically adapts to lower levels of oxygen in the air. If that weren’t the case then anyone who visited a high altitude city like Denver, Colorado, would have died! As we all know, up in Denver the air is thinner, so there are a lot less O2 molecules around. But we adjust, and as long as we don’t play NFL caliber football for an hour, we’re just fine.
The other claim is that these face masks “trap our breath” preventing us from getting oxygen, so that our O2 blood levels fall. But see for yourself – they don’t do that!
Photo credit. Dr. Megan Hall
Dr. Megan Hall writes:
Below is me in 4 scenarios. I wore each mask for 5 minutes and checked my oxygen saturation (shown as the percentage below) along with my heart rate (HR, in beats per minute) using noninvasive pulse oximetry. Keep in mind, immediately prior to this, I had been wearing the surgical mask for 5 hours.
No mask: 98%, HR 64
Surgical mask: 98%, HR 68
N95 mask: 99%, HR 69
N95 plus surgical mask (which is how most healthcare providers are wearing masks): 99%, HR 69.
Finally, if “breathing in your own breath is dangerous” then how come it was perfectly safe – and sometimes necessary! – to perform CPR with mouth to mouth resuscitation?
The air that a person exhales has more than enough O2 to keep someone else alive, and there never was any concern about CO (carbon monoxide) or CO2 from our exhalation harming someone else.
How well do masks work?
They don’t need to stop all droplets. COVID is dangerous not because some particles are airborne (thats true for tons of viruses) but because (a) it transmits more easily, and (b) causes more damage. When we reduce the number of droplets released, then the spread of covid significantly decreases.
Here is a video from Dr. Joe Hanson, from “It’s ok to be smart.” It is an awesome, slow-motion schlieren imaging experiment that demonstrates why masks work.
Oran, Daniel P., and Eric J. Topol. “Prevalence of Asymptomatic SARS-CoV-2 Infection: A Narrative Review.” Annals of Internal Medicine (2020). https://doi.org/10.7326/M20-3012
Chu, Derek K., et al. “Physical distancing, face masks, and eye protection to prevent person-to-person transmission of SARS-CoV-2 and COVID-19: a systematic review and meta-analysis.” The Lancet (2020). https://doi.org/10.1016/S0140-6736(20)31142-9
Stadnytskyi, Valentyn, et al. “The airborne lifetime of small speech droplets and their potential importance in SARS-CoV-2 transmission.” Proceedings of the National Academy of Sciences 117.22 (2020): 11875-11877. https://doi.org/10.1073/pnas.2006874117
Cheng, Vincent CC, et al. “The role of community-wide wearing of face mask for control of coronavirus disease 2019 (COVID-19) epidemic due to SARS-CoV-2.” Journal of Infection (2020). https://doi.org/10.1016/j.jinf.2020.04.024
Eikenberry, Steffen E., et al. “To mask or not to mask: Modeling the potential for face mask use by the general public to curtail the COVID-19 pandemic.” Infectious Disease Modelling (2020). https://doi.org/10.1016/j.idm.2020.04.001
Davies, Anna, et al. “Testing the efficacy of homemade masks: would they protect in an influenza pandemic?.” Disaster medicine and public health preparedness 7.4 (2013): 413-418. https://dx.doi.org/10.1017%2Fdmp.2013.43
In 2001, a major study of human activity patterns found that people in the US spend roughly 90 percent of their time indoors. It is safe to say that, in the age of Covid-19, that number is even higher. (Here in the Roberts household, it feels like we’ve hit 105 percent.)
We also do most of our breathing inside. So it’s a little odd that we don’t think more about indoor air quality. Outdoor air is the subject of titanic legal and regulatory battles going back decades. The six common air pollutants covered by the Clean Air Act — ground-level ozone, particulate matter, carbon monoxide, lead, sulfur dioxide (SO2), and nitrogen dioxide (NO2) — have fallen an average of 74 percent since the Act was passed in 1970.
Yet here’s the doozy:The Environmental Protection Agency (EPA) warns that “studies of human exposure to air pollutants indicate that indoor levels of pollutants may be two to five times — and occasionally more than 100 times — higher than outdoor levels.”
When historians tally up the many missteps policymakers have made in response to the coronavirus pandemic, the senseless and unscientific push for the general public to avoid wearing masks should be near the top.
The evidence not only fails to support the push, it also contradicts it. It can take a while for official recommendations to catch up with scientific thinking. In this case, such delays might be deadly and economically disastrous.
It’s time to make masks a key part of our fight to contain, then defeat, this pandemic. Masks effective at “flattening the curve” can be made at home with nothing more than a T-shirt and a pair of scissors. We should all wear masks — store-bought or homemade — whenever we’re out in public.
At the height of the HIV crisis, authorities did not tell people to put away condoms. As fatalities from car crashes mounted, no one recommended avoiding seat belts. Yet in a global respiratory pandemic, people who should know better are discouraging Americans from using respiratory protection.
… There are good reasons to believe DIY masks would help a lot. Look at Hong Kong, Mongolia, South Korea and Taiwan, all of which have covid-19 largely under control. They are all near the original epicenter of the pandemic in mainland China, and they have economic ties to China.
Yet none has resorted to a lockdown, such as in China’s Wuhan province. In all of these countries, all of which were hit hard by the SARS respiratory virus outbreak in 2002 and 2003, everyone is wearing masks in public.
George Gao, director general of the Chinese Center for Disease Control and Prevention, stated, “Many people have asymptomatic or presymptomatic infections. If they are wearing face masks, it can prevent droplets that carry the virus from escaping and infecting others.”
My data-focused research institute, fast.ai, has found 34 scientific papers indicating basic masks can be effective in reducing virus transmission in public — and not a single paper that shows clear evidence that they cannot.
Studies have documented definitively that in controlled environments like airplanes, people with masks rarely infect others and rarely become infected themselves, while those without masks more easily infect others or become infected themselves.
Masks don’t have to be complex to be effective. A 2013 paper tested a variety of household materials and found that something as simple as two layers of a cotton T-shirt is highly effective at blocking virus particles of a wide range of sizes.
Oxford University found evidence this month for the effectiveness of simple fabric mouth and nose covers to be so compelling they now are officially acceptable for use in a hospital in many situations. Hospitals running short of N95-rated masks are turning to homemade cloth masks themselves; if it’s good enough to use in a hospital, it’s good enough for a walk to the store.
The reasons the WHO cites for its anti-mask advice are based not on science but on three spurious policy arguments.
First, there are not enough masks for hospital workers.
Second, masks may themselves become contaminated and pass on an infection to the people wearing them.
Third, masks could encourage people to engage in more risky behavior.
None of these is a good reason to avoid wearing a mask in public.
Yes, there is a shortage of manufactured masks, and these should go to hospital workers. But anyone can make a mask at home by cutting up a cotton T-shirt, tying it back together and then washing it at the end of the day. Another approach, recommended by the Hong Kong Consumer Council, involves rigging a simple mask with a paper towel and rubber bands that can be thrown in the trash at the end of each day.
… the idea that masks encourage risky behavior is nonsensical. We give cars anti-lock brakes and seat belts despite the possibility that people might drive more riskily knowing the safety equipment is there. Construction workers wear hard hats even though the hats presumably could encourage less attention to safety. If any risky behavior does occur, societies have the power to make laws against it.
Experts said the choir outbreak is consistent with a growing body of evidence that the virus can be transmitted through aerosols — particles smaller than 5 micrometers that can float in the air for minutes or longer.
The World Health Organization has downplayed the possibility of transmission in aerosols, stressing that the virus is spread through much larger “respiratory droplets,” which are emitted when an infected person coughs or sneezes and quickly fall to a surface.
But a study published March 17 in the New England Journal of Medicine found that when the virus was suspended in a mist under laboratory conditions it remained “viable and infectious” for three hours — though researchers have said that time period would probably be no more than a half-hour in real-world conditions.
the question of whether or not the coronavirus can be “airborne” is extremely contentious right now — and it’s a question that has real implications for what people should do to avoid getting infected.
… a committee of independent experts convened by the National Academies of Sciences, Engineering, and Medicine has weighed in, in response to a question from the White House Office of Science and Technology Policy about whether the virus “could be spread by conversation in addition to sneeze/cough-induced droplets.”
“Currently available research supports the possibility that SARS-CoV-2 could be spread via bioaerosols generated directly by patients’ exhalation,” says a letter from the committee chair. By bioaerosols, they are referring to fine particles emitted when someone breathes that can be suspended in the air rather than larger droplets produced through coughs and sneezes.
Even if additional research shows that any virus in such tiny particles is viable, researchers still won’t how much of it would need to be inhaled to make someone sick. But the committee experts also caution that uncertainty about all this is almost a given—because there’s currently no respiratory virus for which we know the exact proportion of infections that come from breathing the virus in versus coming into contact with droplets in the air or on surfaces.
“I personally think that transmission by inhalation of virus in the air is happening,” says Linsey Marr, an aerosol scientist at Virginia Tech. But she says so far, health experts have largely discounted the possibility of transmitting this coronavirus in this way.
“From an infection prevention perspective, these things are not 100% black and white. The reason why we say ‘droplet’ versus ‘airborne’ versus ‘contact’ is to give overall guidance on how to manage patients who are expected to be infectious with a specific pathogen,” said Dr. Hanan Balkhy, assistant director-general for antimicrobial resistance at WHO, in an interview with NPR earlier this week.
As an expert who worked to contain an outbreak of the deadly MERS coronavirus in Saudi Arabia, she believes that this new virus should behave similarly to other severe coronaviruses — and that means, unless health-care workers are doing invasive procedures like putting in breathing tubes, the virus is expected to primarily spread through droplets.
Droplets are larger respiratory particles that are 5 to 10 micrometers in size. Those are considered “big,” even though a 5 micrometer particle would still be invisible to the naked eye. Traditionally, those droplets are thought to not travel more than about three feet or so after exhalation. That would mean the virus can only spread to people who get close to an infected person or who touch surfaces or objects that might have become contaminated by these droplets. This is why public health messages urge people to wash their hands and stand at least 6 feet away from other people.
An “airborne” virus, in contrast, has long been considered to be a virus that spreads in exhaled particles that are tiny enough to linger in the air and move with air currents, letting them be breathed in by passersby who then get sick. Measles is a good example of this kind of virus — an exhaled measles pathogen can hang suspended in a room for a couple hours after an infected person leaves.
The reality of aerosol generation, however, is far more complex than this “droplet” versus “airborne” dichotomy would suggest, says Marr. People produce a wide range of different-sized particles of mucus or saliva. These particles get smaller as they evaporate in the air and can travel different distances depending on the surrounding air conditions.
“The way the definitions have been set up, this “droplet” vs “airborne” distinction, was first established in the 1950s or even earlier,” says Marr. “There was a more limited understanding of aerosol science then.”
Even a 5 micrometer droplet can linger in the air. “If the air were perfectly still, it would take a half hour to fall from a height of 6 feet down to the ground. And, of course, the air isn’t perfectly still,” says Marr. “So it can easily be blown around during that time and stay in the air for longer or shorter.”
What’s more, coughs and sneezes create turbulent clouds of gas that can propel respiratory particles forward.
“For symptomatic, violent exhalations including sneezes and coughs, then the droplets can definitely reach much further than the 1 to 2 meter [3 to 6 feet] cutoff,” says Lydia Bourouiba, an infectious disease transmission researcher at MIT, referring to the distance typically cited as safe for avoiding droplet-carried diseases.
In fact, studies show that “given various combinations of an individual patient’s physiology and environmental conditions, such as humidity and temperature, the gas cloud and its payload of pathogen-bearing droplets of all sizes can travel 23 to 27 feet,” she wrote in a recent article published online by the Journal of the American Medical Association.
…. Some of the strongest evidence that an airborne route of transmission might be possible for this virus comes from a report published last month by the New England Journal of Medicine that described mechanically generating aerosols carrying the SARS-CoV-2 virus in the laboratory. It found that the virus in these little aerosols remained viable and infectious throughout the duration of the experiment, which lasted 3 hours.
WHO mentioned this study in its recent review of possible modes of transmission and noted that “this is a high-powered machine that does not reflect normal human cough conditions … this was an experimentally induced aerosol-generating procedure.”
It may have been artificial, says Marr, but “the conditions they used in that laboratory study are actually less favorable for survival compared to the real world. So it’s more likely that the virus can survive under real world conditions.”
Lydia Bourouiba, JAMA insights, March 26, 2020. doi:10.1001/jama.2020.4756
Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1
March 17, 2020 , DOI: 10.1056/NEJMc2004973
A novel human coronavirus that is now named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (formerly called HCoV-19) emerged in Wuhan, China, in late 2019 and is now causing a pandemic. We analyzed the aerosol and surface stability of SARS-CoV-2 and compared it with SARS-CoV-1, the most closely related human coronavirus.
… We found that the stability of SARS-CoV-2 was similar to that of SARS-CoV-1 under the experimental circumstances tested. This indicates that differences in the epidemiologic characteristics of these viruses probably arise from other factors, including high viral loads in the upper respiratory tract and the potential for persons infected with SARS-CoV-2 to shed and transmit the virus while asymptomatic.
Our results indicate that aerosol and fomite transmission of SARS-CoV-2 is plausible, since the virus can remain viable and infectious in aerosols for hours and on surfaces up to days (depending on the inoculum shed).
These findings echo those with SARS-CoV-1, in which these forms of transmission were associated with nosocomial spread and super-spreading events, and they provide information for pandemic mitigation efforts.
Neeltje van Doremalen, Ph.D., Trenton Bushmaker, B.Sc.
National Institute of Allergy and Infectious Diseases, Hamilton, MT
Dylan H. Morris, M.Phil., Princeton University, Princeton, NJ, Myndi G. Holbrook, B.Sc.
National Institute of Allergy and Infectious Diseases, Hamilton, MT
Amandine Gamble, Ph.D.
University of California, Los Angeles, Los Angeles, CA
Brandi N. Williamson, M.P.H.
National Institute of Allergy and Infectious Diseases, Hamilton, MT
Azaibi Tamin, Ph.D., Jennifer L. Harcourt, Ph.D.
Natalie J. Thornburg, Ph.D., Susan I. Gerber, M.D.
Centers for Disease Control and Prevention, Atlanta, GA
James O. Lloyd-Smith, Ph.D.
University of California, Los Angeles, Los Angeles, CA, Bethesda, MD
Emmie de Wit, Ph.D., Vincent J. Munster, Ph.D.
National Institute of Allergy and Infectious Diseases, Hamilton, MT
Aesthetic judgements of physical attractiveness – beauty – are not arbitrary. Scientific studies show that they are are related to biology and healthy, which is often manifested as facial symmetry.
In physical attractiveness studies, “averageness” describes the physical beauty that results from averaging the facial features of people of the same gender and approximately the same age. This is often called the “averageness-effect.”
Studies use photographic overlays of human faces, in which images are morphed together.
The term “average” here is a mathematical definition = arithmetic mean, = the sum of a collection of numbers divided by the count of numbers in the collection.
It turns out that an averaged face is not unremarkable, but is, in fact, quite good looking.
Image from Koinophilia and human facial attractiveness, Aishwariya Iyengar et al.
Nor is averageness typical in the sense of common or frequently occurring in the population, though it appears familiar, and is typical in the sense that it is a good example of a face that is representative of the category of faces.
The evolutionary explanation for averageness is koinophilia: animals seek mates with average features, because extreme or uncommon features indicate disadvantageous mutations.
Note (1) Grammer, K.; Thornhill, R. (October 1994). “Human (Homo sapiens) facial attractiveness and sexual selection: the role of symmetry and averageness”. Journal of Comparative Psychology. 108 (3): 233–42. doi:10.1037/0735-7036.108.3.233. PMID 7924253. Retrieved 4 May 2019.
Rhodes, Gillian; Zebrowitz, Leslie A. (2002). Facial Attractiveness: Evolutionary, Cognitive, and Social Perspectives. Ablex. ISBN 978-1-56750-636-5.
Jones, B. C., Little, A. C., Tiddeman, B. P., Burt, D. M., & Perrett, D. I. (2001). Facial symmetry and judgements of apparent health Support for a “‘ good genes ’” explanation of the attractiveness – symmetry relationship, 22, 417–429.
Alison Pearce Stevens writes “Research shows that people with more symmetrical faces don’t just look nice. They also tend to be healthier than asymmetrical people. Genes provide the instructions for how a cell is to perform. All people have the same number of genes. But people with more average faces tend to have a greater diversity in the genes they are born with. And that, research has shown, can lead to a stronger immune system and better health.” What makes a pretty face? Science News for Students
Students need to be aware of pseudoscience diets. Some of these claim that by eating more acidic or basic foods you can change your body’s pH level, and thus treat disease.
Not only is this entire idea incorrect, if a person does change their pH beyond even a tiny bit then they will almost immediately die. Changing one’s body pH is almost impossible, but when it happens it is fatal,
What are acids and bases? Acids are bases are complimentary types of chemicals. Acids perform one kind of chemical reaction; bases perform the opposite action. Learn more here about acids and bases.
Here’s the critical point: When it comes to living, what matters is whether acids and bases are working in a safe balance. Cells only work correctly in a very narrow range of conditions.
Too much or too little of any molecule, and they begin to malfunction or die. Homeostasis is the body’s way of keeping chemicals in a safe, dynamic balance.
Is Marijuana as Safe as We Think?
Permitting pot is one thing; promoting its use is another.
By Malcolm Gladwell, The New Yorker, January 14, 2019 Issue
A few years ago, the National Academy of Medicine convened a panel of sixteen leading medical experts to analyze the scientific literature on cannabis. The report they prepared, which came out in January of 2017, runs to four hundred and sixty-eight pages. It contains no bombshells or surprises, which perhaps explains why it went largely unnoticed. It simply stated, over and over again, that a drug North Americans have become enthusiastic about remains a mystery.
For example, smoking pot is widely supposed to diminish the nausea associated with chemotherapy. But, the panel pointed out, “there are no good-quality randomized trials investigating this option.” We have evidence for marijuana as a treatment for pain, but “very little is known about the efficacy, dose, routes of administration, or side effects of commonly used and commercially available cannabis products in the United States.” The caveats continue. Is it good for epilepsy? “Insufficient evidence.” Tourette’s syndrome? Limited evidence. A.L.S., Huntington’s, and Parkinson’s? Insufficient evidence. Irritable-bowel syndrome? Insufficient evidence. Dementia and glaucoma? Probably not. Anxiety? Maybe. Depression? Probably not.
Then come Chapters 5 through 13, the heart of the report, which concern marijuana’s potential risks. The haze of uncertainty continues. Does the use of cannabis increase the likelihood of fatal car accidents? Yes. By how much? Unclear. Does it affect motivation and cognition? Hard to say, but probably. Does it affect employment prospects? Probably. Will it impair academic achievement? Limited evidence. This goes on for pages.
We need proper studies, the panel concluded, on the health effects of cannabis on children and teen-agers and pregnant women and breast-feeding mothers and “older populations” and “heavy cannabis users”; in other words, on everyone except the college student who smokes a joint once a month. The panel also called for investigation into “the pharmacokinetic and pharmacodynamic properties of cannabis, modes of delivery, different concentrations, in various populations, including the dose-response relationships of cannabis and THC or other cannabinoids.”
Figuring out the “dose-response relationship” of a new compound is something a pharmaceutical company does from the start of trials in human subjects, as it prepares a new drug application for the F.D.A. Too little of a powerful drug means that it won’t work. Too much means that it might do more harm than good. The amount of active ingredient in a pill and the metabolic path that the ingredient takes after it enters your body—these are things that drugmakers will have painstakingly mapped out before the product comes on the market, with a tractor-trailer full of supporting documentation.
With marijuana, apparently, we’re still waiting for this information. It’s hard to study a substance that until very recently has been almost universally illegal. And the few studies we do have were done mostly in the nineteen-eighties and nineties, when cannabis was not nearly as potent as it is now. Because of recent developments in plant breeding and growing techniques, the typical concentration of THC, the psychoactive ingredient in marijuana, has gone from the low single digits to more than twenty per cent—from a swig of near-beer to a tequila shot.
Are users smoking less, to compensate for the drug’s new potency? Or simply getting more stoned, more quickly? Is high-potency cannabis more of a problem for younger users or for older ones? For some drugs, the dose-response curve is linear: twice the dose creates twice the effect. For other drugs, it’s nonlinear: twice the dose can increase the effect tenfold, or hardly at all. Which is true for cannabis? It also matters, of course, how cannabis is consumed. It can be smoked, vaped, eaten, or applied to the skin. How are absorption patterns affected?
Last May, not long before Canada legalized the recreational use of marijuana, Beau Kilmer, a drug-policy expert with the rand Corporation, testified before the Canadian Parliament. He warned that the fastest-growing segment of the legal market in Washington State was extracts for inhalation, and that the mean THC concentration for those products was more than sixty-five per cent. “We know little about the health consequences—risks and benefits—of many of the cannabis products likely to be sold in nonmedical markets,” he said. Nor did we know how higher-potency products would affect THC consumption.
When it comes to cannabis, the best-case scenario is that we will muddle through, learning more about its true effects as we go along and adapting as needed—the way, say, the once extraordinarily lethal innovation of the automobile has been gradually tamed in the course of its history. For those curious about the worst-case scenario, Alex Berenson has written a short manifesto, “Tell Your Children: The Truth About Marijuana, Mental Illness, and Violence.”
Berenson begins his book with an account of a conversation he had with his wife, a psychiatrist who specializes in treating mentally ill criminals. They were discussing one of the many grim cases that cross her desk—“the usual horror story, somebody who’d cut up his grandmother or set fire to his apartment.” Then his wife said something like “Of course, he was high, been smoking pot his whole life.”
Of course? I said.
Yeah, they all smoke.
Well . . . other things too, right?
Sometimes. But they all smoke.
Berenson used to be an investigative reporter for the Times, where he covered, among other things, health care and the pharmaceutical industry. Then he left the paper to write a popular series of thrillers. At the time of his conversation with his wife, he had the typical layman’s view of cannabis, which is that it is largely benign. His wife’s remark alarmed him, and he set out to educate himself. Berenson is constrained by the same problem the National Academy of Medicine faced—that, when it comes to marijuana, we really don’t know very much. But he has a reporter’s tenacity, a novelist’s imagination, and an outsider’s knack for asking intemperate questions. The result is disturbing.
The first of Berenson’s questions concerns what has long been the most worrisome point about cannabis: its association with mental illness. Many people with serious psychiatric illness smoke lots of pot. The marijuana lobby typically responds to this fact by saying that pot-smoking is a response to mental illness, not the cause of it—that people with psychiatric issues use marijuana to self-medicate. That is only partly true. In some cases, heavy cannabis use does seem to cause mental illness. As the National Academy panel declared, in one of its few unequivocal conclusions, “Cannabis use is likely to increase the risk of developing schizophrenia and other psychoses; the higher the use, the greater the risk.”
Berenson thinks that we are far too sanguine about this link. He wonders how large the risk is, and what might be behind it. In one of the most fascinating sections of “Tell Your Children,” he sits down with Erik Messamore, a psychiatrist who specializes in neuropharmacology and in the treatment of schizophrenia.
Messamore reports that, following the recent rise in marijuana use in the U.S. (it has almost doubled in the past two decades, not necessarily as the result of legal reforms), he has begun to see a new kind of patient: older, and not from the marginalized communities that his patients usually come from. These are otherwise stable middle-class professionals. Berenson writes, “A surprising number of them seemed to have used only cannabis and no other drugs before their breaks. The disease they’d developed looked like schizophrenia, but it had developed later—and their prognosis seemed to be worse. Their delusions and paranoia hardly responded to antipsychotics.”
Messamore theorizes that THC may interfere with the brain’s anti-inflammatory mechanisms, resulting in damage to nerve cells and blood vessels. Is this the reason, Berenson wonders, for the rising incidence of schizophrenia in the developed world, where cannabis use has also increased?
In the northern parts of Finland, incidence of the disease has nearly doubled since 1993. In Denmark, cases have risen twenty-five per cent since 2000. In the United States, hospital emergency rooms have seen a fifty-per-cent increase in schizophrenia admissions since 2006. If you include cases where schizophrenia was a secondary diagnosis, annual admissions in the past decade have increased from 1.26 million to 2.1 million.
Berenson’s second question derives from the first. The delusions and paranoia that often accompany psychoses can sometimes trigger violent behavior. If cannabis is implicated in a rise in psychoses, should we expect the increased use of marijuana to be accompanied by a rise in violent crime, as Berenson’s wife suggested?
Once again, there is no definitive answer, so Berenson has collected bits and pieces of evidence. For example, in a 2013 paper in the Journal of Interpersonal Violence, researchers looked at the results of a survey of more than twelve thousand American high-school students. The authors assumed that alcohol use among students would be a predictor of violent behavior, and that marijuana use would predict the opposite. In fact, those who used only marijuana were three times more likely to be physically aggressive than abstainers were; those who used only alcohol were 2.7 times more likely to be aggressive. Observational studies like these don’t establish causation. But they invite the sort of research that could.
Berenson looks, too, at the early results from the state of Washington, which, in 2014, became the first U.S. jurisdiction to legalize recreational marijuana. Between 2013 and 2017, the state’s murder and aggravated-assault rates rose forty per cent—twice the national homicide increase and four times the national aggravated-assault increase. We don’t know that an increase in cannabis use was responsible for that surge in violence. Berenson, though, finds it strange that, at a time when Washington may have exposed its population to higher levels of what is widely assumed to be a calming substance, its citizens began turning on one another with increased aggression.
His third question is whether cannabis serves as a gateway drug. There are two possibilities. The first is that marijuana activates certain behavioral and neurological pathways that ease the onset of more serious addictions. The second possibility is that marijuana offers a safer alternative to other drugs: that if you start smoking pot to deal with chronic pain you never graduate to opioids.
Which is it? This is a very hard question to answer. We’re only a decade or so into the widespread recreational use of high-potency marijuana. Maybe cannabis opens the door to other drugs, but only after prolonged use. Or maybe the low-potency marijuana of years past wasn’t a gateway, but today’s high-potency marijuana is. Methodologically, Berenson points out, the issue is complicated by the fact that the first wave of marijuana legalization took place on the West Coast, while the first serious wave of opioid addiction took place in the middle of the country. So, if all you do is eyeball the numbers, it looks as if opioid overdoses are lowest in cannabis states and highest in non-cannabis states.
Not surprisingly, the data we have are messy. Berenson, in his role as devil’s advocate, emphasizes the research that sees cannabis as opening the door to opioid use. For example, two studies of identical twins—in the Netherlands and in Australia—show that, in cases where one twin used cannabis before the age of seventeen and the other didn’t, the cannabis user was several times more likely to develop an addiction to opioids. Berenson also enlists a statistician at N.Y.U. to help him sort through state-level overdose data, and what he finds is not encouraging: “States where more people used cannabis tended to have more overdoses.”
The National Academy panel is more judicious. Its conclusion is that we simply don’t know enough, because there haven’t been any “systematic” studies. But the panel’s uncertainty is scarcely more reassuring than Berenson’s alarmism. Seventy-two thousand Americans died in 2017 of drug overdoses. Should you embark on a pro-cannabis crusade without knowing whether it will add to or subtract from that number?
Drug policy is always clearest at the fringes. Illegal opioids are at one end. They are dangerous. Manufacturers and distributors belong in prison, and users belong in drug-treatment programs. The cannabis industry would have us believe that its product, like coffee, belongs at the other end of the continuum.
“Flow Kana partners with independent multi-generational farmers who cultivate under full sun, sustainably, and in small batches,” the promotional literature for one California cannabis brand reads. “Using only organic methods, these stewards of the land have spent their lives balancing a unique and harmonious relationship between the farm, the genetics and the terroir.”
But cannabis is not coffee. It’s somewhere in the middle. The experience of most users is relatively benign and predictable; the experience of a few, at the margins, is not. Products or behaviors that have that kind of muddled risk profile are confusing, because it is very difficult for those in the benign middle to appreciate the experiences of those at the statistical tails.
Low-frequency risks also take longer and are far harder to quantify, and the lesson of “Tell Your Children” and the National Academy report is that we aren’t yet in a position to do so. For the moment, cannabis probably belongs in the category of substances that society permits but simultaneously discourages. Cigarettes are heavily taxed, and smoking is prohibited in most workplaces and public spaces. Alcohol can’t be sold without a license and is kept out of the hands of children. Prescription drugs have rules about dosages, labels that describe their risks, and policies that govern their availability. The advice that seasoned potheads sometimes give new users—“start low and go slow”—is probably good advice for society as a whole, at least until we better understand what we are dealing with.
Late last year, the commissioner of the Food and Drug Administration, Scott Gottlieb, announced a federal crackdown on e-cigarettes. He had seen the data on soaring use among teen-agers, and, he said, “it shocked my conscience.” He announced that the F.D.A. would ban many kinds of flavored e-cigarettes, which are especially popular with teens, and would restrict the retail outlets where e-cigarettes were available.
In the dozen years since e-cigarettes were introduced into the marketplace, they have attracted an enormous amount of attention. There are scores of studies and papers on the subject in the medical and legal literature, grappling with the questions raised by the new technology. Vaping is clearly popular among kids. Is it a gateway to traditional tobacco use? Some public-health experts worry that we’re grooming a younger generation for a lifetime of dangerous addiction. Yet other people see e-cigarettes as a much safer alternative for adult smokers looking to satisfy their nicotine addiction. That’s the British perspective.
Last year, a Parliamentary committee recommended cutting taxes on e-cigarettes and allowing vaping in areas where it had previously been banned. Since e-cigarettes are as much as ninety-five per cent less harmful than regular cigarettes, the committee argued, why not promote them? Gottlieb said that he was splitting the difference between the two positions—giving adults “opportunities to transition to non-combustible products,” while upholding the F.D.A.’s “solemn mandate to make nicotine products less accessible and less appealing to children.” He was immediately criticized.
“Somehow, we have completely lost all sense of public-health perspective,” Michael Siegel, a public-health researcher at Boston University, wrote after the F.D.A. announcement:
Every argument that the F.D.A. is making in justifying a ban on the sale of electronic cigarettes in convenience stores and gas stations applies even more strongly for real tobacco cigarettes: you know, the ones that kill hundreds of thousands of Americans each year. Something is terribly wrong with our sense of perspective when we take the e-cigarettes off the shelf but allow the old-fashioned ones to remain.
Among members of the public-health community, it is impossible to spend five minutes on the e-cigarette question without getting into an argument. And this is nicotine they are arguing about, a drug that has been exhaustively studied by generations of scientists. We don’t worry that e-cigarettes increase the number of fatal car accidents, diminish motivation and cognition, or impair academic achievement. The drugs through the gateway that we worry about with e-cigarettes are Marlboros, not opioids. There are no enormous scientific question marks over nicotine’s dosing and bio-availability. Yet we still proceed cautiously and carefully with nicotine, because it is a powerful drug, and when powerful drugs are consumed by lots of people in new and untested ways we have an obligation to try to figure out what will happen.
A week after Gottlieb announced his crackdown on e-cigarettes, on the ground that they are too enticing to children, Siegel visited the first recreational-marijuana facility in Massachusetts. Here is what he found on the menu, each offering laced with large amounts of a drug, THC, that no one knows much about:
Prenatal Exposure to Cannabis Affects the Developing Brain
Children born to moms who smoked or ingested marijuana during pregnancy suffer higher rates of depression, hyperactivity, and inattention.
By Andrew Scheyer, The Scientist, 1/1/2019
A Lifetime of Consequences?
Large-scale, longitudinal studies of humans whose mothers smoked marijuana once or more per week and experimental work on rodents exposed to cannabinoids in utero have yielded remarkably consistent intellectual and behavioral correlates of fetal exposure to this drug. Some exposed individuals exhibit deficits in memory, cognition, and measures of sociability.
These aberrations appear during infancy and persist through adulthood and are tied to changes in the expression of multiple gene families, as well as more global measures of brain responsiveness and plasticity. Researchers currently consider these perturbations to be mediated by changes to the endocannabinoid system caused by the active compounds in cannabis.
How Cannabis Affects the Function of Neurons
The human body contains two primary cannabinoid receptors: CB1R and CB2R. CB1R is present in the human fetal cerebrum by the first weeks of the second trimester, and is the brain’s most abundant G-protein coupled receptor. Located at the presynaptic terminal of neurons, CB1R is activated by endocannabinoids, which are synthesized from fatty acids in the postsynaptic neuron.
The receptors’ activation modulates the presynaptic release of neurotransmitters, thereby affecting synaptic function and a range of downstream signaling agents, from glutamate, dopamine, and serotonin to neuropeptides and hormones. The function of CB2Rs in the brain is still poorly understood, but there is some evidence that they exist both pre- and post-synaptically, as well as on glia and astrocytes. One recent paper suggests that, like CB1Rs, CB2Rs regulate neurotransmitter release (Synapse, 72:e22061, 2018).
When people smoke or ingest marijuana, exogenous cannabinoids enter the nervous system and activate these receptors. Stimulation by these high-affinity agonists results in stronger binding and greater activation of CB1R, triggering the process of receptor downregulation. Specifically, the greater binding causes the receptors to be internalized and degraded, such that they are no longer as available for cannabinoid signaling, and can thereby alter neuronal firing and other downstream events.
As the drug becomes more popular, concerns have been raised that its use can lead to psychotic disorders. Here’s what scientists know for sure, and what they don’t.
By Benedict Carey, The New York Times, 1/17/2019
Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone.
Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient.
The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science.
Can heavy use cause schizophrenia or other syndromes?
That is the big question, and so far the evidence is not strong enough to answer one way or the other. Even top scientists who specialize in marijuana research are divided, drawing opposite conclusions from the same data.
“I’ve been doing this research for 25 years, and it’s polarizing even among academics,” said Margaret Haney, a professor of neurobiology at Columbia University Medical Center. “This is what the marijuana field is like.”
The debate centers on the distinction between correlation and causation. People with psychotic problems often use cannabis regularly; this is a solid correlation, backed by numerous studies. But it is unclear which came first, the cannabis habit or the psychoses. Children who later develop schizophrenia often seem to retreat into their own world, stalked periodically by bizarre fears and fantasies well outside the range of usual childhood imagination, and well before they are exposed to cannabis. Those who go on to become regular marijuana users often use other substances as well, including alcohol and cigarettes, making it more difficult for researchers to untangle causation.
Consider cigarettes, the least mind-altering of these substances. In a 2015 study, a team led by Dr. Kenneth S. Kendler of Virginia Commonwealth University analyzed medical data on nearly two million people in Sweden. The data followed the individuals over time, from young adulthood, when most schizophrenia diagnoses occur, to middle age. Smoking was a predictor for later development of the disorder, and in what doctors call a dose-response relationship: the more a person smoked, the higher the risk.
Yet nicotine attracts nowhere near the concern that cannabis does, in part because the two drugs are so different in their everyday effects: mildly stimulated versus stoned. Indeed, some scientists have studied nicotine as a partial treatment for schizophrenia, to blunt the disorders effects on thinking and memory.
Is it biologically plausible that cannabis could cause a psychotic disorder?
Yes. Brain scientists know very little about the underlying biology of psychotic conditions, other than that hundreds of common gene variants are likely involved. Schizophrenia, for instance, is not a uniform disorder but an umbrella term for an array of unexplained problems involving recurrent psychosis, and other common symptoms.
Even so, there is circumstantial evidence for a biological mechanism. Psychotic disorders tend to emerge in late adolescence or early adulthood, during or after a period of rapid brain development. In the teenage years, the brain strips away unneeded or redundant connections between brain cells, in a process called synaptic pruning. This editing is concentrated in the prefrontal cortex, the region behind the forehead where thinking and planning occur — and the region that is perturbed in psychotic conditions.
The region is rich with so-called CB1 receptors, which are involved in the pruning, and are engaged by cannabis use. And alterations to the pruning process may well increase schizophrenia risk, according to recent research at the Broad Institute of M.I.T. and Harvard. In a 2016 analysis, scientists there found that people with the disorder often have a gene variant that appears to accelerate the pruning process.
What does this mean for me?
Experts may debate whether cannabis use can lead to psychotic disorders, but they mostly agree on how to minimize one’s risk.
Psychotic conditions tend to run in families, which suggests there is an inherited genetic vulnerability. Indeed, according to some studies, people prone to or at heightened risk of psychosis seem to experience the effects of cannabis differently than peers without such a history. The users experience a more vivid high, but they also are more likely to experience psychosis-like effects such as paranoia.
The evidence so far indicates that one’s familial risk for psychotic disorders outweighs any added effect of cannabis use. In a 2014 study, a team led by Ashley C. Proal and Dr. Lynn E. DeLisi of Harvard Medical School recruited cannabis users with and without a family history of schizophrenia, as well as non-users with and without such a history. The researchers made sure the cannabis users did not use other drugs in addition, a factor that muddied earlier studies. The result: there was a heightened schizophrenia risk among people with a family history, regardless of cannabis use.
“My study clearly shows that cannabis does not cause schizophrenia by itself,” said Dr. DeLisi. “Rather, a genetic predisposition is necessary. It is highly likely, based on the results of this study and others, that cannabis use during adolescence through to age 25, when the brain is maturing and at its peak of growth in a genetically vulnerable individual, can initiate the onset of schizophrenia.”
Because marijuana has been illegal for so long, research that could settle the question has been sorely lacking, although that has begun to change. The National Institutes of Health have launched a $300 million project that will track thousands of children from the age of 9 or 10 through adolescence, and might help clarify causation.
For the near future, expert opinions likely will be mixed. “Usually it is the research types who are doing ‘the sky is falling’ bit, but here it is switched,” said Dr. Jay Geidd, a professor of psychiatry at the University of California, San Diego. “The researchers are wary of overselling the dangers, as was clearly done in the past. However, clinicians overwhelmingly endorse seeing many more adolescents with ‘paranoia’” of some kind.
In short: Regularly using the new, high-potency cannabis may indeed be a risk for young people who are related to someone with a psychotic condition. On that warning, at least, most experts seem to agree.
Daily Marijuana Use And Highly Potent Weed Linked To Psychosis
NPR, 3/19/2019, by Rhitu Chatterjee
Several past studies have found that more frequent use of pot is associated with a higher risk of psychosis — that is, when someone loses touch with reality. Now a new study published Tuesday in the The Lancet Psychiatry shows that consuming pot on a daily basis and especially using high-potency cannabis increases the odds of having a psychotic episode later.
“This is more evidence that the link between cannabis and psychosis matters,” says Krista M. Lisdahl, a clinical neuropsychologist at the University of Wisconsin, Milwaukee, who wasn’t involved in the study.
The study authors consider high-potency cannabis to be products with more than 10 percent tetrahydrocannabinol or THC, the compound responsible for the drug’s psychoactive effects. The fact that consuming high-THC cannabis products has a greater risk is concerning, Lisdahl says, because these products are more common in the market now.
The study also shows that three European cities — London, Paris and Amsterdam — where high-potency weed is most commonly available actually have higher rates of new cases of psychosis than the other cities in the study.
The researchers identified 901 people aged 18 to 64 who were diagnosed with their first episode of psychosis between May 2010 and April 2015, at a mental health facility anywhere in 11 cities, including London, Paris, Amsterdam, Barcelona, other cities across Europe and one site in Brazil.
The researchers then asked these individuals and a control group of 1,200-plus other healthy people about their habits, including their use of weed. “We asked people if they used cannabis, when did they start using it and what kind of cannabis,” explains study author Marta Di Forti, a psychiatrist and clinician scientist at King’s College London.
People reported the names of weed strains they used, such as skunk in the U.K. or the Dutch Nederwiet, which allowed the researchers to identify the THC content in each product through data gathered by the European Monitoring Center for Drugs and Drug Addiction and national data from the different countries.
The study found that those who used pot daily were three times more likely to have a psychotic episode compared with someone who never used the drug.
Those who started using cannabis at 15 or younger had a slightly more elevated risk than those who started using in later years.
Use of high-potency weed almost doubled the odds of having psychosis compared with someone who had never smoked weed, explains Di Forti.
And for those who used high-potency pot on a daily basis, the risk of psychosis was even greater — four times greater than those who had never used.
The easy availability of high-THC weed is a recent phenomenon, she notes. “Almost 20 years ago, there wasn’t much high-potency cannabis available [in the market].”
One recent study showed that high-potency cannabis is increasingly dominating markets. It found that the average potency of weed in Europe and the U.S. in 2017 was 17.1 percent, up from 8.9 percent in 2008.
And some products can be even more potent. For example, in the Netherlands, the THC content of one product that’s gained popularity, locally produced Dutch resin Nederhasj, can be as high as 67 percent.
“What this paper has done that’s really nice is they look at rates of psychosis and cannabis use in lots of different places where underlying rates of psychosis are different,” says Suzanne Gage, a psychologist and epidemiologist at the University of Liverpool, who wrote a commentary linked to the study in The Lancet Psychiatry.
This allowed the researchers to compare incidence of psychosis with the availability and use of high-THC cannabis in the different cities, she says.
The study found that the three European cities — London, Paris and Amsterdam — had the highest rates of new diagnoses of psychosis — 45.7 per 100,000 person-years in London, 46.1 in Paris and 37.9 in Amsterdam.
These are also cities where high-potency weed is most easily available and commonly used.
Other European cities in Spain, Italy and France on the other hand have less than 10 percent THC content in most popular cannabis products on the market. These cities also have lower rates of new psychosis diagnosis, according to the study.
“One of the things that’s really novel is that they could show that variation of use and potency of cannabis was related to rates of first-episode psychosis,” Lisdahl says.
One critique of the theory that weed contributes to psychosis risk has been that while more people are using weed worldwide, there hasn’t been a corresponding rise in rates of psychosis, Gage explains. But the new study shows that cities with more easily available high-THC weed do have a higher rate of new diagnoses of psychosis.
“That’s a really interesting finding, and that’s not something anyone has done before,” she adds.
However, the study doesn’t prove causality, cautions Dr. Diana Martinez, a psychiatrist and addiction researcher at Columbia University. “You can’t say that cannabis causes psychosis,” she says. “It’s simply not supported by the data,” she says.
Lisdahl agrees. In order to show causality, one would have to follow people over time — before they started using weed to years later when they have their psychotic episodes, she says. “You need twins in the studies, you need genetic information,” among all other kinds of data, she says.
Psychotic disorders such as schizophrenia and bipolar are complicated, “multifaceted disorders,” Gage notes.
“In all psychotic disorders, there is this multiple hit hypothesis,” Martinez says. Many factors influence whether and how these disorders manifest.
Genetics is known to play a major role, as are a host of environmental factors. “Children who have risk of schizophrenia but grow up in stable homes … they may not go on to develop schizophrenia,” she adds.
The Adolescent Brain Cognitive Development study, which is funded by the U.S. National Institutes of Health, is attempting to tease out the various influences, Lisdahl says. “The NIH has now invested in that question.”
In the meantime, the new findings should be of interest to anyone using cannabis, says study author Di Forti. “There are people across the world who use cannabis for a variety of reasons,” she says. “Some of them recreationally, some of them for medicinal purposes.” They should be aware that using high-potency cannabis comes with a risk, she says.
“They need to know what to look for and ask for help, if they come across characteristics of a psychotic disorder,” she adds.
…It is perfectly possible that the association between cannabis and psychosis is bidirectional, as suggested by other work using genetic variables as proxies for the exposures of interest in a Mendelian randomisation design. Di Forti and colleagues’ study adds a new and novel study design to the evidence available, which consistently indicates that for some individuals there is an increased risk of psychosis resulting from daily use of high potency cannabis. Given the changing legal status of cannabis across the world, and the associated potential for an increase in use, the next priority is to identify which individuals are at risk from daily potent cannabis use, and to develop educational strategies and interventions to mitigate this.
Samuel T. Wilkinson, Rajiv Radhakrishnan, and Deepak Cyril D’Souza write:
The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication; acute psychosis that lasts beyond the period of acute intoxication; and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, delta-9-tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case studies indicate that cannabinoids can induce acute psychosis that lasts beyond the period of acute intoxication but resolves within a month. Exposure to cannabis in adolescence is associated with a risk for later psychotic disorder in adulthood; this association is consistent, temporally related, shows a dose response, and is biologically plausible. However, cannabis is neither necessary nor sufficient to cause a persistent psychotic disorder. More likely, it is a component cause that interacts with other factors to result in psychosis. The link between cannabis and psychosis is moderated by age at onset of cannabis use, childhood abuse, and genetic vulnerability. While more research is needed to better characterize the relationship between cannabinoid use and the onset and persistence of psychosis, clinicians should be mindful of the potential risk of psychosis, especially in vulnerable populations, including adolescents and those with a psychosis diathesis.
PreK–12 Standard 10: Tobacco, Alcohol, & Substance Use/Abuse Prevention
Students will acquire the knowledge and skills to be competent in making health-enhancing decisions regarding the use of medications and avoidance of substances, and in communicating about substance use/abuse prevention for healthier homes, schools, and communities.
Through the study of Effects on the Body students will
10.5 Describe addictions to alcohol, tobacco, and other drugs, and methods for intervention, treatment, and cessation
10.6 List the potential outcomes of prevalent early and late adolescent risk behaviors related to tobacco, alcohol, and other drugs, including the general pattern and continuum of risk behaviors involving substances that young people might follow
Students generate ideas of what the term “gateway” means in relation to substance abuse and map out a series of behaviors that begin with such “gateway” behaviors
Through the study of Healthy Decisions students will
10.7 Identify internal factors (such as character) and external factors (such as family, peers, community, faith-based affiliation, and media) that influence the decision of young people to use or not to use drugs
10.8 Demonstrate ways of refusing and of sharing preventive health information about tobacco, alcohol, and other drugs with peers. Students research and give an oral report on the effects of second-hand smoke.
By the end of grade 12
Through the study of Effects on the Body students will
10.9 Describe the relationship between multi-drug use and the increased negative effects on the body, including the stages of addiction, and overdose. Students research the increased chances of death from alcohol poisoning when alcohol is combined with marijuana.
10.10 Describe the harmful effects of tobacco, alcohol, and other substances on pregnant women and their unborn children.
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