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Health24.com | Can marijuana bring on psychosis in young users?

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The idea of marijuana causing a psychotic breakdown sounds like something out of the camp film classic “Reefer Madness”, but many experts argue it’s not that far-fetched.

As legalisation of recreational marijuana spreads across the United States, more people are showing up in ERs with psychotic symptoms after consuming too much pot, said Dr Itai Danovitch, chairman of psychiatry and behavioural neurosciences at Cedars-Sinai in Los Angeles.

Full-fledged psychotic disorder

“If somebody gets too high, they use more than intended, they can have psychotic symptoms. That typically resolves as the drug wears off,” Danovitch said. “After it’s worn off, there’s no subsequent psychosis. That’s just a direct effect of over-intoxication.”

But some unlucky souls with a family history of mental illness might wind up with a full-fledged psychotic disorder that will require extended treatment, Danovitch noted.

“That risk is concentrated among a minority of people who have an existing vulnerability to develop a psychotic disorder, a family history of psychosis,” Danovitch said. “There are environmental factors that influence whether somebody develops schizophrenia who has a risk. It appears cannabis probably is one of those factors.”

Vaping a potent form of THC – the intoxicating ingredient in pot – prompted a psychotic episode last year in 24-year-old Madison McIntosh of Scottsdale, Ariz., according to USA Today.

McIntosh appeared at the driving range where he worked on his day off, wandering around and talking babble for 12 hours straight. His family rushed him to a hospital, where he told his father that he was seeing double rainbows. Doctors diagnosed him with cannabis use disorder and unspecified psychosis.

McIntosh remembers feeling “out of it, delusional” at the driving range, where he thought people were following him. “I was pretty scared,” he told USA Today of the March incident. “I didn’t know where I was at.”

Strong causal relationship

Despite anecdotes like these, sceptics argue that the science on a potential link between pot and psychosis remains far from solid.

“It would appear to be premature, at best, and sensational, at worst, to opine that a strong causal relationship exists between cannabis exposure and psychiatric disorders, given the lack of consensus among experts in the field and the fact that rates of psychosis and mental illness have largely remained static over the decades while at the same time rates of cannabis use have fluctuated dramatically,” said Paul Armentano. He is deputy director of NORML, a non-profit calling for the reform of marijuana laws.

“This latter fact undermines the theory that cannabis exposure is a direct cause of psychiatric illness in otherwise non-predisposed subjects, and instead indicates that those most likely to express psychotic symptoms possess a predisposition to both cannabis use and psychotic behaviours,” Armentano added.

Still, a study published recently in the Lancet journal found that daily marijuana use may increase the risk of a first-time psychotic episode by three to five times, depending on the potency of the pot.

The Lancet study reported that in the three sites with the greatest consumption of high-potency cannabis, daily use of high-potency cannabis was associated with the greatest increase in the odds for psychotic disorder – four times greater in Paris, five times greater in London, and more than nine times greater in Amsterdam.

These temporary psychotic episodes are “not a common marijuana experience, but it’s common given how prevalently marijuana is used,” Danovitch said.

Lasting psychosis

The risk of so-called “transient psychosis” has grown with both the increasing potency of new pot strains and the increased use of edible marijuana products, said Dr Scott Krakower, assistant unit chief of psychiatry at Zucker Hillside Hospital in Glen Oaks, New York.

“You can ingest a large amount of high-potency agents in a quick period of time,” Krakower explained. “It’s not going to take you a lot with edibles to hit a very high dose of marijuana. If you’re not regulating yourself, you could go up pretty fast without even realising it.”

But there’s a small proportion of people whose existing vulnerability to mental illness makes them more likely to have lasting psychosis if they use too much pot, studies have found.

The risk for schizophrenia following substance-induced psychosis is about 11%, with the strongest association among vulnerable users of pot, according to a 2019 study in the American Journal of Psychiatry.

Danovitch said he counsels young people to consider their genetic risk for mental illness before they use marijuana.

“If they have a family history of serious mental illness, their risk may be really different from that of their peers,” Danovitch said. “It’s important that they be aware and informed about that.”

Harms amplified in adolescents

Emily Feinstein, executive vice president at the Center on Addiction, seconded those concerns regarding young users.

“The research is clear that adolescent marijuana use is associated with an increased risk of schizophrenia or psychotic symptoms in young people with a potential vulnerability to mental illness,” Feinstein said.

“The harms of marijuana are amplified in adolescents and young adults, whose developing brains are more vulnerable to the impact of THC,” she noted. “Parents should be especially concerned if their children are using high-concentrate THC products.”

Armentano agreed that the “growing concerns over this potential relationship ought to be taken seriously and they provide an argument in favour of better regulation of the plant so that it can be better kept out of the hands of young people and so that targeted warnings be directed toward those adults who may be at higher risk for an adverse reaction.

“Maintaining cannabis prohibition, unfortunately, achieves neither result,” Armentano said.

Image credit: iStock

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HIV infections among gay and bi men fall by 71% in UK

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New figures suggest the UK is on track to eliminate HIV transmission by 2030.

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Health24.com | Why gyms are fertile grounds for germs

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Going to the gym is supposed to improve your health, but it can also be a hotbed of cold and flu bugs, an expert warns.

“The biggest thing about the gym is there are a lot of areas where germs, viruses and fungus can be year-round,” said Bryan Combs, a nurse practitioner in the University of Alabama at Birmingham’s School of Nursing.

Wipe your equipment

Handlebars on elliptical machines, treadmills, stationary bicycles and weight machines are among the dirtiest places in gyms.

“Even if the handlebars are cleaned regularly, handlebars are going to be covered in bacteria,” said Combs, who added that you should clean the machines before and after each time you use them.

“You need to use wipes or a disinfectant spray to wipe down the machines or weights before and after,” Combs said in a university news release. “Once you clean the equipment, hang your towel on an area that you know is clean. When you get done, clean it again for the next person.”

Towels are another potential problem. “While the towels have been washed, a lot of gyms use the same container to carry dirty towels to the washing area and then use the same one to bring clean towels back, so they can become contaminated again,” Combs said.

Bring your own clean towel to the gym and wash your towel after each workout.

It’s also important to wash your water bottles with soap and hot water after every use.

A haven for bacteria

“Some people use the same water bottle each time they go to the gym. If you don’t take it home and wash it, and you go to the gym a few or several days a week, the water bottle could be covered in bacteria,” Combs said.

Your gym bag can also be a haven for bacteria, so regular treatment with a disinfectant spray is a good idea.

Always wear shoes in all areas of the gym, especially in locker rooms and in the shower. If you sit down, place a clean towel on top of the bench or seat.

“Walking barefoot in locker rooms or showers is an easy way to contract MRSA or pick up a fungal infection like athlete’s foot. By wearing clean shoes, you can prevent catching something that is spread by skin contact,” Combs said.

Change your clothes after each workout. “As soon as you leave the gym, you should change clothes as soon as possible. A lot of people continue to wear their sweaty clothes for an hour or hour and a half. It’s important to take those off and shower as soon as you can after a workout,” Combs said.

Image credit: iStock

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NHS tells betting firms to stop ‘vicious gambling cycle’

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Free bets and other incentives should be banned to make gambling safer, a letter to companies says.

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Discovery reveals how remora fishes know when to hitch a ride aboard their hosts

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Remoras are among the most successful marine hitchhikers, thanks to powerful suction discs that allow them to stay tightly fastened to the bodies of sharks, whales and other hosts despite incredible drag forces while traveling through the ocean. But how do these suckerfish sense the exact moment when they must “stick their landing” and board their speedy hosts in the first place?

A team of biologists at New Jersey Institute of Technology (NJIT), Friday Harbor Labs at University of Washington (FHL-UW) and The George Washington University (GWU) now offers an answer.

In findings published in the Journal of the Royal Society Open Science, researchers have detailed the discovery of a tactile-sensory system stowed within the suction disc of remora, believed to enable the fish to acutely sense contact pressure with host surfaces and gauge ocean forces in order to determine when to initiate their attachment, as well as adjust their hold on hosts while traversing long distances.

Specifically, the study describes the discovery of groupings of push-rod-like touch receptors, or mechanoreceptor complexes, embedded in the outer lip of the remora adhesive disc, which have been known to aid other organisms in responding to touch and shear forces.

Researchers say the finding marks the first time such touch-sensory complexes have been described in fishes, as the structure was previously only known in extant monotremes — platypus and echidnas.

“One of the wildest things about this work was not only finding a mechanoreceptor complex not previously known to fishes, but that the only other organisms known to possess them are monotremes,” said Brooke Flammang, NJIT professor of biological sciences and lead author of the study. “This is exciting because it shows how much we as integrative comparative biologists still have to learn about the sensory world of organisms.”

“When I was in graduate school, conventional wisdom was that fishes did not have such mechanoreceptors,” said Patricia Hernandez, one of the study’s authors at The George Washington University. “The discovery that these fishes share convergent receptors with echidnas is really exciting and points us in the right direction for discovering similar convergence in other fishes.”

While conducting various imaging studies to examine the head and disc of Echeneis naucrates, a common sharksucker remora, the team successfully identified the complexes: dome-like protrusions along the surface of the soft tissue lip surrounding the remora’s adhesive disc. Each dome packs below it a column of cells with three vesicle chains containing sensory nerves that stretch from the disc’s epidermal layer down to its dermal layer. In addition to sensing contact, these complexes are thought to respond to shear stress, which would provide feedback information to the remora if it was losing its grip and sliding backward on its host.

“When we first noticed these structures we were a little thrown off,” said Karly Cohen, a Ph.D. biology student at FHL-UW and an author on the study. “We knew they had to be sensory because of the plethora of nerves, but they didn’t look like lateral line structures, which are one of the main ways fishes sense their environment. We dove into the literature to try and find structures that fit the morphology of those we saw in the remora histology. Finally landing on the push-rod receptors known in echidnas was so exciting. … It was validation of the morphology we were seeing and it took us into a realm of mechnosensation that we were not necessarily considering when thinking about how the remora stick.”

Notably, in further examining seven other remora species, the team found that those species known to frequently piggyback on larger and faster hosts, like pelagic billfish, are equipped with nearly double the mechanoreceptor complexes of remora species that typically hitchhike on slower swimmers, such as reef fishes.

“On animals swimming very fast where the remora may be under increased drag conditions, the need to recognize loss of contact and make an instant correction is more crucial than on slower swimming hosts,” noted Flammang.

Flammang and colleagues say that the touch-signaling complexes found in remoras suggest not only that fishes may be able to sense their environment in ways not previously realized, but that specialized mechanoreceptors may also be a much more common feature among basal vertebrates than was previously thought as well.

“The interesting aspect here is that push-rods are only otherwise known in platypus and echidnas,” said Flammang. “Obviously, there is no close phylogenetic relationship between remoras and monotremes, so this likely means that there are a lot of mechanoreceptors in vertebrates that just haven’t been found in a wide breadth of organisms. We hope this paper brings this structure to the attention of other researchers for comparative study on how their organisms sense the environment.”

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Molecular understanding of drug interactions suggests pathway to better malaria treatments

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The process of crystallization is central to drug development, petrochemical processing and other industrial actions, but scientists say they still are learning about the complex interactions involved in the building and dissolution of crystals.

Researchers from the University of Houston and the Université libre de Bruxelles reported in the journal Nature that they have for the first time demonstrated at the molecular level what happens when two compounds known to inhibit crystal growth — in this case, antimalarial drugs — were combined. The results were unexpected.

“You would expect using two drugs that attacked crystallization in two different ways would be synergistic, or at the very least additive,” said Jeffrey Rimer, Abraham E. Dukler Professor of Chemical and Biomolecular Engineering at UH and a co-author of the paper. “Instead, we found that they can work against each other.”

Working against each other, known as antagonistic cooperation, meant that the drugs were actually less effective in tandem than individually. Peter Vekilov, John and Rebecca Moores Professor of Chemical and Biomolecular Engineering and Chemistry at UH and another co-author, said the work will allow the design of more effective treatments for malaria, a mosquito-borne disease that killed 435,000 people in 2017, most of them children in Africa.

But more broadly, it suggests a new way to screen molecules for their potential in drug development, allowing new treatments to be developed more quickly.

“When you are using modifiers, a small change in the molecule’s structure can dramatically alter its performance,” Rimer said.

Malaria is caused by a parasite, which consumes hemoglobin and leaves behind a compound known as hematin, which the parasite sequesters inside a crystal. Antimalarial treatments work by inhibiting the crystal growth, freeing hematin to attack the parasite.

For this work, the researchers studied the growth of hematin crystals in the presence of four antimalarial drugs — chloroquine, quinine, mefloquine and amodiaquine — which work in one of two distinct ways.

Both computationally and experimentally, including through the use of atomic force microscopy, the researchers demonstrated how compounds which attack crystallization by two different mechanisms behave when combined. The resulting molecular-level understanding of that behavior suggests a new mechanism for materials science, Vekilov said.

“This mechanism may provide guidance in the search for suitable inhibitor combinations to control crystallization of pathological, biomimetic, and synthetic materials,” the researchers wrote. “In a broader context, our results highlight modifier interactions mediated by the dynamics and structures on the crystal interface as a prime element of the regulation of the shapes and patterns of crystalline structures in nature and industry.”

In addition to Vekilov and Rimer, researchers involved with the project include UH Ph.D. student Wenchuan Ma and collaborator Dr. James Lutsko of the Université libre de Bruxelles.

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Materials provided by University of Houston. Original written by Jeannie Kever. Note: Content may be edited for style and length.

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With these neurons, extinguishing fear is its own reward

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When you expect a really bad experience to happen and then it doesn’t, it’s a distinctly positive feeling. A new study of fear extinction training in mice may suggest why: The findings not only identify the exact population of brain cells that are key for learning not to feel afraid anymore, but also show these neurons are the same ones that help encode feelings of reward.

The study, published Jan. 14 in Neuron by scientists at MIT’s Picower Institute for Learning and Memory, specifically shows that fear extinction memories and feelings of reward alike are stored by neurons that express the gene Ppp1r1b in the posterior of the basolateral amygdala (pBLA), a region known to assign associations of aversive or rewarding feelings, or “valence,” with memories. The study was conducted by Xiangyu Zhang, a graduate student, Joshua Kim, a former graduate student, and Susumu Tonegawa, Professor of Biology and Neuroscience at RIKEN-MIT Laboratory of Neural Circuit Genetics at the Picower Institute for Learning and Memory at MIT and Howard Hughes Medical Institute.

“We constantly live at the balance of positive and negative emotion,” Tonegawa said. “We need to have very strong memories of dangerous circumstances in order to avoid similar circumstances to recur. But if we are constantly feeling threatened we can become depressed. You need a way to bring your emotional state back to something more positive.”

Overriding fear with reward

In a prior study, Kim showed that Ppp1r1b-expressing neurons encode rewarding valence and compete with distinct Rspo2-expressing neurons in the BLA that encode negative valence. In the new study, Zhang, Kim and Tonegawa set out to determine whether this competitive balance also underlies fear and its extinction.

In fear extinction, an original fearful memory is thought to be essentially overwritten by a new memory that is not fearful. In the study, for instance, mice were exposed to little shocks in a chamber, making them freeze due to the formation of fearful memory. But the next day, when the mice were returned to the same chamber for a longer period of time without any further little shocks, freezing gradually dissipated and hence this treatment is called fear extinction training. The fundamental question then is whether the fearful memory is lost or just suppressed by the formation of a new memory during the fear extinction training.

While the mice underwent fear extinction training the scientists watched the activity of the different neural populations in the BLA. They saw that Ppp1r1b cells were more active and Rspo2 cells were less active in mice that experienced fear extinction. They also saw that while Rspo2 cells were mostly activated by the shocks and were inhibited during fear extinction, Ppp1r1b cells were mostly active during extinction memory training and retrieval, but were inhibited during the shocks.

These and other experiments suggested to the authors that the hypothetical fear extinction memory may be formed in the Ppp1r1b neuronal population and the team went on to demonstrate this vigorously. For this, they employed the technique previously pioneered in their lab for the identification and manipulation of the neuronal population that holds specific memory information, memory “engram” cells. Zhang labeled Ppp1r1b neurons that were activated during retrieval of fear extinction memory with the light-sensitive protein channelrhodopsin. When these neurons were activated by blue laser light during a second round of fear extinction training it enhanced and accelerated the extinction. Moreover, when the engram cells were inhibited by another optogenetic technique, fear extinction was impaired because the Ppp1r1b engram neurons could no longer suppress the Rspo2 fear neurons. That allowed the fear memory to regain primacy.

These data met the fundamental criteria for the existence of engram cells for fear extinction memory within the pBLA Ppp1r1b cell population: activation and reactivation by recall and enduring and off-line maintenance of the acquired extinction memory.

Because Kim had previously shown Ppp1r1b neurons are activated by rewards and drive appetitive behavior and memory, the team sequentially tracked Ppp1r1b cell activity in mice that eagerly received water reward followed by food reward followed by fear extinction training and fear extinction memory retrieval. The overlap of Ppp1r1b neurons activated by fear extinction vs. water reward was as high as the overlap of neurons activated by water vs. food reward. And finally, artificial optogenetic activation of Ppp1r1b extinction memory engram cells was as effective as optogenetic activation of Ppp1r1b water reward-activated neurons in driving appetitive behaviors. Reciprocally, artificial optogenetic activation of water-responding Ppp1r1b neurons enhanced fear extinction training as efficiently as optogenetic activation of fear extinction memory engram cells. These results demonstrate that fear extinction is equivalent to bona fide rewards and therefore provide the neuroscientific basis for the widely held experience in daily life: omission of expected punishment is a reward.

What next?

By establishing this intimate connection between fear extinction and reward and by identifying a genetically defined neuronal population (Ppp1r1b) that plays a crucial role in fear extinction this study provides potential therapeutic targets for treating fear disorders like PTSD and anxiety, Zhang said.

From the basic scientific point of view, Tonegawa said, how fear extinction training specifically activates Ppp1r1b neurons would be an important question to address. More imaginatively, results showing how Ppp1r1b neurons override Rspo2 neurons in fear extinction raises an intriguing question about whether a reciprocal dynamic might also occur in the brain and behavior. Investigating “joy extinction” via these mechanisms might be an interesting research topic.

The research was supported by the RIKEN Brain Science Institute, the Howard Hughes Medical Institute and the JPB Foundation funded the research.

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Health24.com | Man grows ‘eggshell’ around testicle because of parasitic worm

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An 80-year old man from India developed a layer of eggshell-like material around his testicle. According to a report published on 6 January 2020 in the BMJ Case Reports, this happened because of a rare reaction to a chronic infection.

The man visited the doctor after experiencing symptoms similar to a urinary tract infection – blood in his urine and discomfort when passing urine.

During the examination, doctors discovered that his one testicle was enlarged and felt “hard and stony” to the touch. CT scans revealed a fluid-filled sac around his testicle – which had hardened due to calcification, like an eggshell.

According to the report, this fluid-filled sac, also called a hydrocele, is not typically found in the scrotum but can develop as a response to an infection. This sometimes happens in newborns and the elderly, especially in response to inflammation and injury.

Caused by a worm

In this case, the infection was diagnosed as lymphatic filariasis (commonly known as elephantiasis), caused by parasitic worms classified as nematodes.

Humans come into contact with the larvae of parasitic worms when they are transmitted through mosquito bites and develop into lymphatic vessels. The worms are found in tropical regions, including India where the patient lives.

According the World Health Organization (WHO), although the formation of hydroceles occurs in millions of men globally, it is very rare for the sac to calcify and form the so-called “eggshell”. According to a previous case report on the matter, the hardening of the sac can indicate a chronic infection.

The treatment

These infections are normally treated with anti-filarial drugs, but may require surgery. The authors of the case study didn’t mention how this specific patient was treated.

The authors recommend that people living in areas with high risks of infections related to parasitic worms should be treated annually with anti-filarial drugs. 

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Compiled by Marelize Wilke

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MND: The search for new treatments

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A major study will assess if new – and existing – drugs can help people with motor neurone disease.

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Health24.com | Burnout can raise the risk of a dangerous heart disorder

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Feeling exhausted, with too few hours in the day to do what needs to be done?

Be careful of burnout – especially after a new study finds it can raise your risk for the dangerous irregular heartbeat known as atrial fibrillation.

“A-fib” – long tied to higher odds for heart attack and stroke – is the most common form of heart arrhythmia. It’s estimated that 10 million people in the United States will have the condition by next year.

The new study found burnout might help trigger a-fib.

“Vital exhaustion is associated with increased inflammation and heightened activation of the body’s physiologic stress response,” explained study author Parveen Garg, of the University of Southern California, Los Angeles.

“When these two things are chronically triggered, that can have serious and damaging effects on the heart tissue, which could then eventually lead to the development of this arrhythmia,” he explained.

In the study, Garg’s group surveyed more than 11,000 people about whether or not they had symptoms of burnout and then followed them for nearly 25 years.

Profound stress at work or home

Burnout “is typically caused by prolonged and profound stress at work or home,” said Garg. His team published its findings January 13 in the European Journal of Preventive Cardiology.

Burnout “differs from depression, which is characterised by low mood, guilt and poor self-esteem,” Garg said in a journal news release.

While the new study couldn’t prove cause-and-effect, it found that people with the highest levels of burnout had a 20% higher odds of developing a-fib during the follow-up period, compared to those with little or no burnout.

The study did not find any link between a-fib and a number of other psychological issues, such as anger, antidepressant use or poor social support.

“The findings for anger and social support are consistent with prior research, but two previous studies did find a significant association between antidepressant use and an increased risk of atrial fibrillation,” Garg noted. “Clearly, more work still needs to be done.”

But when it comes to the impact of burnout on heart health, the findings “further establish the harm that can be caused in people who suffer from exhaustion that goes unchecked”, he added.

Be more aware of stress

Two heart specialists unconnected to the study agreed.

“There is a strong mind-heart relationship,” said Dr Satjit Bhusri, a cardiologist at Lenox Hill Hospital in New York City. “When the mind is under stress, the heart will respond, either with an appropriate heart rhythm or an abnormal one, namely atrial fibrillation.”

Dr Marcin Kowalski directs cardiac electrophysiology at Staten Island University Hospital, also in New York City. He believes that “physicians and patients should be more aware of stress as a contributing factor to cardiac arrhythmias”, and stressed patients should be counseled to help them avoid burnout.

“Hopefully, future studies can show the reduction in stress can lead to in reduction of cardiac arrhythmia,” Kowalski said.

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