Have you ever loved a woman
Wednesday, July 31, 2019
A photographer in Monterey Bay spotted a humpback accidentally trapping a sea lion when both species were snacking on the same bait ball.
PHOTOGRAPH BY CHASE DEKKER
How a humpback whale ended up with a sea lion in its mouth
In an extremely rare occurrence, a photographer captured a sea lion getting snagged in the open mouth of a humpback whale.
BY SARAH KEARTES
PUBLISHED JULY 30, 2019
During a whale-watching trip last week, wildlife photographer Chase Dekker stared in awe as a humpback surfaced and engulfed a sea lion in its mouth.
The humpback whale, the largest of the three the group was observing—likely measuring around 50 feet long—opened its mouth to consume fish and
Tuesday, July 30, 2019
Monday, July 29, 2019
T.V. and the Inebriated Audience
"We have lived a love of burning, pure crystal." -- Albert Camus to Maria Casares
If you're chasing money, you'll always be lacking. Chase purpose and money will chase you! - Tony Gaskins #quote
@alixsarbh
"Explanation separates us from astonishment, which is the only gateway to the incomprehensible." Eugène Ionesco
LSD helps to treat alcoholism
LSD helps to treat alcoholism
Retrospective analysis shows hallucinogenic drug helped problem drinkers.
An analysis of old studies suggests LSD may have a role to play in treating alcoholism.
The powerful hallucinogen LSD (lysergic acid diethylamide) has potential as a treatment for alcoholism, according to a retrospective analysis of studies published in the late 1960s and early 1970s.
The study1, by neuroscientist Teri Krebs and clinical psychologist Pål-Ørjan Johansen of the Norwegian University of Science and Technology in Trondheim, is the first-ever quantitative meta-analysis of LSD–alcoholism clinical trials. The researchers sifted through thousands of records to collect data from randomized, double-blind trials that compared one dose of LSD to a placebo.
Of 536 participants in six trials, 59% of people receiving LSD reported lower levels of alcohol misuse, compared to 38% of people who received a placebo. “We were surprised that the effect was so clear and consistent,” says Krebs. She says that the problem with most studies done at that time was that there were too few participants, which limited statistical power. “But when you combine the data in a meta-analysis, we have more than 500 patients and there is definitely an effect,” she says. In general, the reported benefits lasted three to six months. Their findings are published today in the Journal of Psychopharmacology.
Psychedelics were promoted by psychiatrists in the 1950s as having a range of medical uses — to treat conditions such as schizophrenia, for example — before political pressures in the United States and elsewhere largely ended the work. “Alcoholism was considered one of the most promising clinical applications for LSD,” says Johansen. Alcoholics Anonymous co-founder Bill Wilson is said to have espoused the benefits of LSD in the book Pass It On: The Story of Bill Wilson and How the AA Message Reached the World.
In the last decade or so, however, a new generation of researchers have been interested in harnessing the therapeutic benefits of illicit drugs — such as 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) for post-traumatic stress disorder, ayahuasca for drug and alcohol dependency, and psilocybin, the active ingredient in hallucinogenic mushrooms, for smoking cessation.
The snow globe of perception?
How psychedelics exert such effects, especially after a single dose, remains unclear. LSD and its chemical cousins share structural similarities with the neurotransmitter serotonin, which is linked to many aspects of mood, memory and pleasure. These psychedelics also bind the same receptor sites in the brain as serotonin, but there the similarity may end — studies have shown that the hallucinogens elicit chemical cascades different from other compounds that bind at the same receptor2. To complicate matters further, LSD also acts at other receptors3.
For the moment, studying human behavioural responses rather than brain chemistry may be more helpful in understanding how the drugs work. Robin Carhart-Harris, a psychopharmacologist at Imperial College London who has researched how psilocybin could treat depression, says that psychedelics must work at both biological and psychological levels. “Psychedelics probably work in addiction by making the brain function more chaotically for a period — a bit like shaking up a snow globe — weakening reinforced brain connections and dynamics,” he says.
Roland Griffiths, a behavioural biologist at the Johns Hopkins University School of Medicine in Baltimore, Maryland, is investigating the influence of psilocybin on smoking cessation, and says that psychedelics sometimes give rise to distinctive, insightful experiences that can produce enduring positive changes in attitude, mood and behaviour.
“This is impressive and important work,” says Matthew Johnson, a psychiatrist also at Johns Hopkins University who is now running a small trial looking at the effectiveness of psilocybin to treat nicotine addiction. “Although this meta-analysis does not replace the need to test the approach in new, well-designed and rigorous clinical trials, it puts some more muscle behind the interpretation that the older literature shows hints that psychedelic therapy might really help addiction.”
However, Ken Checinski, a consultant addiction psychiatrist and independent researcher based in London, says that although the results are exciting, no pharmacological treatment should be seen as a magic bullet and that modern therapeutic techniques have improved. “The included LSD trials pre-date the use of psychological techniques such as motivational interviewing and cognitive behaviour therapy,” he says.
- Nature
- doi:10.1038/nature.2012.10200
Sunday, July 28, 2019
Shunning booze may improve women’s mental health: study
Shunning booze may improve women’s mental health: study
Winding down with some wine may not be so relaxing after all.
Researchers at the University of Hong Kong found that quitting alcohol completely may actually be more relaxing than a nightly glass of vino.
For the study, published this week in the Canadian Medical Association Journal, researchers examined the self-reported changes in physical and mental well-being amongst more than 10,000 men and women in Hong Kong and 31,000 in the US. However, the study only looked at moderate drinkers; those who self-reported as heavy drinkers were not included.
Those who quit imbibing reported feeling more “calm and peaceful” than when they were moderate drinkers. While people who quit drinking reported the biggest changes in their mental well-being, those who never drank at all were actually found to have the “highest level of mental well being,” the author’s note.
One notable outcome: The women who quit alcohol self-reported more favorable changes in their mental well-being.
“Women who quit drinking were found to have a greater improvement in mental well-being than lifetime abstainers,” the researchers report in the study.
For the Chinese population, researchers used the FAMILY Cohort study — a longitudinal study of health, happiness, and family harmony that looked at individuals, households, and neighborhoods in Hong Kong. For the US population, the National Epidemiologic Survey on Alcohol and Related Conditions was used to assess the subjects. The study’s results “remained consistent” after it was adjusted for factors including BMI, smoking status, and self-reported diseases.
Still, the researchers note the women in the Chinese cohort were very light drinkers to begin with: “Most Chinese women in Hong Kong use alcohol fewer than 4 times per month, which may not have a physiologic effect,” they write. “The explanation for our findings and the underlying mechanism are not clear.”
One area of the study that warrants a further look: Can quitting alcohol reverse previous mental health damage caused by alcohol use?
Another interesting tidbit: The study says that quitting alcohol could help reduce stress from life events that would normally have you hitting the bottle.
“Alcohol cessation may also reduce stressful life events, such as conflict within family, difficulties in employment and legal troubles, resulting in improved mental well-being.”
Thinking of giving up booze? New York’s bustling sober scene is surging in popularity.
Link: https://nypost.com/2019/07/10/shunning-booze-may-improve-womens-mental-health-study/?utm_source=url_sitebuttons&utm_medium=site%20buttons&utm_campaign=site%20buttons
Tuesday, June 4, 2019
Kurt Vonnegut > Quotes
“I tend to think of human beings as huge, rubbery test tubes, too, with chemical reactions seething inside. When I was a boy, I saw a lot of people with goiters. So did Dwayne Hoover, the Pontiac dealer who is the hero of this book. Those unhappy Earthlings had such swollen thyroid glands that they seemed to have zucchini squash growing from their throats.
All they had to do in order to have ordinary lives, it turned out, was to consume less than one-millionth of an ounce of iodine every day.
My own mother wrecked her brains with chemicals, which were supposed to make her sleep.
When I get depressed, I take a little pill, and I cheer up again.
And so on.
So it is a big temptation to me, when I create a character for a novel, to say that he is what he is because of faulty wiring, or because of microscopic amounts of chemicals which he ate or failed to eat on that particular day.”
― Kurt Vonnegut, Breakfast of Champions
Read more quotes from Kurt Vonnegut
A Landmark Study on the Origins of Alcoholism
“We cured alcoholism in every rat we ever tried,” says Heilig, who is now at Linköping University in Sweden. “And at the end of every paper, we wrote: This will lead to an exciting treatment.
But everything we took from these animal models to the clinic failed. We needed to go back to the drawing board.” Heilig doesn’t buy that mice and rats have nothing to teach us about addiction. It’s more that researchers have been studying them in the wrong way."
A Landmark Study on the Origins of Alcoholism
SCIENCE
A Landmark Study on the Origins of Alcoholism
By studying rats in a smarter way, scientists are finally learning something useful about why some drinkers become addicted and others don’t.
A Landmark Study on the Origins of Alcoholism
SCIENCE
A Landmark Study on the Origins of Alcoholism
By studying rats in a smarter way, scientists are finally learning something useful about why some drinkers become addicted and others don’t.
JUN 21, 2018
For Markus Heilig, the years of dead ends were starting to grate.
A seasoned psychiatrist, Heilig joined the National Institutes of Health in 2004 with grand ambitions of finding new ways to treat addiction and alcoholism.
Only 15% of regular drinkers become dependent on alcohol.
AXEL BUECKERT / SHUTTERSTOCK
A seasoned psychiatrist, Heilig joined the National Institutes of Health in 2004 with grand ambitions of finding new ways to treat addiction and alcoholism.
“It was the age of the neuroscience revolution, and all this new tech gave us many ways of manipulating animal brains,” he recalls.
By studying addictive behavior in laboratory rats and mice, he would pinpoint crucial genes, molecules, and brain regions that could be targeted to curtail the equivalent behaviors in people.
It wasn’t to be.
It wasn’t to be.
The insights from rodent studies repeatedly proved to be irrelevant. Many researchers and pharmaceutical companies became disillusioned.
“We cured alcoholism in every rat we ever tried,” says Heilig, who is now at Linköping University in Sweden.
“And at the end of every paper, we wrote: This will lead to an exciting treatment.
But everything we took from these animal models to the clinic failed. We needed to go back to the drawing board.”
Heilig doesn’t buy that mice and rats have nothing to teach us about addiction. It’s more that researchers have been studying them in the wrong way.
Typically, they’ll let the animals self-administer drugs by pressing a lever, which they almost always learn to do. That should have been a red flag.
When humans regularly drink alcohol, only 15 percent or so become dependent on the stuff.
Why them and not the other 85 percent?
That’s the crucial question, and you won’t answer it with an experiment in which every rodent becomes addicted.
Eric Augier, who recently joined Heilig’s team, tried a different approach—one pioneered in his former laboratory to study cocaine addiction. After training rats to self-administer alcohol, he offered them some sugary water, too. This better mimics real life, in which drugs exist simultaneously with other pleasurable substances. Given a choice between booze and nectar, most rats chose the latter. But not all of them:
Of the 32 rats that Augier first tested, four ignored the sugar and kept on shooting themselves up with alcohol.
“Four rats is laughable,” says Heilig, referring to the study’s small size, “but 620 rats later, no one’s laughing.” Augier repeated the experiment with more rats of various breeds, and always got the same results.
Consistently, 15 percent of them choose alcohol over sugar—the same number as the proportion of human drinkers who progress to alcoholism.
Those alcohol-preferring rats showed other hallmarks of human addiction, too.
1)They spend more effort to get a sip of alcohol than their sugar-preferring peers, and
2) they kept on drinking even when their booze supply was spiked with an intensely bitter chemical or paired with an electric shock.
“That was striking to me, as a clinician,” says Heilig.
“Embedded in the criteria for diagnosing alcoholism is that people continue to take drugs despite good knowledge of the fact that it will harm or kill them.”
Many lab studies treat animals as if they were identical, and any variation in their behavior is just unhelpful noise.
But in Augier’s work, the variation is the important bit. It’s what points to the interesting underlying biology.
“This is a really good study,” says Michael Taffe, a neuroscientist at the Scripps Research Institute who studies drug addiction. “Since only a minority of humans experience a transition to addiction, [an approach] such as this is most likely to identify the specific genetic variants that convey risk.”
That is exactly what the team did next. They compared the alcohol-preferring and sugar-preferring rats and looked for differences in the genes that were active in their brains.
They focused on six regions that are thought to be involved in addiction, and found no differences in five. “But in the sixth, we did,” says Heilig. “And it made me smile because I started out doing my Ph.D. on the amygdala.”
The amygdala is an almond-shaped region that sits deep within the brain, and is heavily
involved in processing emotions.
When Augier looked at the amygdala of alcoholic rats, he found signs of unusually low activity in several genes, all of which are linked to a chemical called gaba.
Gaba is a molecular red light: Certain neurons make and release it to stop their neighbors from firing. Once that’s done, the gaba-making neurons use an enzyme called GAT3 to pump the molecule back into themselves, so they can reuse it.
But in the amygdala of alcohol-preferring rats, the gene that makes GAT3 is much less active, and makes just half the usual levels of the pump. Gaba accumulates around the neighboring neurons, making them abnormally inactive.
The consequences of this are unclear, but Heilig thinks that all this extra gabahampers the rats’ ability to deal with fear and stress. They are naturally more anxious, which might explain their vulnerability to alcohol.
He predicts it will take another five years of work to fully close this loop. But for now, his team have definitely shown that GAT3—the gaba-recycling pump—is important.
They took rats that prefer sugar and deliberately reduced the levels of GAT3 in their amygdala. This simple procedure was enough to convert those resilient rodents into addiction-prone, alcohol-preferring 15-percenters.
At this point, the team submitted their result to a journal, which agreed to publish them.
Good news—but after Heilig’s long history with rat-shaped dead-ends, he wanted to do one more experiment. “Curing alcoholism in rats is not important,” he says. “What’s important is what this looks like in humans with alcohol addiction.”
As it happens, it looks much the same. Heilig’s colleagues examined postmortem tissue samples from people who had donated their brains to research, some of whom had alcohol addiction. As in the rats, they found nothing unusual in five of six brain regions. But in the amygdala, they found low levels of GAT3.
Others scihing out the details behind these somewhat hazy links.
“It is a very significant studentists have found connections between alcoholism, the amygdala, and gaba-related genes. But by identifying rats that are particularly vulnerable to alcoholism, Heilig’s team has begun flesy that will impact the alcohol research field deeply,” says Jun Wang from Texas A&M University.
“Identifying GAT3 is not that important because alcoholism is controlled by multiple genes, but [the team’s new approach] will help to find those genes. It’s a wonderful method for modeling human alcoholism.”
There are other signs that what Heilig found is relevant to humans as well as rats.
A decade ago, a French cardiologist named Olivier Ameisen claimed to have cured his own alcoholism by taking a drug called baclofen.
“That was met with skepticism, and there was no basic science to support his claims,” says Heilig. But there is now: Baclofen stops neurons from releasing gaba. If individuals with alcoholism aren’t good at recycling this chemical, it might be possible to compensate by producing less of it in the first place.
But baclofen is controversial. It has been tested in several clinical trials, to mixed results.
Two recent studies, which analyzed the results from these trials, concluded that the drug’s ability to treat alcoholism is only “slightly above placebo effects” and its growing use is “premature.” It can be harmful, too.
People quickly build up a tolerance to it, which prompts them to seek higher doses.
They can experience severe side effects, and France has seen more than 100 cases of people inadvertently poisoning themselves with baclofen. “It’s a terrible drug,” Heilig says.
Other drugs like benzodiazepines also exert their effects through gaba, but like baclofen, they’re easily abused themselves. “They’re a good alternative for alcoholism in the short term but they’re not safe in the long term,” says Lara Ray from UCLA.
But Heilig’s study suggests that other chemicals, which could influence gaba levels in more subtle ways, might help people to control their addictions. Several such substances are in development, and Heilig’s team can see if they change the choices of their alcohol-preferring rats.
“It’s just such an impressive breakthrough for the field of alcoholism, with real potential for therapies,” Ray adds.
ED YONG is a staff writer at The Atlantic, where he covers science.
But everything we took from these animal models to the clinic failed. We needed to go back to the drawing board.”
Heilig doesn’t buy that mice and rats have nothing to teach us about addiction. It’s more that researchers have been studying them in the wrong way.
Typically, they’ll let the animals self-administer drugs by pressing a lever, which they almost always learn to do. That should have been a red flag.
When humans regularly drink alcohol, only 15 percent or so become dependent on the stuff.
Why them and not the other 85 percent?
That’s the crucial question, and you won’t answer it with an experiment in which every rodent becomes addicted.
Eric Augier, who recently joined Heilig’s team, tried a different approach—one pioneered in his former laboratory to study cocaine addiction. After training rats to self-administer alcohol, he offered them some sugary water, too. This better mimics real life, in which drugs exist simultaneously with other pleasurable substances. Given a choice between booze and nectar, most rats chose the latter. But not all of them:
Of the 32 rats that Augier first tested, four ignored the sugar and kept on shooting themselves up with alcohol.
“Four rats is laughable,” says Heilig, referring to the study’s small size, “but 620 rats later, no one’s laughing.” Augier repeated the experiment with more rats of various breeds, and always got the same results.
Consistently, 15 percent of them choose alcohol over sugar—the same number as the proportion of human drinkers who progress to alcoholism.
Those alcohol-preferring rats showed other hallmarks of human addiction, too.
1)They spend more effort to get a sip of alcohol than their sugar-preferring peers, and
2) they kept on drinking even when their booze supply was spiked with an intensely bitter chemical or paired with an electric shock.
“That was striking to me, as a clinician,” says Heilig.
“Embedded in the criteria for diagnosing alcoholism is that people continue to take drugs despite good knowledge of the fact that it will harm or kill them.”
Many lab studies treat animals as if they were identical, and any variation in their behavior is just unhelpful noise.
But in Augier’s work, the variation is the important bit. It’s what points to the interesting underlying biology.
“This is a really good study,” says Michael Taffe, a neuroscientist at the Scripps Research Institute who studies drug addiction. “Since only a minority of humans experience a transition to addiction, [an approach] such as this is most likely to identify the specific genetic variants that convey risk.”
That is exactly what the team did next. They compared the alcohol-preferring and sugar-preferring rats and looked for differences in the genes that were active in their brains.
They focused on six regions that are thought to be involved in addiction, and found no differences in five. “But in the sixth, we did,” says Heilig. “And it made me smile because I started out doing my Ph.D. on the amygdala.”
The amygdala is an almond-shaped region that sits deep within the brain, and is heavily
involved in processing emotions.
When Augier looked at the amygdala of alcoholic rats, he found signs of unusually low activity in several genes, all of which are linked to a chemical called gaba.
Gaba is a molecular red light: Certain neurons make and release it to stop their neighbors from firing. Once that’s done, the gaba-making neurons use an enzyme called GAT3 to pump the molecule back into themselves, so they can reuse it.
But in the amygdala of alcohol-preferring rats, the gene that makes GAT3 is much less active, and makes just half the usual levels of the pump. Gaba accumulates around the neighboring neurons, making them abnormally inactive.
The consequences of this are unclear, but Heilig thinks that all this extra gabahampers the rats’ ability to deal with fear and stress. They are naturally more anxious, which might explain their vulnerability to alcohol.
He predicts it will take another five years of work to fully close this loop. But for now, his team have definitely shown that GAT3—the gaba-recycling pump—is important.
They took rats that prefer sugar and deliberately reduced the levels of GAT3 in their amygdala. This simple procedure was enough to convert those resilient rodents into addiction-prone, alcohol-preferring 15-percenters.
At this point, the team submitted their result to a journal, which agreed to publish them.
Good news—but after Heilig’s long history with rat-shaped dead-ends, he wanted to do one more experiment. “Curing alcoholism in rats is not important,” he says. “What’s important is what this looks like in humans with alcohol addiction.”
As it happens, it looks much the same. Heilig’s colleagues examined postmortem tissue samples from people who had donated their brains to research, some of whom had alcohol addiction. As in the rats, they found nothing unusual in five of six brain regions. But in the amygdala, they found low levels of GAT3.
Others scihing out the details behind these somewhat hazy links.
“It is a very significant studentists have found connections between alcoholism, the amygdala, and gaba-related genes. But by identifying rats that are particularly vulnerable to alcoholism, Heilig’s team has begun flesy that will impact the alcohol research field deeply,” says Jun Wang from Texas A&M University.
“Identifying GAT3 is not that important because alcoholism is controlled by multiple genes, but [the team’s new approach] will help to find those genes. It’s a wonderful method for modeling human alcoholism.”
There are other signs that what Heilig found is relevant to humans as well as rats.
A decade ago, a French cardiologist named Olivier Ameisen claimed to have cured his own alcoholism by taking a drug called baclofen.
“That was met with skepticism, and there was no basic science to support his claims,” says Heilig. But there is now: Baclofen stops neurons from releasing gaba. If individuals with alcoholism aren’t good at recycling this chemical, it might be possible to compensate by producing less of it in the first place.
But baclofen is controversial. It has been tested in several clinical trials, to mixed results.
Two recent studies, which analyzed the results from these trials, concluded that the drug’s ability to treat alcoholism is only “slightly above placebo effects” and its growing use is “premature.” It can be harmful, too.
People quickly build up a tolerance to it, which prompts them to seek higher doses.
They can experience severe side effects, and France has seen more than 100 cases of people inadvertently poisoning themselves with baclofen. “It’s a terrible drug,” Heilig says.
Other drugs like benzodiazepines also exert their effects through gaba, but like baclofen, they’re easily abused themselves. “They’re a good alternative for alcoholism in the short term but they’re not safe in the long term,” says Lara Ray from UCLA.
But Heilig’s study suggests that other chemicals, which could influence gaba levels in more subtle ways, might help people to control their addictions. Several such substances are in development, and Heilig’s team can see if they change the choices of their alcohol-preferring rats.
“It’s just such an impressive breakthrough for the field of alcoholism, with real potential for therapies,” Ray adds.
ED YONG is a staff writer at The Atlantic, where he covers science.
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