Great Sex Never Gets Old – by Kimberly Cunningham – by Kimberly Cunningham
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Here some readers may be thinking “after 40? But I am 70 already” or such, so be assured, there’s no upper limit on the applicability of this book’s writings. The number of 40 was chosen more as the start point of things, because it is an age after which the majority of hormonal declines happen (and with them, often, sex drive and/or physical ability). But, as she explains, this is by no means necessarily an end, and can instead be an exciting new beginning.
She kicks things off with a “wellness check”, before diving into the science of the menopause—and yes, the andropause too.
She doesn’t stop there though, and discusses other hormones besides the obvious ones, and other non-hormonal factors that can affect sex in what for most people is the later half of life.
Nurse Cunningham, much like most of modern science, is strongly pro-HRT, and/but doesn’t claim it to be a magic bullet (though honestly, it can feel like it is! But here we’re reviewing the book, not HRT, so let’s continue), or else this book could have been a leaflet. Instead, she talks about the side-effects to expect (mostly good or neutral, but still, things you don’t want to be taken by surprise by), and what things will just be “a little different” now if you’re running on exogenous bioidentical hormones rather than ones your own body made. A lot of this comes down to how and when one takes them, by the way, since this can be different to your body making its own natural peaks and troughs.
But it’s not all about hormones; there are also plenty of chapters on social and psychological issues, as well as medical issues other than hormones.
The style is very light and conversational, while also casually dropping about 30 pages of scientific references. Like many nurses, the author knows at least as much as doctors when it comes to her area of expertise, and it shows.
Bottom line: if your sex has ever hit a slump, and/or you simply recognize that it could, this book could make a very important difference.
Click here to check out Great Sex Never Gets Old, and enjoy the best of life in the bedroom too!
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Is alcohol good or bad for you? Yes.
10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.
This article originally appeared in Harvard Public Health magazine.
It’s hard to escape the message these days that every sip of wine, every swig of beer is bad for your health. The truth, however, is far more nuanced.
We have been researching the health effects of alcohol for a combined 60 years. Our work, and that of others, has shown that even modest alcohol consumption likely raises the risk for certain diseases, such as breast and esophageal cancer. And heavy drinking is unequivocally harmful to health. But after countless studies, the data do not justify sweeping statements about the effects of moderate alcohol consumption on human health.
Yet we continue to see reductive narratives, in the media and even in science journals, that alcohol in any amount is dangerous. Earlier this month, for instance, the media reported on a new study that found even small amounts of alcohol might be harmful. But the stories failed to give enough context or probe deeply enough to understand the study’s limitations—including that it cherry-picked subgroups of a larger study previously used by researchers, including one of us, who concluded that limited drinking in a recommended pattern correlated with lower mortality risk.
“We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.”
Those who try to correct this simplistic view are disparaged as pawns of the industry, even when no financial conflicts of interest exist. Meanwhile, some authors of studies suggesting alcohol is unhealthy have received money from anti-alcohol organizations.
We believe it’s worth trying, again, to set the record straight. We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.
It’s important to keep in mind that alcohol affects many body systems—not just the liver and the brain, as many people imagine. That means how alcohol affects health is not a single question but the sum of many individual questions: How does it affect the heart? The immune system? The gut? The bones?
As an example, a highly cited study of one million women in the United Kingdom found that moderate alcohol consumption—calculated as no more than one drink a day for a woman—increased overall cancer rates. That was an important finding. But the increase was driven nearly entirely by breast cancer. The same study showed that greater alcohol consumption was associated with lower rates of thyroid cancer, non-Hodgkin lymphoma, and renal cell carcinoma. That doesn’t mean drinking a lot of alcohol is good for you—but it does suggest that the science around alcohol and health is complex.
One major challenge in this field is the lack of large, long-term, high-quality studies. Moderate alcohol consumption has been studied in dozens of randomized controlled trials, but those trials have never tracked more than about 200 people for more than two years. Longer and larger experimental trials have been used to test full diets, like the Mediterranean diet, and are routinely conducted to test new pharmaceuticals (or new uses for existing medications), but they’ve never been done to analyze alcohol consumption.
Instead, much alcohol research is observational, meaning it follows large groups of drinkers and abstainers over time. But observational studies cannot prove cause-and-effect because moderate drinkers differ in many ways from non-drinkers and heavy drinkers—in diet, exercise, and smoking habits, for instance. Observational studies can still yield useful information, but they also require researchers to gather data about when and how the alcohol is consumed, since alcohol’s effect on health depends heavily on drinking patterns.
For example, in an analysis of over 300,000 drinkers in the U.K., one of us found that the same total amount of alcohol appeared to increase the chances of dying prematurely if consumed on fewer occasions during the week and outside of meals, but to decrease mortality if spaced out across the week and consumed with meals. Such nuance is rarely captured in broader conversations about alcohol research—or even in observational studies, as researchers don’t always ask about drinking patterns, focusing instead on total consumption. To get a clearer picture of the health effects of alcohol, researchers and journalists must be far more attuned to the nuances of this highly complex issue.
One way to improve our collective understanding of the issue is to look at both observational and experimental data together whenever possible. When the data from both types of studies point in the same direction, we can have more confidence in the conclusion. For example, randomized controlled trials show that alcohol consumption raises levels of sex steroid hormones in the blood. Observational trials suggest that alcohol consumption also raises the risk of specific subtypes of breast cancer that respond to these hormones. Together, that evidence is highly persuasive that alcohol increases the chances of breast cancer.
Similarly, in randomized trials, alcohol consumption lowers average blood sugar levels. In observational trials, it also appears to lower the risk of diabetes. Again, that evidence is persuasive in combination.
As these examples illustrate, drinking alcohol may raise the risk of some conditions but not others. What does that mean for individuals? Patients should work with their clinicians to understand their personal risks and make informed decisions about drinking.
Medicine and public health would benefit greatly if better data were available to offer more conclusive guidance about alcohol. But that would require a major investment. Large, long-term, gold-standard studies are expensive. To date, federal agencies like the National Institutes of Health have shown no interest in exclusively funding these studies on alcohol.
Alcohol manufacturers have previously expressed some willingness to finance the studies—similar to the way pharmaceutical companies finance most drug testing—but that has often led to criticism. This happened to us, even though external experts found our proposal scientifically sound. In 2018, the National Institutes of Health ended our trial to study the health effects of alcohol. The NIH found that officials at one of its institutes had solicited funding from alcohol manufacturers, violating federal policy.
It’s tempting to assume that because heavy alcohol consumption is very bad, lesser amounts must be at least a little bad. But the science isn’t there, in part because critics of the alcohol industry have deliberately engineered a state of ignorance. They have preemptively discredited any research, even indirectly, by the alcohol industry—even though medicine relies on industry financing to support the large, gold-standard studies that provide conclusive data about drugs and devices that hundreds of millions of Americans take or use daily.
Scientific evidence about drinking alcohol goes back nearly 100 years—and includes plenty of variability in alcohol’s health effects. In the 1980s and 1990s, for instance, alcohol in moderation, and especially red wine, was touted as healthful. Now the pendulum has swung so far in the opposite direction that contemporary narratives suggest every ounce of alcohol is dangerous. Until gold-standard experiments are performed, we won’t truly know. In the meantime, we must acknowledge the complexity of existing evidence—and take care not to reduce it to a single, misleading conclusion.
This article first appeared on The Journalist’s Resource and is republished here under a Creative Commons license.
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What’s the difference between a psychopath and a sociopath? Less than you might think
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Articles about badly behaved people and how to spot them are common. You don’t have to Google or scroll too much to find headlines such as 7 signs your boss is a psychopath or How to avoid the sociopath next door.
You’ll often see the terms psychopath and sociopath used somewhat interchangeably. That applies to perhaps the most famous badly behaved fictional character of all – Hannibal Lecter, the cannibal serial killer from The Silence of the Lambs.
In the book on which the movie is based, Lecter is described as a “pure sociopath”. But in the movie, he’s described as a “pure psychopath”. Psychiatrists have diagnosed him with something else entirely.
So what’s the difference between a psychopath and a sociopath? As we’ll see, these terms have been used at different times in history, and relate to some overlapping concepts.
Benoit Daoust/Shutterstock What’s a psychopath?
Psychopathy has been mentioned in the psychiatric literature since the 1800s. But the latest edition of the Diagnostic Statistical Manual of Mental Disorders (known colloquially as the DSM) doesn’t list it as a recognised clinical disorder.
Since the 1950s, labels have changed and terms such as “sociopathic personality disturbance” have been replaced with antisocial personality disorder, which is what we have today.
Was Hannibal Lecter from The Silence of the Lambs a psychopath, a sociopath or something else entirely? Ralf Liebhold/Shutterstock Someone with antisocial personality disorder has a persistent disregard for the rights of others. This includes breaking the law, repeated lying, impulsive behaviour, getting into fights, disregarding safety, irresponsible behaviours, and indifference to the consequences of their actions.
To add to the confusion, the section in the DSM on antisocial personality disorder mentions psychopathy (and sociopathy) traits. In other words, according to the DSM the traits are part of antisocial personality disorder but are not mental disorders themselves.
US psychiatrist Hervey Cleckley provided the first formal description of psychopathy traits in his 1941 book The Mask of Sanity. He based his description on his clinical observations of nine male patients in a psychiatric hospital. He identified several key characteristics, including superficial charm, unreliability and a lack of remorse or shame.
Canadian psychologist Professor Robert Hare refined these characteristics by emphasising interpersonal, emotional and lifestyle characteristics, in addition to the antisocial behaviours listed in the DSM.
When we draw together all these strands of evidence, we can say a psychopath manipulates others, shows superficial charm, is grandiose and is persistently deceptive. Emotional traits include a lack of emotion and empathy, indifference to the suffering of others, and not accepting responsibility for how their behaviour impacts others.
Finally, a psychopath is easily bored, sponges off others, lacks goals, and is persistently irresponsible in their actions.
So how about a sociopath?
The term sociopath first appeared in the 1930s, and was attributed to US psychologist George Partridge. He emphasised the societal consequences of behaviour that habitually violates the rights of others.
Academics and clinicians often used the terms sociopath and psychopath interchangeably. But some preferred the term sociopath because they said the public sometimes confused the word psychopath with psychosis.
“Sociopathic personality disturbance” was the term used in the first edition of the DSM in 1952. This aligned with the prevailing views at the time that antisocial behaviours were largely the product of the social environment, and that behaviours were only judged as deviant if they broke social, legal, and/or cultural rules.
Some of these early descriptions of sociopathy are more aligned with what we now call antisocial personality disorder. Others relate to emotional characteristics similar to Cleckley’s 1941 definition of a psychopath.
In short, different people had different ideas about sociopathy and, even today, sociopathy is less-well defined than psychopathy. So there is no single definition of sociopathy we can give you, even today. But in general, its antisocial behaviours can be similar to ones we see with psychopathy.
Over the decades, the term sociopathy fell out of favour. From the late 60s, psychiatrists used the term antisocial personality disorder instead.
Born or made?
Both “sociopathy” (what we now call antisocial personality disorder) and psychopathy have been associated with a wide range of developmental, biological and psychological causes.
For example, people with psychopathic traits have certain brain differences especially in regions associated with emotions, inhibition of behaviour and problem solving. They also appear to have differences associated with their nervous system, including a reduced heart rate.
However, sociopathy and its antisocial behaviours are a product of someone’s social environment, and tends to run in families. These behaviours has been associated with physical abuse and parental conflict.
What are the consequences?
Despite their fictional portrayals – such as Hannibal Lecter in Silence of the Lambs or Villanelle in the TV series Killing Eve – not all people with psychopathy or sociopathy traits are serial killers or are physically violent.
But psychopathy predicts a wide range of harmful behaviours. In the criminal justice system, psychopathy is strongly linked with re-offending, particularly of a violent nature.
In the general population, psychopathy is associated with drug dependence, homelessness, and other personality disorders. Some research even showed psychopathy predicted failure to follow COVID restrictions.
But sociopathy is less established as a key risk factor in identifying people at heightened risk of harm to others. And sociopathy is not a reliable indicator of future antisocial behaviour.
In a nutshell
Neither psychopathy nor sociopathy are classed as mental disorders in formal psychiatric diagnostic manuals. They are both personality traits that relate to antisocial behaviours and are associated with certain interpersonal, emotional and lifestyle characteristics.
Psychopathy is thought to have genetic, biological and psychological bases that places someone at greater risk of violating other people’s rights. But sociopathy is less clearly defined and its antisocial behaviours are the product of someone’s social environment.
Of the two, psychopathy has the greatest use in identifying someone who is most likely to cause damage to others.
Bruce Watt, Associate Professor in Psychology, Bond University and Katarina Fritzon, Associate Professor of Psychology, Bond University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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It’s Not A Bloody Trend – by Kat Brown
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This one’s not a clinical book, and the author is not a clinician. However, it’s not just a personal account, either. Kat Brown is an award-winning journalist (with ADHD) and has approached this journalistically.
Not just in terms of investigative journalism, either. Rather, also with her knowledge and understanding of the industry, doing for us some meta-journalism and explaining why the press have gone for many misleading headlines.
Which in this case means for example it’s not newsworthy to say that people have gone undiagnosed and untreated for years and that many continue to go unseen; we know this also about such things as endometriosis, adenomyosis, and PCOS. But some more reactionary headlines will always get attention, e.g. “look at these malingering attention-seekers”.
She also digs into the common comorbidities of various conditions, the differences it makes to friendships, families, relationships, work, self-esteem, parenting, and more.
This isn’t a “how to” book, but there’s a lot of value here if a) you have ADHD, and/or b) you spend any amount of time with someone who does.
Bottom line: if you’d like to understand “what all the fuss is about” in one book, this is the one for ADHD.
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Reporting on psychedelics research or legislation? Proceed with caution
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More cities and states are introducing bills to decriminalize and regulate access to psychedelic drugs, which could potentially become another option to treat mental health conditions and substance use disorders. But the substances remain illegal under U.S. federal law and scientific evidence about their effectiveness is still far from conclusive.
This month alone, California lawmakers introduced a bill to allow people 21 and older to consume psychedelic mushrooms under medical supervision. In Massachusetts, lawmakers are working on a bill that would legalize psilocybin, the active ingredient of psychedelic mushrooms. And Arizona legislators have also introduced a bill that would make psychedelic mushrooms available as a mental health treatment option.
Last December, Congress passed legislation that included funding for psychedelic clinical trials for active-duty service members. And in January this year, the Department of Veterans Affairs announced that it will begin funding research on MDMA, also known as ecstasy, and psilocybin, to treat veterans with post-traumatic stress disorder and depression. This is the first time since the 1960s that the VA is funding research on such compounds, according to the department.
The rise of proposed and passed legislation in recent years necessitates more journalistic coverage. But it’s important for journalists to go beyond what the bills and lawmakers say and include research studies about psychedelics and note the limitations of those studies.
Major medical organizations, including the American Psychiatric Association, have not yet endorsed psychedelics to treat psychiatric disorders, except in clinical trials, due to inadequate scientific evidence.
The authors of a 2023 study published in the journal Therapeutic Advances in Psychopharmacology, also advise “strong caution” regarding the hype around the potential medical use of psychedelics. “There is not enough robust evidence to draw any firm conclusions about the safety and efficacy of psychedelic therapy,” they write.
Scientists are still trying to better understand how psychedelics work, what’s the best dose for treating different mental health conditions and how to reduce the risk of potential side effects such as intense emotional experiences or increased heart rate and blood pressure, the authors of a February 2024 study published in the journal Progress in Neuro-Psychopharmacology and Biological Psychiatry write.
In a 2022 study published in JAMA Psychiatry, Dr. Joshua Siegel and his colleagues at Washington University in St. Louis write that while legislative reform for psychedelic drugs is moving forward rapidly, several issues have not been addressed, including:
- A mechanism for verifying the chemical content of drugs that are obtained from outside the medical establishment.
- Licensure and training criteria for practitioners who wish to provide psychedelic treatment.
- Clinical and billing infrastructure.
- Assessing potential interactions with other drugs.
- How the drugs should be used in populations such as youths, older adults and pregnant people.
“Despite the relative rapidity with which some have embraced psychedelics as legitimate medical treatments, critical questions about the mechanism of action, dose and dose frequency, durability of response to repeated treatments, drug-drug interactions, and the role that psychotherapy plays in therapeutic efficacy remain unanswered,” Siegel and colleagues write.
What are psychedelics?
Psychedelics are among the oldest class of mind-altering substances, used by humans for thousands of years in traditional or religious rituals.
In 2021, 74 million people 12 years and older reported using hallucinogens, according to the National Survey on Drug Use and Health.
The terms “psychedelics” and “hallucinogens” are used interchangeably in public discourse, but scientifically, hallucinogens fall into three groups based on chemical structure and mechanism of action, according to NIH’s National Institute on Drug Abuse:
- Psychedelic drugs, also called “classic psychedelics” or simply “psychedelics,” mainly affect the way the brain processes serotonin, a chemical that carries messages between nerve cells in the brain and the body. These drugs can bring on vivid visions and affect a person’s sense of self, according to NIDA. Drugs in this category include:
- Psilocybin is the active ingredient in psychedelic mushrooms, also known as “magic” mushrooms or shrooms. It’s a Schedule 1 drug in the U.S. under the Controlled Substances Act, which means it has a high potential for abuse and has no accepted medical use. However, some states have decriminalized it, according to NIDA. The drug has also been given the Breakthrough Therapy designation from the FDA, a process to speed up the development and review of drugs, for the treatment of major depressive disorder.
- LSD, or lysergic acid diethylamide, is a synthetic chemical made from a fungus that infects rye. It’s a Schedule 1 drug.
- DMT, or dimethyltryptamine, found in certain plants native to the Amazon rainforest, has been used in religious practices and rituals. The plants are sometimes used to make a tea called ayahuasca. DMT can also be made in the lab as a white powder. DMT is generally smoked or consumed in brews like ayahuasca. It’s a Schedule 1 drug.
- Mescaline, a chemical compound found in a small cactus called peyote, has been used by Indigenous people in northern Mexico and the southwestern U.S. in religious rituals. Mescaline can also be produced in the lab. Mescaline and peyote are Schedule 1 drugs.
- Dissociative drugs affect how the brain processes glutamate, an abundant chemical released by nerve cells in the brain that plays an important role in learning and memory. These drugs can make people feel disconnected from their bodies and surroundings. Drugs in this category include:
- PCP, or phencyclidine, was developed in the 1950s as an injectable anesthetic but was discontinued because patients became agitated and delusional. Today it is an illegal street drug. It’s a Schedule 2 drug, which means it has a high potential for abuse, but lower compared to Schedule 1 drugs.
- Ketamine, a drug developed in the 1960s and used as an anesthetic in the Vietnam War, is approved by the FDA as an anesthetic. It has been shown to play a role in pain management and treatment of depression. It is also illegally used for its hallucinogenic effects. It is a Schedule 3 drug, which means it has a moderate to low potential for physical and psychological dependence. A chemically-similar drug called esketamine is approved by the FDA for the treatment of depression that doesn’t respond to standard treatment.
- Other hallucinogens, which affect different brain functions and can cause psychedelic and potentially dissociative effects, include:
- MDMA, or ecstasy, is a synthetic drug that’s a stimulant and hallucinogen. It is a Schedule 1 drug. It has been given the Breakthrough Therapy designation from the FDA for the treatment of PTSD.
- Salvia is an herb in the mint family that has hallucinogenic effects. It is not a federally controlled drug, but it is controlled in some states, according to the DEA.
- Ibogaine is derived from the root bark of a West African shrub and is a stimulant and hallucinogen. It is a Schedule 1 drug.
Research on psychedelics
There was a wave of studies on psychedelics, particularly LSD, in the 1950s and 1960s, but they came to a halt when the U.S. declared a “War on Drugs” in 1971 and tightened pharmaceutical regulations. There was little research activity until the early 1990s when studies on drugs such as MDMA and DMT began to emerge.
In 2006, researchers at Johns Hopkins University published a seminal double-blind study in which two-thirds of participants — who had never taken psychedelics previously — said their psychedelic sessions were among the most meaningful experiences of their lives.
“These studies, among others, renewed scientific interest in psychedelics and, accordingly, research into their effects has continued to grow since,” Jacob S. Aday and colleagues write in a 2019 study published in Drug Science, Policy and Law.
In their paper, Aday and colleagues argue that 2018 may be remembered as the true turning point in psychedelic research due to “advances within science, increased public interest, and regulatory changes,” such as psilocybin receiving the “breakthrough therapy” status from the FDA.
Today, there are numerous ongoing clinical trials on the therapeutic potential of psychedelics for different conditions, including substance use disorders and mental health conditions such as depression, anxiety and post-traumatic stress disorder.
Given the growing number of studies on psychedelics, the Food and Drug Administration issued a draft guidance in June 2023 for clinical trials with psychedelic drugs, aiming to help researchers design studies that will yield more reliable results for drug development.
The systematic reviews highlighted below show that there’s a lack of robust study designs in many psychedelic clinical trials. Some have small sample sizes. Some include participants who have used psychedelics before, so when they participate in a randomized controlled clinical trial, they know whether they are receiving psychedelic treatment or a placebo. Or, some include participants who may have certain expectations due to positive coverage in the lay media, hence creating bias in the results.
If you’re covering a study about psychedelics…
It’s important for journalists to pay close attention to study design and speak with an expert who is not involved in the study.
In a February 2024 blog post from Harvard Law School’s Petrie-Flom Center, Leiden University professors Eiko I. Fried and Michiel van Elk share several challenges in psychedelic research:
- “Conclusions are dramatically overstated in many studies. This ranges from conclusions in the results sections, abstracts, and even titles of papers not consistent with the reported results.”
- “There is emerging evidence that adverse events resulting from psychedelic substances are both common and underreported.”
- Some studies don’t have control groups, which can create problems for interpreting results, “because treatments like psychedelics need to be compared against a placebo or other treatment to conclude that they work beyond the placebo effect or already existing, readily available treatments.”
- “Participants in psychedelic studies usually know if they are in the treatment or control group, which artificially increases the apparent efficacies of psychedelics in clinical studies.”
- Small sample sizes can affect the statistical power and generalizability of the findings. “Small samples also mean that results are not representative. For example, participants with severe or comorbid mental health problems are commonly excluded from psychedelic studies, and therefore results may look better in these studies than in real-world psychiatric settings.”
- Many studies do not include long-term follow-ups of participants. “Studying how these people are feeling a few days or weeks after they receive treatment is not sufficient to establish that they are indeed cured from depression.”
Fried and van Elk also have a useful checklist for assessing the quality and scientific rigor of psychedelic research in their 2023 study “History Repeating: Guidelines to Address Common Problems in Psychedelic Science,” published in the journal Therapeutic Advances in Psychopharmacology.
Journalists should also remind their audiences that the drugs are still illegal under federal law and can pose a danger to health.
In California, the number of emergency room visits involving the use of hallucinogens increased by 54% between 2016 and 2022, according to a January 2024 study published in Addiction. Meanwhile, the law enforcement seizure of psychedelic mushrooms has risen dramatically, increasing nearly four-fold between 2017 and 2022, according to a February 2024 study published in the journal Drug and Alcohol Dependence.
Below, we have curated and summarized five recent studies, mostly systematic reviews and meta-analyses, which examine various aspects of psychedelic drugs, including legislative reform; long-term effects; efficacy and safety for the treatment of anxiety, depression and PTSD; and participation of older adults in clinical trials. The research summaries are followed by recommended reading.
Research roundup
Psychedelic Drug Legislative Reform and Legalization in the US
Joshua S. Siegel, James E. Daily, Demetrius A. Perry and Ginger E. Nicol. JAMA Psychiatry, December 2022.The study: Most psychedelics are Schedule I drugs federally, but state legislative reforms are changing the prospects of the drugs’ availability for treatment and their illegal status. For a better understanding of the legislative reform landscape around Schedule I psychedelic drugs, researchers collected all bills and ballot initiatives related to psychedelic drugs that were introduced into state legislatures between 2019 and September 2022. They used publicly available sources, including BillTrack50, Ballotpedia and LexisNexis.
The findings: In total, 25 states considered 74 bills, although the bills varied widely in their framework. A majority proposed decriminalization but only a few would require medical oversight and some would not even require training or licensure, the authors write. Ten of those bills became law in seven states — Colorado, Connecticut, Hawaii, New Jersey, Oregon, Texas and Washington. As of August 1, 2022, 32 bills were dead and 32 remained active.
The majority of the bills — 67 of them — referred to psilocybin; 27 included both psilocybin and MDMA; 43 proposed decriminalization of psychedelic drugs.
To predict the future legalization of psychedelics, the authors also created two models based on existing medical and recreational marijuana reform. Using 2020 as the year of the first psychedelic decriminalization in Oregon, their models predict that 26 states will legalize psychedelics between 2033 and 2037.
In the authors’ words: “Despite the relative rapidity with which some have embraced psychedelics as legitimate medical treatments, critical questions about the mechanism of action, dosing and dose frequency, durability of response to repeated treatments, drug-drug interactions, and the role psychotherapy plays in therapeutic efficacy remain unanswered. This last point is critical, as a significant safety concern associated with drugs like psilocybin, MDMA, or LSD is the suggestibility and vulnerability of the patient while under the influence of the drug. Thus, training and clinical oversight is necessary to ensure safety and also therapeutic efficacy for this divergent class of treatments.”
Who Are You After Psychedelics? A Systematic Review and a Meta-Analysis of the Magnitude of Long-Term Effects of Serotonergic Psychedelics on Cognition/Creativity, Emotional Processing and Personality
Ivana Solaja, et al. Neuroscience & Behavioral Reviews, March 2024.The study: Many anecdotal reports and observational studies have reported that psychedelics, even at microdoses, which are roughly one-tenth of a typical recreational dose, may enhance certain aspects of cognition and/or creativity, including coming up with new, useful ideas. Cognition is a “range of intellectual functions and processes involved in our ability to perceive, process, comprehend, store and react to information,” the authors explain. There are established relationships between impaired cognitive functioning and mental health disorders.
Due to limitations such as a lack of rigorous study designs, various populations in the studies and lack of documented dosage, it’s difficult to draw any conclusions about changes that last at least one week as a result of consuming psychedelics.
The authors screened 821 studies and based on the criteria they had set, found 10 to be eligible for the review and meta-analysis. The drugs in the studies include psilocybin, ayahuasca and LSD.
The findings: Overall, there was little evidence that these psychedelics have lasting effects on creativity. Also, there was not sufficient evidence to determine if this group of psychedelics enhances cognition and creativity in healthy populations or improves cognitive deficits in the study populations.
Pooled data from three studies showed lasting improvement in emotional processing — perceiving, expressing and managing emotions.
The studies offered little evidence suggesting lasting effects of psychedelics on personality traits.
In the authors’ words: “Results from this study showed very limited evidence for any lasting beneficial effects across these three psychological constructs. However, preliminary meta-analytic evidence suggested that these drugs may have the potential to cause lasting improvement in emotional recognition time. Future studies investigating these constructs should employ larger sample sizes, better control conditions, standardized and validated measures and longer-term follow-ups.”
The Impact of Psychedelics on Patients with Alcohol Use Disorder: A Systematic Review with Meta-Analysis
Dakota Sicignano, et al. Current Medical Research and Opinion, December 2023.The study: Researchers are exploring the psychedelics’ potential for the treatment of alcohol use disorder, which affected nearly 30 million Americans in 2022. The authors of this study searched PubMed from 1960 to September 2023 for studies on the use of psychedelics to treat alcohol use disorder. Out of 174 English-language studies, they selected six studies that met the criteria for their analysis.
The findings: LSD and psilocybin are promising therapies for alcohol use disorder, the authors report. However, five of the six trials were conducted in the 1960s and 1970s and may not reflect the current treatment views. Also, four of the six studies included patients who had used psychedelics before participating in the study, increasing the risk of bias.
In the authors’ words: “Despite the existence of several clinical trials showing relatively consistent benefits of psychedelic therapy in treating alcohol use disorder, there are important limitations in the dataset that must be appreciated and that preclude a conclusive determination of its value for patient care at this time.”
Older Adults in Psychedelic-Assisted Therapy Trials: A Systematic Review
Lisa Bouchet, et al. Journal of Psychopharmacology, January 2024.The study: People 65 years and older have been underrepresented in clinical trials involving psychedelics, including the use of psilocybin for the treatment of depression and anxiety. About 15% of adults older than 60 suffer from mental health issues, the authors note. They wanted to quantify the prevalence of older adults enrolled in psychedelic clinical trials and explore safety data in this population. They searched for English-language studies in peer-reviewed journals from January 1950 to September 2023. Of 4,376 studies, the authors selected 36. The studies involved psilocybin, MDMA, LSD, ayahuasca, and DPT (dipropyltryptamine), which is a less-studied synthetic hallucinogen.
The findings: Of the 1,400 patients participating in the selected studies, only 19 were 65 and older. Eighteen received psychedelics for distress related to cancer or other life-threatening illnesses. In a trial of MDMA-assisted therapy for PTSD, only one older adult was included. Adverse reactions to the drugs among older patients, including heart and gastrointestinal issues were resolved within two days and didn’t have a long-lasting impact.
In the authors’ words: “Although existing data in older adults is limited, it does provide preliminary evidence for the safety and tolerability of [psychedelic-assisted therapy] in older patients, and as such, should be more rigorously studied in future clinical trials.”
Efficacy and Safety of Four Psychedelic-Assisted Therapies for Adults with Symptoms of Depression, Anxiety, and Posttraumatic Stress Disorder: A Systematic Review and Meta-Analysis
Anees Bahji, Isis Lunsky, Gilmar Gutierrez and Gustavo Vazquez. Journal of Psychoactive Drugs, November 2023.The study: LSD, psilocybin, ayahuasca and MDMA have been approved for clinical trials on psychedelic-assisted therapy of mental health conditions in Canada and the U.S. However, major medical associations, including the American Psychiatric Association, have argued that there is insufficient scientific evidence to endorse these drugs for treating mental health disorders. To better understand the current evidence, researchers reviewed 18 blinded, randomized controlled trials, spanning 2008 through 2023. Most studies were conducted in the U.S. or Switzerland.
The findings: The studies overall suggest preliminary evidence that psychedelic drugs are mostly well-tolerated. Psilocybin and MDMA therapies may offer relief from depression and PTSD symptoms for at least a year. Most studies also used therapy and psychological support along with psychedelics.
In the authors’ words: “Despite the promising evidence presented by our study and previous reviews in the field, the evidence base remains limited and underpowered. Long-term efficacy and safety data are lacking,” the authors write. “Future steps should encourage and highlight the need for more robust larger scale randomized controlled trials with longer follow-up periods, and efforts to address regulatory and legal barriers through the collaborations between researchers, healthcare professionals, regulatory bodies, and policymakers.”
This article first appeared on The Journalist’s Resource and is republished here under a Creative Commons license.
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A short history of sunscreen, from basting like a chook to preventing skin cancer
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Australians have used commercial creams, lotions or gels to manage our skin’s sun exposure for nearly a century.
But why we do it, the preparations themselves, and whether they work, has changed over time.
In this short history of sunscreen in Australia, we look at how we’ve slathered, slopped and spritzed our skin for sometimes surprising reasons.
At first, suncreams helped you ‘tan with ease’
This early sunscreen claimed you could ‘tan with ease’.
Trove/NLASunscreens have been available in Australia since the 30s. Chemist Milton Blake made one of the first.
He used a kerosene heater to cook batches of “sunburn vanishing cream”, scented with French perfume.
His backyard business became H.A. Milton (Hamilton) Laboratories, which still makes sunscreens today.
Hamilton’s first cream claimed you could “
Sunbathe in Comfort and TAN with ease”. According to modern standards, it would have had an SPF (or sun protection factor) of 2.The mirage of ‘safe tanning’
A tan was considered a “modern complexion” and for most of the 20th century, you might put something on your skin to help gain one. That’s when “safe tanning” (without burning) was thought possible.
This 1967 Coppertone advertisement urged you to ‘tan, not burn’.
SenseiAlan/Flickr, CC BY-SASunburn was known to be caused by the UVB component of ultraviolet (UV) light. UVA, however, was thought not to be involved in burning; it was just thought to darken the skin pigment melanin. So, medical authorities advised that by using a sunscreen that filtered out UVB, you could “safely tan” without burning.
But that was wrong.
From the 70s, medical research suggested UVA penetrated damagingly deep into the skin, causing ageing effects such as sunspots and wrinkles. And both UVA and UVB could cause skin cancer.
Sunscreens from the 80s sought to be “broad spectrum” – they filtered both UVB and UVA.
Researchers consequently recommended sunscreens for all skin tones, including for preventing sun damage in people with dark skin.
Delaying burning … or encouraging it?
Up to the 80s, sun preparations ranged from something that claimed to delay burning, to preparations that actively encouraged it to get that desirable tan – think, baby oil or coconut oil. Sun-worshippers even raided the kitchen cabinet, slicking olive oil on their skin.
One manufacturer’s “sun lotion” might effectively filter UVB; another’s merely basted you like a roast chicken.
Since labelling laws before the 80s didn’t require manufacturers to list the ingredients, it was often hard for consumers to tell which was which.
At last, SPF arrives to guide consumers
In the 70s, two Queensland researchers, Gordon Groves and Don Robertson, developed tests for sunscreens – sometimes experimenting on students or colleagues. They printed their ranking in the newspaper, which the public could use to choose a product.
An Australian sunscreen manufacturer then asked the federal health department to regulate the industry. The company wanted standard definitions to market their products, backed up by consistent lab testing methods.
In 1986, after years of consultation with manufacturers, researchers and consumers, Australian Standard AS2604 gave a specified a testing method, based on the Queensland researchers’ work. We also had a way of expressing how well sunscreens worked – the sun protection factor or SPF.
This is the ratio of how long it takes a fair-skinned person to burn using the product compared with how long it takes to burn without it. So a cream that protects the skin sufficiently so it takes 40 minutes to burn instead of 20 minutes has an SPF of 2.
Manufacturers liked SPF because businesses that invested in clever chemistry could distinguish themselves in marketing. Consumers liked SPF because it was easy to understand – the higher the number, the better the protection.
Australians, encouraged from 1981 by the Slip! Slop! Slap! nationwide skin cancer campaign, could now “slop” on a sunscreen knowing the degree of protection it offered.
How about skin cancer?
It wasn’t until 1999 that research proved that using sunscreen prevents skin cancer. Again, we have Queensland to thank, specifically the residents of Nambour. They took part in a trial for nearly five years, carried out by a research team led by Adele Green of the Queensland Institute of Medical Research. Using sunscreen daily over that time reduced rates of squamous cell carcinoma (a common form of skin cancer) by about 60%.
Follow-up studies in 2011 and 2013 showed regular sunscreen use almost halved the rate of melanoma and slowed skin ageing. But there was no impact on rates of basal cell carcinoma, another common skin cancer.
By then, researchers had shown sunscreen stopped sunburn, and stopping sunburn would prevent at least some types of skin cancer.
What’s in sunscreen today?
An effective sunscreen uses one or more active ingredients in a cream, lotion or gel. The active ingredient either works:
“chemically” by absorbing UV and converting it to heat. Examples include PABA (para-aminobenzoic acid) and benzyl salicylate, or
“physically” by blocking the UV, such as zinc oxide or titanium dioxide.
Physical blockers at first had limited cosmetic appeal because they were opaque pastes. (Think cricketers with zinc smeared on their noses.)
With microfine particle technology from the 90s, sunscreen manufacturers could then use a combination of chemical absorbers and physical blockers to achieve high degrees of sun protection in a cosmetically acceptable formulation.
Where now?
Australians have embraced sunscreen, but they still don’t apply enough or reapply often enough.
Although some people are concerned sunscreen will block the skin’s ability to make vitamin D this is unlikely. That’s because even SPF50 sunscreen doesn’t filter out all UVB.
There’s also concern about the active ingredients in sunscreen getting into the environment and whether their absorption by our bodies is a problem.
Sunscreens have evolved from something that at best offered mild protection to effective, easy-to-use products that stave off the harmful effects of UV. They’ve evolved from something only people with fair skin used to a product for anyone.
Remember, slopping on sunscreen is just one part of sun protection. Don’t forget to also slip (protective clothing), slap (hat), seek (shade) and slide (sunglasses).
Laura Dawes, Research Fellow in Medico-Legal History, Australian National University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Huperzine A: A Natural Nootropic
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Huperzine A: A Natural Nootropic
Huperzine A is a compound, specifically a naturally occurring sesquiterpene alkaloid, that functions as an acetylcholinesterase inhibitor. If that seems like a bunch of big words, don’t worry, we’ll translate in a moment.
First, a nod to its origins: it is found in certain kinds of firmoss, especially the “toothed clubmoss”, Huperzia serrata, which grows in many Asian countries.
What’s an acetylcholinesterase inhibitor?
Let’s do this step-by-step:
- An acetylcholinesterase inhibitor is a compound that inhibits acetylcholinesterase.
- Acetylcholinesterase is an enzyme that catalyzes (speeds up) the breakdown of acetylcholine.
- Acetylcholine is a neurotransmitter; it’s an ester of acetic acid and choline.
- This is the main neurotransmitter of the parasympathetic nervous system, and is also heavily involved in cognitive functions including memory and creative thinking.
What this means: if you take an acetylcholinesterase inhibitor like huperzine A, it will inhibit acetylcholinesterase, meaning you will have more acetylcholine to work with. That’s good.
What can I expect from it?
Huperzine A has been well-studied for a while, mostly for the prevention and treatment of Alzheimer’s disease:
- New insights into huperzine A for the treatment of Alzheimer’s disease
- Huperzine A: Is it an Effective Disease-Modifying Drug for Alzheimer’s Disease?
- Huperzine A and Its Neuroprotective Molecular Signaling in Alzheimer’s Disease
However, research has suggested that huperzine A is much better as a prevention than a treatment:
❝A central event in the pathogenesis of Alzheimer’s disease (AD) is the accumulation of senile plaques composed of aggregated amyloid-β (Aβ) peptides.
Ex vivo electrophysiological experiments showed that 10 μM of Aβ1-40 significantly decreased the effect of the AChE inhibitor huperzine A on the synaptic potential parameters. ❞
~ Dr. Irina Zueva
In other words: the answer to the titular question is “Yes, yes it can”
And, to translate Dr. Zueva’s words into simple English:
- People with Alzheimer’s have amyloid-β plaque in their brains
- That plaque reduces the effectiveness of huperzine A
So, what if we take it in advance? That works much better:
❝Pre-treatment with [huperzine A] at concentrations of 50, 100, and 150 µg/mL completely inhibited the secretion of PGE2, TNF-α, IL-6, and IL-1β compared to post-treatment with [huperzine A].
This suggests that prophylactic treatment is better than post-inflammation treatment. ❞
~ Dr. Thu Kim Dang
Source: Anti-neuroinflammatory effects of alkaloid-enriched extract from Huperzia serrata
As you may know, neuroinflammation is a big part of Alzheimer’s pathology, so we want to keep that down. The above research suggests we should do that sooner rather than later.
Aside from holding off dementia, can it improve memory now, too?
There’s been a lot less research done into this (medicine is generally more concerned with preventing/treating disease, than improving the health of healthy people), but there is some:
^This is a small (n=68) old (1999) study for which the full paper has mysteriously disappeared and we only get to see the abstract. It gave favorable results, though.
The effects of huperzine A and IDRA 21 on visual recognition memory in young macaques
^This, like most non-dementia research into HupA, is an animal study. But we chose to spotlight this one because, unlike most of the studies, it did not chemically lobotomize the animals first; they were and remained healthy. That said, huperzine A improved the memory scores most for the monkeys that performed worst without it initially.
Where can I get it?
As ever, we don’t sell it, but here’s an example product on Amazon for your convenience
Enjoy!
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