Tag: brain function

Exploring Nootropic Psychedelics for Cognitive Health
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Posted by veriheal on 03/26/2024 in Alternative Medicine

Nootropics are a diverse class of substances known to improve thinking, learning, and memory. Their ability to improve cognitive function is why nootropics are often referred to as “smart drugs.”

It should be noted that “nootropics” is an incredibly broad term. It includes everything from herbal extracts like ginseng to prescription drugs like Ritalin and rivastigmine. Do you drink coffee or tea? Guess what, those two substances are also nootropics. Simply put, if a substance affects your brain in a way that improves cognitive function, then it is a nootropic.

As if that wasn’t enough to keep track of, new research indicates that psychedelics may also fit under the wide nootropic umbrella. We’ll dive into the growing evidence surrounding psychedelics’ nootropic properties and explain how they compare to established nootropic substances.

Nootropics in Psychedelics

Psychedelic research is an incredibly new field made possible by recent shifts in public opinion and regulatory changes. As such, we are only now beginning to understand the effects of psychedelics and their underlying causes.

Here’s what we currently know about the therapeutic effects of psychedelics:
- DMT-heavy ayahuasca is believed to facilitate memory reconstruction and neural health.
- Psilocybin is believed to alleviate prescription-resistant depression in addition to alleviating anxiety and providing an overall mood boost.
- Ketamine, similarly, shows great promise in alleviating depression while also showing the potential to treat PTSD, bipolar disorder, and OCD.
What these psychedelics have in common is that their therapeutic effects seem to be made possible by their ability to promote either neuroprotection, neuroplasticity, or neurogenesis. This seems to indicate that psychedelics possess cognitive boosting nootropic properties.

A 2022 study sought to verify the psychedelic-nootropic connection through the lens of LSD. Similar to the psychedelics mentioned above, the substance has been shown to increase “openness to experience, well-being, satisfaction with life, mindfulness, and optimism.”

The team behind the study ran three sets of tests, each meant to verify LSD’s ability to boost a different area of cognitive health. The study found that LSD increased plasticity in human brain organoids, increased novelty preference in tats, and improved memory consolidation and recall in humans. This was enough for researchers to say, “Altogether, the results suggest that LSD has nootropic effects.”

The Wide World of Nootropics

So, now that we’ve established the scientific momentum propelling psychedelics to nootropic status — where do psychedelics fit in the nootropic landscape? Given how broad the term “nootropics” is, it’s best to start by differentiating traditional nootropics based on their strength.

On the lower end, you have natural substances like coffee and tea as well as dietary substances like ginseng and ginkgo (though these last two have been the subject of much scientific discourse and disagreement). These are best used for gradual cognitive improvements linked with learning.

In the middle, you have prescription drugs, mostly stimulants, like Ritalin and modafinil. These are best for individuals looking to regulate the symptoms of their ADHD or associated attention disorders.

On the very end of the spectrum, you have incredibly potent nootropics used to treat serious brain damage brought upon by brain trauma, infection, or Alzheimer’s. These should only be used under the supervision of a medical professional.

What differentiates psychedelics from (most) of these established nootropics is their effects. As their nickname suggests, established “smart drugs” primarily affect cognitive function when it comes to the processing, retention, and recall of information — things innate to the conventional idea of “intelligence.” Psychedelics, meanwhile, affect cognitive function when it comes to the healing, protecting, and building of new neural connections that facilitate emotional growth previously inhibited by trauma, depression, or anxiety.

With this in mind, consider the “strength” scale we discussed earlier and apply it to psychedelics. On the low end, you have microdoses which can be helpful in boosting gradual emotional-cognitive improvements. At the other end of the scale, you have high-dosage ketamine and DMT treatments, which can help individuals with deep-seated emotional trauma or PTSD, but should only be used under the supervision of a professional. The middle of the scale is where it gets complicated and where further research will help better define the dosage and consumptions best suited for “prescription” psychedelic dosages.

Conclusion

Nootropics represent a wide breadth of substances used to improve cognitive health. Although we are only now beginning to understand how psychedelics work, early research into their therapeutic benefits seems to indicate that they can serve a similar (if not identical) function as nootropics. Unlike traditional nootropics, however, psychedelics address emotional cognitive health. Continued research into psychedelics will be crucial in ensuring the population at large can properly benefit from their therapeutic qualities.
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July 17, 2024
We Have No Drugs to Treat the Deadliest Eating Disorder

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In the 1970s, they tried lithium. Then it was zinc and THC. Anti-anxiety drugs had their turn. So did Prozac and SSRIs and atypical antidepressants. Nothing worked. Patients with anorexia were still unable to bring themselves to eat, still stuck in rigid thought patterns, still chillingly underweight.

A few years ago, a group led by Evelyn Attia, the director of the Center for Eating Disorders at New York Presbyterian Hospital and the New York State Psychiatric Institute, tried giving patients an antipsychotic drug called olanzapine, normally used to treat schizophrenia and bipolar disorder, and known to cause weight gain as a side effect. Those patients in her study who were on olanzapine increased their BMI a bit more than others who were taking a placebo, but the two groups showed no difference in their cognitive and psychological symptoms. This was the only medication trial for treating anorexia that has shown any positive effect at all, Attia told me, and even then, the effects were “very modest.”

Despite nearly half a century of attempts, no pill or shot has been identified to effectively treat anorexia nervosa. Anorexia is well known to be the deadliest eating disorder; the only psychiatric diagnosis with a higher death rate is opioid-use disorder. A 2020 review found people who have been hospitalized for the disease are more than five times likelier to die than their peers without it. The National Institutes of Health has devoted more than $100 million over the past decade to studying anorexia, yet researchers have not found a single compound that reliably helps people with the disorder.

Other eating disorders aren’t nearly so resistant to treatment. The FDA has approved fluoxetine (a.k.a. Prozac) to treat bulimia nervosa and binge-eating disorder (BED); doctors prescribe additional SSRIs off-label to treat both conditions, with a fair rate of success. An ADHD drug, Vyvanse, was approved for BED within two years of the disorder’s official recognition. But when it comes to anorexia, “we’ve tried, I don’t know, eight or 10 fundamentally different kinds of approaches without much in the way of success,” says Scott Crow, an adjunct psychology professor at the University of Minnesota and the vice president of psychiatry for Accanto Health.

The discrepancy is puzzling to anorexia specialists and researchers. “We don’t fully understand why medications work so differently in this group, and boy, do they ever work differently,” Attia told me. Still, experts have some ideas. Over the past few decades, they have been learning about the changes in brain activity that accompany anorexia. For example, Walter Kaye, the founder and executive director of the Eating Disorders Program at UC San Diego, told me that the neurotransmitters serotonin and dopamine, both of which are involved in the brain’s reward system, seem to act differently in anorexia patients.

Perhaps some underlying differences in brain chemistry and function play a role in anorexia patients’ extreme aversion to eating. Or perhaps, the experts I spoke with suggested, these brain changes are at least in part a result of patients’ malnourishment. People with anorexia suffer from many effects of malnutrition: Their bones are more brittle; their brain is smaller; their heart beats slower; their breath comes shorter; their wounds fail to heal. Maybe their neurons respond differently to psychoactive drugs too.

Read: The challenge of treating anorexia in adults

Psychiatrists have found that many patients with anorexia don’t improve with treatment even when medicines are prescribed for conditions other than their eating disorder. If an anorexia patient also has anxiety, for example, taking an anti-anxiety drug would likely fail to relieve either set of symptoms, Attia told me. “Time and again, investigators have found very little or no difference between active medication and placebo in randomized controlled trials,” she said. The fact that fluoxetine seems to help anorexia patients avoid relapse—but only when it’s given after they’ve regained a healthy weight—also supports the notion that malnourished brains don’t respond so well to psychoactive medication. (In that case, the effect might be especially acute for people with anorexia nervosa, because they tend to have lower BMIs than people with other eating disorders.)

Why exactly this would be true remains a mystery. Attia noted that proteins and certain fats have been shown to be crucial for brain function; get too little of either, and the brain might not metabolize drugs in expected ways. Both she and Kaye suggested a possible role for tryptophan, an amino acid that humans get only from food. Tryptophan is converted into serotonin (among other things) when we release insulin after a meal, Kaye said, but in anorexia patients, whose insulin levels tend to be low, that process could end up off-kilter. “We suspect that that might be the reason why [SSRIs] don’t work very well,” he said, though he emphasized that the theory is very speculative.

In the absence of meaningful pharmacologic intervention, doctors who treat anorexia rely on methods such as nutrition counseling and psychotherapy. But even non-pharmaceutical interventions, such as cognitive behavioral therapy, are more effective at treating bulimia and binge-eating disorder than anorexia. Studies from around the world have shown that as many as half of people with anorexia relapse.

Colleen Clarkin Schreyer, a clinical psychologist at Johns Hopkins University, sees both patients with anorexia nervosa and those with bulimia nervosa, and told me that the former can be more difficult to treat—“but not just because of the fact that we don’t have any medication to help us along. I often find that patients with anorexia nervosa are more ambivalent about making behavior change.” Bulimia patients, she said, tend to feel shame about their condition, because binge eating is stigmatized and, well, no one likes vomit. But anorexia patients might be praised for skipping meals or rapidly losing weight, despite the fact that their behaviors can be just as dangerous over the long term as binging and vomiting.

Read: Raising a daughter with a body like mine

Researchers are still trying to find substances that can help anorexia patients. Crow told me that case studies testing a synthetic version of leptin, a naturally occurring human hormone, have produced interesting data. Meanwhile, some early research into using psychedelics, including ketamine, psilocybin, and ayahuasca, suggests that they may relieve some symptoms in some cases. But until randomized, controlled trials are conducted, we won’t know whether or how well any psychedelic really works. Kaye is currently recruiting participants for such a study of psilocybin, which is planned to have multiple sites in the U.S. and Europe.

Pharmaceutical companies just don’t seem that enthusiastic about testing treatments for anorexia, Crow said. “I think that drug makers have taken to heart the message that the mortality is high” among anorexia patients, he told me, and thus avoid the risk of having deaths occur during their clinical trials. And drug development isn’t the only area where the study of anorexia has fallen short. Research on eating disorders tends to be underfunded on the whole, Crow said. That stems, in part, from “a widely prevailing belief that this is something that people could or should just stop … I wish that were how it works, frankly. But it’s not.”

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Rachel Gutman-Wei

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September 7, 2023
Study Confirms Memory, Concentration Issues After Lyme Disease

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Nov. 15, 2022 – People who have been treated for Lyme disease, but continue to have symptoms, have changes in their brains that confirm the memory and concentration problems many of them have reported, a new study has found.

Many people with what’s known as post-treatment Lyme disease – or PTLD – complain about problems with memory and concentration, which sometimes come with fatigue, muscle pain, insomnia, and depression.

To understand potential changes in brain function that might explain these cognitive difficulties, researchers used specialized imaging techniques to compare the brains of 12 adults with PTLD and 18 adults with no history of Lyme disease.

The researchers found changes in the white matter of the brains of those with PTLD. White matter is found in the deeper brain tissues and contains nerve fibers that are extensions of nerve cells.

“We found that … white matter function increased while participants with PTLD were performing a cognitive task,” says lead investigator Cheri Marvel, PhD, an associate professor of neurology and psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine in Baltimore.

“I think if patients heard this, they might feel validated that there is a biologic basis for their persistent symptoms, even if there is no good way to treat the cognitive difficulties yet,” she says. This may be similar to what patients with long COVID experience, Marvel says.

The study was published online Oct. 26 in the journal PLOS One.

‘We Could Begin to Connect the Dots’

“Objective biologic measures” of PTLD symptoms “typically can’t be identified using regular MRIs, CT scans, or blood tests,” senior author John Aucott, MD, director of the Johns Hopkins Lyme Disease Clinical Research Center, said in a news release.

Because of the number of people affected by this condition — 10%-20% of the nearly half a million Americans who contract the disease each year — the researchers felt they needed to “expand” the evaluation methods.

“We were motivated by the persistent complaints of cognitive difficulties by patients who have been treated for their Lyme disease, with a lack of data to explain the reason behind these symptoms,” Marvel says.

It seemed logical “that if there were cognitive and neurological symptoms involved, then the brain may reveal something about this. Then we could begin to connect the dots between the patient experience and the underlying mechanisms driving them,” she says.

To investigate, Marvel’s team used functional magnetic resonance (fMRI), an imaging technique that measures blood flow to areas of the brain, often while specific tasks are performed — in this case, short-term memory tasks that involved memorizing and recalling capital and lowercase letters as well as the alphabetical order of multiple letters.

Those with PTLD performed more slowly on some of the memory tasks, although their slower speed did not affect the accuracy of their performance.

The researchers found unusual activity in the white matter of the frontal lobe — an area of the brain involved in cognitive tasks, such as memory recall and concentration — in the PTLD group.

Typically, this type of tissue sees less blood flow, compared to gray matter in the brain, and is responsible for moving information around the brain and “delivering” it to the gray matter. The amount of activity they saw “is unusual to observe with the MRI methods we used, and we did not see such activity in the healthy control group,” Marvel says.

Sign of Healing?

To confirm the finding, the investigators used a second imaging technique called diffusion tensor imaging in all 12 PTLD patients and 12 of the 18 people without PTLD. The imaging technique detects whether there is water moving within the brain tissue and what direction it goes.

In the patients with PTLD, the researchers found what’s called axon diffusion – or leakage – from the white matter was tied to better brain function. The water that was diffusing was found in the same white matter regions that the first imaging test had identified.

“This led us to speculate that the white matter changes are a healthy response to Lyme disease’s effect on the brain,” Marvel says. She suggests that the increased white matter leakage “may be a marker of healing during PTLD and represent a healthier outcome.”

In the meantime, the researchers want to work with other experts to answer their remaining questions, she says.

“It is important for clinicians to know that PTLD leads to real, quantifiable brain changes and that patients’ cognitive complaints may be a direct consequence of these brain changes, rather than a side effect of other symptoms, such as fatigue, for example,” Marvel said.

Commenting on the study for this report, John Keilp, PhD, an associate professor of clinical psychology at Columbia University in New York City, says it is an “important, carefully executed study that expands upon earlier brain imaging studies of patients with PTLD” using “state-of-the-art brain imaging and analysis methods.”

The researchers “have shown us a way forward to examine these patients and this disorder in greater detail as we attempt to unlock the uncertainties surrounding the physiological basis of these patients’ symptoms,” says Keilp, who heads the neuropsychology laboratory in the division of Molecular Imaging and Neuropathology at the New York State Psychiatric Institute.

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November 15, 2022