PEOPLE BEFORE PROFIT

Behind the 2025 “shroom boom” hides a bad trip

Political economist warns psychedelics may be too unruly to become profitable products for mental health treatment.

City St George’s, University of London

FacebookXLinkedInWeChatBlueskyMessageWhatsAppEmail

Investor appetite in corporate psychedelia is returning, but the sector faces fundamental barriers to profitability, according to new research.

The paper by Dr Sandy Brian Hager, Reader in International Political Economy at City St George’s, University of London is published in Finance and Society and argues there’s a mismatch between psychedelics and the economics of drug development.

Consequently, pharmaceutical startups might change the face of psychedelics: some are looking to develop extremely intense, short-term effect drugs; others are looking to engineer the trip out of the experience entirely.

From boom to bust

The paper analyses the financial results of the top five for-profit psychedelic pharmaceutical companies between the industry’s inception in 2016 and 2021 and draws on economic theory around capital and financial cycles.

Hype around the revolutionary benefits of psychedelics in treating mental health inspired an economic boom. Hundreds of startups launched and investor money poured in.

A series of setbacks rattled investors – weak trial results, rising interest rates, the US Food and Drug Administration (FDA) rejecting MDMA treatment for post-traumatic stress disorder – and the industry went into freefall.

Now in 2025, political winds are shifting, trials are delivering stronger results, and Big Pharma, long wary of psychedelics, is finally showing interest, hinting at the promise of another “shroom boom”.

Dr Hager’s paper suggests investors should remain cautious, as issues around patenting and drug trials may yet choke drug development.

Economic and medical constraints choke development

The research identifies two major obstacles to profitability: weak intellectual property (IP) protection, and the unpredictable nature of the psychedelic experience making conducting standardised medical trials challenging.

Developing a new drug can cost $1-2 billion, and investors will only put up that money if they believe companies can recoup it later through patents. IP is therefore a major concern.

Some psychedelics, like magic mushrooms (psilocybin), are naturally occurring and unpatentable; others, such as ayahuasca, have long histories of Indigenous use, leaving little scope for patent law. Even synthetic drugs like LSD have patents that expired decades ago.

Because drugs like psilocybin work best alongside hours-long guided therapy, their effects are hard to standardise and test in lab settings, making commercial scaling difficult.

This unruliness casts doubt over the future of corporate psychedelia.

A changing face of psychedelics

Pharmaceutical companies may yet find ways around the obstacles, whether through short-acting compounds or entirely new drug classes.

Some are developing short-duration psychedelics such as 5-MeO-DMT, which cause extremely intense trips lasting only minutes.

Other companies are looking to engineer the trip out of the experience altogether, creating a new class of drugs called neuroplastogens.

These aim to trigger the same brain changes as classic psychedelics without the hallucinations.

Dr Hager said:

“When startups first began launching, corporate psychedelia looked set to fulfil its vision: delivering big returns for investors and offering a long-awaited solution to the global mental health crisis.

“Then weak trial results and rising interest rates sent the sector into a freefall.

“The unruliness of psychedelics gives us reasons to be cautious about the long-term future of for-profit psychedelic medicine.

“In bending psychedelics to fit the pharmaceutical model, they risk becoming indistinguishable from the very drugs they were meant to replace.

“For all the hype of a mental health revolution, psychedelics may deliver nothing more radical than business as usual.”

Read the full article here.

ENDS
 

Media enquiries

To be put in touch with the study author, please contact:

Eve Lacroix, Press Officer at City St George’s, University of London

• Phone: +44 (0)7867 285 573 / +44 (0)20 7040 8788  
• Email: eve.lacroix@citystgeorges.ac.uk / pressoffice@citystgeorges.ac.uk 

Notes for Editors

About City St George’s, University of London 

Please refer to us as City St George's, University of London in the first instance, which can then be shortened to City St George's. 

City St George’s is the University of business, practice and the professions. 

Our academic range is broadly-based with world-leading strengths in business; law; health and medical sciences; mathematics; computer science; engineering; social sciences including international politics, economics and sociology; and the arts including journalism, dance and music. 

Our research is impactful, engaged and at the frontier of practice. In the last REF (2021) 86 per cent of City research was rated as ‘world-leading’ 4* (40%) and ‘internationally excellent’ 3* (46%) and 100 per cent of St George’s impact case studies were judged as ‘world-leading’ or ‘internationally excellent’. As City St George’s we will seize the opportunity to carry out interdisciplinary research which will have positive impact on the world around us. 

---

Journal

Finance and Society

DOI

10.1017/fas.2025.10014 

Method of Research

Data/statistical analysis

Subject of Research

Not applicable

Article Title

The shifting fortunes of corporate psychedelia

 

Gene variant increases brain inflammation in those with repetitive head impacts

Findings underscore the importance of TMEM106B as a potential therapeutic target in CTE and related diseases

Boston University School of Medicine

FacebookXLinkedInWeChatBlueskyMessageWhatsAppEmail

 

Boston—Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head impacts (RHI). However, individuals with similar RHI exposure have shown differing pathology, suggesting a role for genetic variation. While a common Transmembrane Protein106B (TMEM106B) risk variant has been associated with greater CTE severity, its mechanism has remained unclear until now.

 

TMEM106B helps regulate lysosomes—tiny recycling centers inside cells—and is especially important for microglia, the brain’s immune cells. Changes in this gene can alter how microglia clear waste and respond to damage, affecting inflammation throughout the brain.

 

A new study from BU’s CTE Center has found that a genetic difference in the TMEM106B gene can make brain inflammation worse in people who have repeated head injuries, making them more likely to develop serious brain problems like CTE and dementia. This is the first time anyone has shown that this gene variant changes how the brain’s immune cells (called microglia) react in CTE, connecting a genetic factor directly to the way the brain responds to repeated head injuries. This finding could lead to its use as a genetic marker predicting who may be most vulnerable.

 

“These findings explain why some athletes and others with repeated head injuries are at higher risk for brain diseases. Knowing this gene increases risk means we may someday be able to identify people who should be extra careful to protect their brains or could benefit from new treatments,” says corresponding author Thor Stein, MD, PhD, associate professor of pathology & laboratory medicine at Boston University Chobanian & Avedisian School of Medicine and VA Boston Healthcare System.

 

Retrospective clinical data including contact sports history, levels (high school, college, etc.) played and years played at each level, was collected through online surveys, telephone interviews with next-of-kin and by reviewing clinical records. Additionally, the researchers examined brains from the Understanding Neurologic Injury and Traumatic Encephalopathy (UNITE) Brain Bank of people who had a history of repeated head injuries. They analyzed their DNA to see if they had a certain type of TMEM106B gene. They then compared signs of brain inflammation, damage and memory problems between people with and without the gene variant.

 

In people older than 65, having the TMEM106B risk gene more than doubled the chances of developing worse CTE, similar to the effect of playing over eight years of contact sports. For those 65 or younger, carrying the TMEM106B gene variant was linked to a much higher risk of dementia.

 

“These results pave the way for more personalized approaches to preventing and treating brain diseases caused by repeated head injuries,” adds Stein. “Our hope is that understanding the role of TMEM106B will open up new possibilities to improve brain health and protect those most at risk.”
 

These findings appear online in the journal Acta Neuropathologica.

 

About the BU CTE Center

The BU CTE Center is an independent academic research center at the Boston University Avedisian & Chobanian School of Medicine. It conducts pathological, clinical and molecular research on CTE and other long-term consequences of repetitive brain trauma in athletes and military personnel. For people considering brain donation, click here. To support its research, click here. 

 

 

 

This study was supported by National Institute of Aging Boston University AD Research Center, P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee,P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee, P30AG072978-McKee, National Institute of Aging Boston University AD Research, P30AG072978-McKee, National Institute of Aging, R01AG090553, R01NS132290, R01AG087199,R01NS139383, P30AG066514-06, R01NS139383, R01AG075876-Zhang, Stein, Zaia, National Institute of Neurological Disorders and Stroke, R01NS142076, R01 NS119651, R01NS093870, RF1NS122854- Alosco, U54NS115266-McKee, U54NS115266, U54NS115266-McKee, Veterans Affairs, BX004349, National Center for PTSD, U.S. Department of Veterans Affairs, NIH/NIA, 3P30-AG13846-23,EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT, 5R01HD104772, National Institute of Nursing Research, 5R01 NR020752-03, NIA, R01AG061028, National institute of Aging, 1RF1NS122854, National Institute of Aging, National Institute of Neurological Disorders and Stroke, 5R01 NS119651-04, National Institutes of Health, 75N92024R0245,National Institute of Neurological disorders and Stroke, 1U01 NS137483-01, Concussion Legacy Foundation, Andlinger Foundation, WWE, United States Department of Veterans Affairs, Veterans Health Administration, Veterans Affairs Biorepository, BX002466, BLRD Merit Award,I01BX005933 (CTE-AD), Alzheimer’s Association, NIRG-305779, NIRG-362697, National Institute of Neurological Disorders and Stroke, RF1NS122854- Alosco, National Heart, Lung and Blood Institute, 75N92019D00031, Department of Defense Peer Reviewed Alzheimer’s Research Program, PRARP #13267017, and Military Exposures Research Program Award United States (U.S.) Department of Veterans Affairs Biomedical Laboratory R& D Service (ALS MERP), 1I01BX005161.

 

Note to Editors:

Michael L Alosco receives research support from Life Molecular Imaging Inc. He also receives Royalities from Oxford University Press Inc and receive honorarium from Michael J Fox Foundation for services unrelated to this study. Yorghos Tripodis reports payment to self by the American Medical Association for editorial services. Douglas Katz receives Royalties from Demos/Springer publishers for Textbook on TBI with chapter on CTE Daniel H. Daneshvar conducts Expert medico-legal work related to TBI and SCI, receives research and clinical support from the NFLPA, and is a Member of NFLPA Mackey-White Health and Safety Committee.

 

 

 

---

Journal

Acta Neuropathologica

DOI

10.1007/s00401-025-02955-7 

Method of Research

Data/statistical analysis

Subject of Research

Human tissue samples

Article Title

Genetic variation in TMEM106B alters microglial activation and cytokine responses in chronic traumatic encephalopathy

Article Publication Date

20-Nov-2025

COI Statement

Michael L Alosco receives research support from Life Molecular Imaging Inc. He also receives Royalities from Oxford University Press Inc and receive honorarium from Michael J Fox Foundation for services unrelated to this study. Yorghos Tripodis reports payment to self by the American Medical Association for editorial services. Douglas Katz receives Royalties from Demos/Springer publishers for Textbook on TBI with chapter on CTE Daniel H. Daneshvar conducts Expert medico-legal work related to TBI and SCI, receives research and clinical support from the NFLPA, and is a Member of NFLPA Mackey-White Health and Safety

 

For young children, finger-counting a stepping stone to higher math skills

Common strategy helps kids develop more abstract skills, study finds

American Psychological Association

FacebookXLinkedInWeChatBlueskyMessageWhatsAppEmail

Children who count on their fingers between ages 4 and 6 1/2 have better addition skills by age 7 than those who don’t use their fingers, suggesting that finger counting is an important stepping stone to higher math skills, according to research published by the American Psychological Association.

“Finger counting is not just a tool for immediate success in young children, but a way to support the development of advanced abstract arithmetic skills,” said lead author Catherine Thevenot, PhD, of the University of Lausanne in Switzerland.

Finger counting is widely used by young children as a strategy to solve math problems. However, many elementary school teachers expect children to move on from finger counting at a very young age. One French study found that 30% of first grade teachers view it as a sign that a child is struggling to understand numerical concepts. 

Previous research generally only assessed children at one point in time and found that children who use their fingers to count perform better in arithmetic than those who don’t -- until about age 7. After age 7, however, the relationship reverses and children who don’t use their fingers perform better than those who do. What remained unclear, however, was whether the non-finger users at age 7 had never used their fingers, or whether they were “former finger users” who had moved on from the practice. 

“Our study aimed to clarify this distinction and to better understand what finger use, or its absence, truly reveals about children’s arithmetic development,” Thevenot said.

To do so, she and her colleague Marie Krenger, PhD, followed 211 Swiss children from ages 4 ½ to 7 ½ (pre-K to second grade) to assess how their finger-counting strategies changed over time and how they related to mathematical skill. Twice a year, the researchers asked the children to answer up to three sets of addition problems of increasing difficulty: adding two digits between 1 and 5, adding one digit between 1 and 5 to another between 6 and 9, and adding two digits between 6 and 9. At each test, the researchers only moved on to the next level of difficulty if the child was able to answer 80% of the previous set correctly.

The researchers videotaped the children and observed whether they used their fingers during the addition tasks. Overall, they found that finger counting peaked around age 5 ½ to 6. Up to age 5, more children added without their fingers than with them. However, by age 6 ½, 92% of kids had used their fingers during at least one testing point. By age 7 ½, 43% of children were “ex-finger counters” – they had used their fingers during at least one test but no longer did – while 50% were current finger counters and only 7% had never counted on their fingers.

Overall, the researchers found that the highest-performing children were those who had used their fingers in the past but no longer relied on them. From age 6 on, these former finger users outperformed both children who had never used their fingers and those who still used them. 

“This has important implications, as it shows that there is no reason to discourage children in school from using their fingers to solve arithmetic problems on the grounds that this strategy could prevent them from shifting to faster, internalized procedures once the numbers become too large to be represented on fingers,” Thevenot said. “This research supports encouraging children to use their fingers in arithmetic without fear that they will become stuck in limited strategies.”

Article: “The Role of Children’s Finger Counting History on their Addition Skills,” by Marie Krenger, PhD, University of Lausanne, and Catherine Thevenot, PhD, University of Lausanne. Developmental Psychology, published online Nov. 20, 2025. 
 
CONTACT: Catherine Thevenot, PhD, can be reached at catherine.thevenot@unil.ch. 

The American Psychological Association, in Washington, D.C., is the largest scientific and professional organization representing psychology in the United States. APA’s membership includes  173,000 researchers, educators, clinicians, consultants and students. Through its divisions in 54 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance the creation, communication and application of psychological knowledge to benefit society and improve lives.

---

Journal

Developmental Psychology

DOI

10.1037/dev0002099 

Method of Research

Observational study

Subject of Research

People

Article Title

The Role of Children’s Finger Counting History on Their Addition Skills

Article Publication Date

20-Nov-2025

Ancient arctic adaptations may influence modern disease risk

University of Copenhagen

FacebookXLinkedInWeChatBlueskyMessageWhatsAppEmail

Over the past 25 years, Greenlanders have experienced a dramatic increase in cardiometabolic diseases, including type 2 diabetes and cardiovascular disease. Scientists have already linked their increased risk of these diseases to genetic variants that are common in the Inuit Greenlandic population but rare in other populations. These variants likely provided survival advantages in the harsh Arctic environment and with traditional diets based on marine mammals, which are rich in protein and polyunsaturated fatty acids.

What is less well understood is how these variants increase the risk of disease. Our genome plays a crucial role in regulating the levels of proteins in the bloodstream, which in turn control inflammation, metabolism, immune responses, and cardiovascular function. If a genetic variant affects both protein levels and disease risk, it suggests that the protein is likely involved in the disease's development.

In a new study published in the American Journal of Human Genetics, an international team of researchers identified 251 genetic variants that significantly affect circulating protein levels in Greenlanders. The study revealed that genetic control over certain proteins is substantially stronger in Greenlandic Inuit than in Europeans, and uncovered 70 previously unreported associations. Their discoveries provide crucial insights into how Arctic-adapted genes influence modern disease risk.

"By understanding how genetic variants regulate proteins in the blood, we can identify new drug targets and understand why certain populations are more susceptible to specific diseases. This is especially important for populations like Greenland, where unique genetic adaptations that once provided survival advantages now contribute to elevated disease risks,” said Professor Torben Hansen from the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen, who co-led the study.

Linking ancient adaptations to modern disease

In the study, the scientists analyzed blood samples from 3,707 Greenlandic individuals collected through population health surveys conducted between 1998 and 2019. Using advanced proteomics technology, they measured levels of 177 proteins related to inflammation and cardiovascular health. They then examined how genetic variation across the genome influenced these protein levels.

The research revealed several significant associations between Arctic-enriched genetic variants and disease-related proteins. The CPT1A variant, which likely enabled the Inuit to process traditional high-fat Arctic diets, was associated with lower levels of 55 inflammatory and cardiovascular proteins in carriers. The TBC1D4 variant, which contributes to up to 10% of diabetes cases in Greenland, is associated with altered levels of nine immune-related proteins, including key inflammatory markers. Additionally, the researchers discovered a novel genetic variant affecting IL-6 levels that was associated with a 31% increased risk of cardiovascular disease in Greenlanders.

Importantly, this study found that genetic control over protein levels is stronger in Greenlandic Inuit than in Europeans. For certain key proteins, such as IL-27 and Gal-9, genetic variants account for 30-44% of their levels in Greenlanders but less than 20% in Europeans. This demonstrates that isolated populations can harbor high-impact genetic variants that reveal fundamental biological mechanisms invisible in more commonly studied populations.

The Case for Diverse Genomic Research

This research builds on a comprehensive genetic study of Greenlanders published in Nature earlier this year. While that study mapped the population's unique genetic architecture and identified disease-associated variants, this new work reveals the biological mechanisms behind these associations and demonstrates how Arctic-adapted genetic variants influence circulating protein levels and disease development.

Nearly all previous studies linking genetic variants to protein levels have focused on individuals of European ancestry, which leaves a significant gap in scientific knowledge. By revealing how Arctic-adapted variants influence protein levels and disease risk, this study demonstrates that genetic architecture varies substantially across populations. In so doing, it provides insights relevant to both Greenlandic health interventions and global understanding of cardiometabolic disease mechanisms.

“Indigenous and underrepresented populations have been largely excluded from genomic research. Without studying diverse populations, we miss critical pieces of human biology and perpetuate health disparities," said Sara Stinson, who carried out the research while she was a Postdoc at the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen and co-first author of the study together with Postdoc Renzo Balboa from the University of Copenhagen.

About the Study

The research was conducted by an international team led by the Novo Nordisk Foundation Center for Basic Metabolic Research and the Department of Biology at the University of Copenhagen, in collaboration with the National Institute of Public Health at the University of Southern Denmark, the Greenland Center for Health Research, and Steno Diabetes Center Greenland.

The study was funded by the Novo Nordisk Foundation, the Independent Research Fund Denmark, and other sources. Data were collected through three population-based health surveys conducted in Greenland with ethics approval and participant consent.

---

Journal

American Journal of Human Genetics

DOI

10.1016/j.ajhg.2025.10.013 

Article Title

Genetic regulation of the plasma proteome and its link to cardiometabolic disease in Greenlandic Inuit

Article Publication Date

22-Nov-2025