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Provenance research at Goethe University anticipates further extensive restitutions
The Johann Christian Senckenberg University Library (UB) at Goethe University Frankfurt has been systematically reviewing its collections since 2020 to identify Nazi-looted property and return it to its rightful owners. The provenance research is supported by the German Lost Art Foundation. For the first time, volumes have now been restituted to the Jewish Community of Frankfurt, including books from the collection of one of the city's prominent Jewish families.
FRANKFURT. In numerical
terms, it was a comparatively small restitution: five volumes were handed over within
the premises of the University Library (UB). What made the occasion exceptional
was that this marked the first time the UB returned books to Frankfurt's Jewish
Community. Among them were volumes previously owned by individuals of central
importance to the predecessor community. Julius Blau (*1861), an attorney and
notary, served as chair of the Israelite Community from 1903 until his death in
1939 and was actively involved in numerous Jewish aid organizations. His term
of office included milestones such as the construction of the Westend Synagogue
(1910) and the Philanthropin – the city's historic Jewish school – on
Hebelstraße (1908), but also the early years of the Nazi era. His son Ernst
(*1892) worked as a librarian for the Israelite Community, emigrated to France
in 1939, and died in 1941 at the Gurs concentration camp. Two additional books
originated from the community library itself or from the “Tagesheim der
erwerbslosen jüdischen Jugend" [Day
Home for Unemployed Jewish Youth].
“Mr. Justizrat Dr. Blau with best regards
from Vf" is handwritten in a publication about the “Frankfurter Sammelkatalog",
bound together with other booklets in a single volume. Another booklet in the
same volume bears a personalized bookplate identifying “Dr. Ernst Blau," Julius
Blau's son, as the owner. A copy of Nahum Norbert Glatzer's “History of the
Talmudic Era" is identifiable by a stamp from the Israelite Community, while the
“General Encyclopedia" carries a stamp from the Day Home for Unemployed Jewish
Youth. Such clear evidence of previous ownership
is not always available to the UB's provenance research team. The exact route
by which the books entered the library's collection can no longer be
reconstructed. Based on cataloging data, however, it is clear that the volumes
must have arrived before the end of the Nazi regime.
Although the restituted books are neither
valuable nor rare editions, their return is nonetheless of great significance to
Frankfurt's Jewish Community: “For us, this is a very important acknowledgment
of the injustice inflicted on Jews in Frankfurt," says Rachel Heuberger, a
member of the Jewish Community Frankfurt's five-person board and a former
University Library employee, where she led the renowned Judaica collection
until 2019. She welcomes the fact that, with funding from the German Lost Art
Foundation, the UB is now able to systematically review its holdings. Julius
and Ernst Blau are well-known figures within the community, and their memory is
held in high regard. In 1936, the Israelite Community was designated as the
Blau family's sole heir through an inheritance contract. In 1964, it received
limited “compensation" for the family's losses, including payments related to the
Jewish Property Tax, the Reich Flight Tax, and the Dego levy imposed at the
time of Ernst Blau's emigration. The family home was burned down during the November
Pogroms of 1938.
Before the Nazi era, the Israelite
Community's library comprised 11,531 works in 14,085 volumes, as recorded by
librarian Dr. Ernst Blau in 1932. These included the valuable book collection
of the Marburg philosopher Hermann Cohen and, on loan, the collection of
Frankfurt Orientalist Raphael Kirchheim. Like most Jewish property, the library
was later confiscated by the Nazis. The recovered books are now being
integrated into the Jewish Community's current collection. Given the scale of
the losses, reconstruction of the original library is not possible, Heuberger explains.
However, following the identification of additional suspected cases of Nazi-looted
property, the University Library expects to carry out further restitutions. “We
still have a lot of work ahead of us," says provenance researcher Darleen
Pappelau.
Goethe University's Executive Board
established the Forum for University History with the goal of bringing together
and making accessible projects focused on exploring the history of the
university and its collections. Provenance research at the UB is part of this
growing network.
About the
University Library Johann Christian Senckenberg (UB JCS)
The University Library Johann Christian
Senckenberg is one of Germany's leading academic libraries, known for its
extensive collections and resources. It serves multiple roles: as a university
library with numerous state-level responsibilities, as a scientific library for
the city of Frankfurt and the Rhine-Main region, and as a specialized library
contributing to nationwide literature and information services.
https://www.ub.uni-frankfurt.de/
Images
for download: Link
einsetzen
Captions:
Image 1: Following the handover of the
books on the University Library's grounds in Bockenheim: Dr. Daniel Korn (Member
of the Board, Jewish Community Frankfurt), Dr. Rachel Heuberger (Member of the
Board, Jewish Community Frankfurt), Bernhard Wirth (Head of UB's Provenance
Research Project), Daniel Dudde (Member of the Provenance Research Project), Darleen
Pappelau (Member of the Provenance Research Project), Dr. Mathias Jehn (Head of
UB's Curation, Specialized Information and
Engagement Department).
(Photo: Baunemann)
Image 2: The first five books returned by
the University Library to Frankfurt's Jewish Community. (Photo: Baunemann)
Image 3: The volumes from the collection
of librarian Dr. Ernst Blau are adorned with a beautiful bookplate. (Photo:
Baunemann)
Image 4: Stamps indicate the Israelite
Community or the Home for Unemployed Jewish Youth as the previous owners. (Photo:
Baunemann)
Further Information
Dr. Mathias Jehn
Head of UB's Curation, Specialized Information and Engagement Department
Freimannplatz 1
60325 Frankfurt
Phone +49 (0)69 798-39007
E-Mail m.jehn@ub.uni-frankfurt.de
Dr. Anke Sauter, Science Communication, PR &
Communications Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt, Tel. +49
(0)69 798-13066, sauter@pvw.uni-frankfurt.de
Frankfurt researchers discover an unusual metabolic pathway in the gut bacterium Blautia luti
Researchers at Goethe University Frankfurt have discovered a surprising role for formic acid in the human gut: The small molecule acts as a kind of “taxi" for electrons – both within bacteria and, likely, also between different microorganisms. The gut bacterium Blautia luti produces formic acid as part of a metabolic trick that allows it to respond flexibly to what is available in the gut. In addition to carbohydrates, the bacterium can also metabolize toxic carbon monoxide derived from the body's own hemoglobin degradation.
FRANKFURT. Among the many trillions of microorganisms in the human gut is Blautia luti. Like many gut bacteria, it metabolizes indigestible dietary components, such as fiber in the form of carbohydrates. This process produces, among other things, acetic acid (acetate), an important energy source for our intestinal cells and a signaling molecule that can even influence our well-being via the gut-brain axis.
Taxis for electron transport
B. luti lives in the gut without oxygen and cannot respire, but only ferment. During this process, carbohydrates are converted into lactate, succinate, ethanol, carbon dioxide, and hydrogen, which are excreted as metabolic end products. Too much hydrogen in the gut is unhealthy because it inhibits further fermentation. Therefore, small single-celled organisms known as archaea consume the hydrogen, convert it into methane, and thus regulate hydrogen levels in the gut. Hydrogen thus acts, so to speak, as an electron taxi within a bacterium and between different bacteria. However, this process involves a substantial loss of energy and is therefore disadvantageous for the bacteria.
B. luti has an additional, better option. Raphael Trischler and Prof. Volker Müller, Chair of Molecular Microbiology and Bioenergetics at Goethe University Frankfurt, found that B. luti produces formic acid (formate) instead of carbon dioxide (CO₂) and hydrogen, with hydrogen bound to CO₂. In this case, formic acid is the electron taxi, allowing the energetically costly production of hydrogen to be bypassed.
Formic acid as an electron store
To produce formic acid, B. luti uses the enzyme pyruvate formate lyase. This enzyme is rather unusual in acetogenic bacteria. “The electrons are essentially stored in the formic acid," explains Trischler. However, formic acid is also unhealthy at high concentrations.
B. luti detoxifies formic acid together with CO₂ via a special metabolic pathway, the Wood-Ljungdahl pathway (WLP), converting it into acetate. In the WLP, CO₂ is transformed via two different “branches" and ultimately assembled into acetic acid. In the first branch, CO₂ is normally converted into formic acid by a specific enzyme – formate dehydrogenase – using hydrogen. “But B. luti completely lacks formate dehydrogenase," explains Raphael Trischler, who studied the bacterium for his doctoral thesis. Instead, B. luti uses formic acid directly. Sugar breakdown on one side and acetic acid production on the other are thus linked via formic acid – a clever strategy that gives the bacterium an energetic advantage.
Useful side effects
In the laboratory culture studied, B. luti excretes formic acid. In the complex food web of the gut, however, the situation is different, and formic acid does not accumulate there. Methane-producing archaea can convert formic acid into methane, but B. luti has another trick up its sleeve. Reducing formic acid in the WLP requires electrons that originate from carbohydrate fermentation. But B. luti can also use gases produced by other bacteria for this purpose. “In the presence of hydrogen, the formic acid disappears completely," reports Trischler.
Particularly remarkable is B. luti's ability to utilize carbon monoxide. This highly toxic gas is produced in the human body during the natural breakdown of hemoglobin, the red blood pigment. “Bacteria like B. luti can thus detoxify carbon monoxide produced by the body itself using formic acid," explains Müller. This also explains why so many gut microbes possess the enzyme carbon monoxide dehydrogenase.
B. luti has yet another property beneficial to humans: In addition to acetate, it produces succinate (succinic acid). Succinate promotes the growth of other beneficial gut bacteria, stimulates the immune system, and is also an industrially valuable raw material for biotechnological applications.
The study highlights how diverse metabolic strategies in the gut are. “Even within related groups of bacteria, there are fascinating differences," says Müller. “Understanding this helps us better decipher the interactions between different gut bacteria and their role in human well-being."
Publication: Raphael Trischler, Volker Müller: Formate as electron carrier in the gut acetogen Blautia luti: a model for electron transfer in the gut microbiome. Gut Microbes (2026) https://doi.org/10.1080/19490976.2025.2609406
Picture download:
https://www.uni-frankfurt.de/183002483
Caption:
1) Interspecies formate transfer. Formate is produced by various bacteria and taken up by B. luti, which converts it into acetate. B. luti can also produce formate itself. Image: Raphael Trischler, Goethe-Universität Frankfurt/AI
2) In the lab: Raphael Trischler (seated) and Volker Müller in the laboratory at an anaerobic chamber. The chamber contains no oxygen but nitrogen, allowing oxygen-sensitive bacteria such as B. luti to be handled safely. Photo: Jennifer Roth, Goethe-Universität Frankfurt
3) Formate as a taxi for electrons. Top: During interspecies formate transfer, B. luti consumes carbohydrates and produces short-chain fatty acids such as lactate, acetate, or succinate, but also formate. The short-chain fatty acids are then absorbed by the intestine. Formate is absorbed by other intestinal microbes and converted into short-chain fatty acids and methane (not shown). Below: During intraspecies formate transfer, B. luti metabolizes the formate with carbon monoxide (CO) or hydrogen (not shown) to produce short-chain fatty acids such as acetate. Short-chain fatty acids contribute to intestinal health. Image: Volker Müller, Goethe-University Frankfurt
Contact:
Professor Volker Müller
Molecular Microbiology and Bioenergetics
Institute for Molecular Biosciences
Goethe University Frankfurt
Tel: +49 (0)69 798-29507
vmueller@bio.uni-frankfurt.de
https://www.mikrobiologie-frankfurt.de/
http://acinetobacter.de
German Research Foundation admits “Advanced Clinician Scientist” Dr. Sebastian Scheich to early-career program
Dr. Sebastian Scheich of University Hospital Frankfurt will receive around €2 million over the next six years through the Emmy Noether Program for his research into an aggressive form of lymph node cancer, diffuse large B-cell lymphoma. Through this program, the German Research Foundation (DFG) supports outstanding researchers, enabling them to qualify for appointment as university professors.
FRANKFURT. Diffuse large B-cell lymphoma (DLBCL) is an aggressive and rapidly progressing form of lymph node cancer that affects around 6,000 people in Germany each year. In this disease, certain immune cells—B cells—become malignant. The effectiveness of therapies and patient prognoses vary widely, as DLBCL occurs in several genetically distinct variants.
As part of the DFG's Emmy Noether program, Dr. Sebastian Scheich and his research group at Medical Clinic 2 of Universitätsmedizin Frankfurt are investigating which signaling networks DLBCL cancer cells use to promote their own growth and ensure survival.
To this end, the researchers aim to elucidate how various proteins in malignant B cells are modified with sugar residues. This process, known as glycosylation, influences protein stability, function, and cellular localization, among other factors. Glycosylation also determines how cells receive and process signals, as it regulates the organization of signaling receptors on the cell surface.
In recent studies, Scheich's team has shown that changes in the enzymes catalyzing glycosylation contribute to the activation of disease-relevant signaling networks. One key network is the NF-B signaling pathway, which conveys the message to cancer cells: “Grow, divide, and do not die." Moreover, the group's findings suggest that glycosylation mechanisms may also influence how well DLBCL tumors respond to targeted therapies, cellular therapies, and immunotherapies.
The Emmy Noether funding enables Scheich to expand his junior research group and supports his dual career path in research and clinical practice. The physician explains: “We want to systematically investigate how altered glycosylation controls oncogenic signaling pathways in lymphoma cells. Our goal is to identify starting points for innovative therapies for aggressive lymphomas. As an Advanced Clinician Scientist, I lead a laboratory while also treating patients on a daily basis. This helps me align scientific questions with clinical relevance."
Dr. Sebastian Scheich, born in 1988, studied medicine at Justus Liebig University Giessen, where he also earned his doctorate. Starting 2019, he worked for four years as a postdoctoral researcher at the National Cancer Institute in the United States. Since 2023, he has been conducting research and working at Medical Clinic 2 – Hematology and Oncology at Universitätsmedizin Frankfurt and at the University Cancer Center Frankfurt (UCT). In the same year, he began establishing and leading a junior research group at the LOEWE Center Frankfurt Cancer Institute (FCI). Sebastian Scheich is funded as an Advanced Clinician Scientist through the INITIALISE program (Innovations in Infection Medicine) of Germany's Federal Ministry of Research, Technology and Space, and is affiliated with the Mildred Scheel Early Career Center (MSNZ) Frankfurt-Marburg. He is also actively involved, via the Frankfurt/Mainz site of the German Cancer Consortium (DKTK), in the Alliance of Rhine-Main Universities (RMU).
The Emmy Noether Program of the German Research Foundation (DFG) supports exceptionally qualified researchers at an early stage of their careers and enables them, by leading an independent junior research group for up to six years, to obtain the qualifications required for a professorship.
Picture download:
https://www.uni-frankfurt.de/182872402
Caption: Dr. Sebastian Scheich, Head of Emmy Noether Group at Medical Clinic 2 – Hematology and Oncology, Universitätsmedizin Frankfurt. Photo: Klaus Wäldele
Contact:
Dr. Sebastian Scheich
Medical Clinic 2 – Hematology and Oncology
and University Cancer Center Frankfurt
Universitätsmedizin Frankfurt
Tel: +49 69 6301-37 67
sebastian.scheich@unimedizin-ffm.de
https://lymphoma-leukemia-research-frankfurt.de/ag-scheich-home/research-scheich-lab
Bluesky: @goetheuni.bsky.social
LinkedIn: @Goethe-Universität Frankfurt @Universitätsmedizin Frankfurt @UCT University Cancer Center Frankfurt @Georg Speyer Haus @Sebastian Scheich
Goethe University-led study reveals how mutations in the repair enzyme SPRTN trigger inflammation and premature ageing – new insight into Ruijs-Aalfs syndrome
If severe DNA damage is not repaired, the consequences for the health of cells and tissues are dramatic. A study led by researchers at Goethe University Frankfurt, part of the Rhine-Main University Alliance, shows that the failure of a key DNA repair enzyme called SPRTN not only results in genetic damage, but also triggers chronic inflammatory responses that accelerate aging and lead to developmental abnormalities. The findings shed light on the rare hereditary disorder Ruijs-Aalfs syndrome and may open new avenues for therapeutic intervention.
FRANKFURT. Although DNA is tightly packed and protected within the cell nucleus, it is constantly threatened by damage from normal metabolic processes or external stressors such as radiation or chemical substances. To counteract this, cells rely on an elaborate network of repair mechanisms. When these systems fail, DNA damage can accumulate, impair cellular function, and contribute to cancer, aging, and degenerative diseases.
One particularly severe form of DNA damage are the so-called DNA–protein crosslinks (DPCs), in which proteins become attached to DNA. DPCs can arise from alcohol consumption, exposure to substances such as formaldehyde or other aldehydes, or from errors made by enzymes involved in DNA replication and repair. Because DPCs can cause serious errors during cell division by stalling DNA replication, DNA–protein crosslinks pose a serious threat to genome integrity.
The enzyme SPRTN removes DPCs by cleaving the DNA-protein crosslinks. SPRTN malfunctions, for example as a result of mutations, may predispose individuals to develop bone deformities and liver cancer in their teenage years. This rare genetic disorder is known as Ruijs-Aalfs syndrome. Its underlying mechanism remains poorly understood, and there are no specific therapies.
Now a research team led by Prof. Ivan Ðikić from the Institute of Biochemistry II at Goethe University demonstrated that the loss of a functional SPRTN enzyme not only leads to the accumulation of damaged DNA in the cell nucleus. Using cell culture experiment and genetically modified mice they found out that, in addition, DNA from the nucleus also leaks into the interior of the cell, the cytoplasm.
DNA in the cytoplasm is recognized by the cell as a danger signal, as such DNA usually originates from invading viruses or bacteria or from malignant transformation. Cytoplasmic DNA therefore activates defense mechanisms in the cell by initiating the so-called cGAS-STING signaling pathway. Furthermore, the cell releases messenger substances that attract immune cells, leading to chronic inflammation.
The Frankfurt-led research team observed that this chronic inflammatory response is especially pronounced in the mouse embryos and persists in adulthood, particularly in the lung and liver. As a result, the mice died early or showed signs of premature ageing similar to those seen in people with Ruijs-Aalfs syndrome. Blocking the relevant immune response alleviated many of the symptoms.
“Unrepaired DNA-protein crosslinks have broader systemic consequences," explains Ðikić. “They not only compromise genome stability but also drive chronic inflammation that can significantly influence lifespan."
The physician and molecular biologist sees potential for the development of therapies: “In addition to Ruijs-Aalfs syndrome, there are other rare genetic diseases in which DNA-protein crosslinks play an important role. With our work, we have laid an important foundation for future therapeutic approaches to these diseases as well. By studying the underlying mechanisms of these rare diseases, we discovered a new link between DNA damage, inflammatory responses, and the lifespan of an organism. This also contributes to the understanding of the biology of ageing."
Partners in the research project included Goethe University and Johannes Gutenberg University Mainz (Institute of Molecular Biology/Professor Petra Beli and Institute of Transfusion Medicine/Professor Daniela Krause) within the Rhine-Main Universities alliance (RMU), the German Consortium for Translational Cancer Research (DKTK), the German Cancer Research Center (DKFZ), EPFL Lausanne, Charité Berlin and the Universities of Cologne and Split (Croatia).
Publication: Ines Tomaskovic, Cristian Prieto-Garcia, Maria Boskovic, Mateo Glumac, Tsung-Lin Tsai, Thorsten Mosler, Rubina Kazi, Rajeshwari Rathore, Jorge Andrade, Marina Hoffmann, Giulio Giuliani, Anne-Claire Jacomin, Raquel S. Pereira, Elias Knop, Laurens Wachsmuth, Petra Beli, Koraljka Husnjak, Manolis Pasparakis, Andrea Ablasser, Daniela S. Krause, Michael Potente, Stamatis Papathanasiou, Janos Terzic, Ivan Dikic. DNA-Protein crosslinks promote cGAS-STING-driven premature aging and embryonic lethality. Science (2026) https://doi.org/10.1126/science.adx9445
Picture download:
https://www.uni-frankfurt.de/182738939
Captions:
1 Fatal error: The failure of the repair enzyme SPRTN in these cultured cells leads to fatal errors in cell division, e.g. by distributing the chromosomes (red) to three daughter cell nuclei instead of two (arrow). Green: Cell division apparatus/cytoskeleton. Photo: Institute of Biochemistry II, Goethe University Frankfurt
2 SPRTN protects the DNA like a helmet by reparing DNA-protein crosslinks. Artist's impression: Anne-Claire Jacomin, Goethe University Frankfurt
Contact:
Professor Ivan Ðikić
Institute of Biochemistry II
and Buchmann Institute for Molecular Life Sciences
Goethe University Frankfurt
Tel: +49 (0)69 6301-5964
dikic@biochem2.uni-frankfurt.de
https://biochem2.com/research-group/molecular-signaling
Bluesky: @goetheuni.bsky.social @ibc2-gu.bsky.social @idikic.bsky.social @rheinmainunis.bsky.social @unimainz.bsky.social @Johannes Gutenberg-Universität Mainz
Linkedin: @Goethe-Universität Frankfurt @Institute of Biochemistry II (IBC2) @Rhein-Main-Universitäten @Universitätsmedizin Mainz @Johannes Gutenberg-Universität Mainz
The Collaborative Research Center “Treatment Expectation” focuses on risks, chances of recovery, and side-effect rates in patient education.
FRANKFURT, MARBURG, ESSEN. Similar – yet not the same: Many studies show that patients often struggle to interpret numerical information in medical contexts, especially probabilities related to recovery and side effects. In a recently published Letter in the prestigious journal JAMA (Journal of the American Medical Association), Professors Tobias Kube (Goethe University Frankfurt) and Winfried Rief (University of Marburg) explain which phrasing can help prevent nocebo effects in communication in outpatient and clinical settings.
Is “three out of 100” the same as 3%? Mathematically, yes – psychologically, not necessarily. While the numbers are identical, patients often perceive the two descriptions differently. This is one of the key points highlighted by Prof. Tobias Kube (Clinical Psychology and Psychopathology, Goethe University Frankfurt) and Prof. Winfried Rief, Chair of Clinical Psychology and Psychotherapy at the University of Marburg. Rief also serves as deputy spokesperson for the Collaborative Research Center (CRC) “Treatment Expectation,” which investigates placebo and nocebo effects; Kube is an associate member of the CRC. One of the CRC’s central research questions is how healthcare providers can strengthen placebo effects and avoid nocebo effects through medical communication. Which pitfalls should clinicians avoid when discussing risks, chances of recovery, and side-effect rates during patient consultations?
Numbers and Numeracy
Many people struggle with basic mathematical tasks. In a study of 4,637 adults in the United States, only 34 percent were able to identify the largest value in an unordered sequence of numbers. Brian Zikmund-Fisher, Professor of Health Behavior and Health Equity at the University of Michigan, reported this in JAMA in late October 2025. The situation in Germany is likely not fundamentally different. Zikmund-Fisher recommends five clear strategies for presenting numbers in an understandable way and advises against vague verbal descriptors such as “frequent,” “very rare,” or “unlikely.” Without context and comparison, such terms offer little guidance and can amplify fear as well as unintended expectation effects.
However, as Kube notes in the recent JAMA commentary, numbers in medical contexts also carry risks. What the U.S. professor did not address in his JAMA article are so-called framing effects. Kube and Rief therefore show that patients can perceive numerically identical test results and probability statements very differently depending on how they are presented.
Positive Percentages
“There is no mathematical difference between saying ‘90 percent of patients recover from the infection’ and ‘10 percent do not recover,’ but the first phrasing emphasizes the high likelihood of a favorable outcome,” explains Prof. Tobias Kube (Goethe University Frankfurt). “That is positive framing.” The first formulation tends to be reassuring, while the second can provoke anxiety. “That’s why we should aim for positive framing in clinical practice – especially when communicating potentially distressing information. In such situations, explanations such as the likelihood that a treatment will work or the probability of severe side effects should be placed in a positive context.”
The Framing Effect
This “framing effect” describes why we evaluate the same information differently depending on how it is phrased. Psychologists Daniel Kahneman and Amos Tversky showed in their early, pioneering work on decision-making that two statements with identical content can trigger very different emotional responses – and therefore different decisions – depending on linguistic framing. The same information can thus be experienced differently in perception, emotional state, and evaluation. This is why wording matters: the brain responds not only to content, but also strongly to emotional tone. Kube goes a step further: “Beyond positive versus negative framing, it also matters whether probabilities are presented as percentages or as frequencies.” For example, the statement “one in a hundred will die” often feels far more alarming than “one percent will die.” “When communicating medical risks using negative framing, it is often better to use percentages, because patients perceive them more abstractly. That makes it less likely they will immediately imagine themselves as the one person out of a hundred who is affected,” advises Prof. Rief (University of Marburg).
The Recommendation
Numbers are a central component of medical communication, but they should be chosen carefully with regard to framing effects. Patients who are highly anxious require special attention and expanded communication. “Highly anxious and very concerned patients should be given a detailed explanation of how these numbers are to be understood,” explains Kube.
Conclusion
“Many patients do not fully understand what a doctor has said – or, more importantly, what was meant – during consultations,” confirms neurologist Prof. Ulrike Bingel, Head of University Pain Medicine at Universitätsmedizin Essen and spokesperson for the CRC “Treatment Expectation.” She adds: “Effective health communication primarily requires time – and that time is often lacking in clinical practice.”
Especially given tight time resources in the healthcare system, Kube sees substantial potential in careful risk communication: “Positive framing costs nothing and does not require additional time in consultations – which makes it particularly easy to implement.”
“Every patient asks about risks and benefits because information provides reassurance. That’s precisely why we need to train therapists and clinicians to communicate diagnoses, treatments, and potential side effects in a way that is sensitive to expectations,” emphasizes Bingel. Current studies provide clear guidance on what matters. Patients should not be left to search for explanations online on their own, Bingel warns.
Link to the Jama Letter
https://jamanetwork.com/journals/jama/article-abstract/2844450#
Original Work:
Zikmund-Fisher, B. J., Thorpe, A. & Fagerlin, A. How to Communicate Medical Numbers. JAMA (2025). https://doi.org:10.1001/jama.2025.13655
Kube T, Riecke J, Heider J, Glombiewski JA, Rief W, Barsky AJ. Same same, but different: effects of likelihood framing on concerns about a medical disease in patients with somatoform disorders, major depression, and healthy people. Psychol Med. 2023 Dec;53(16):7729-7734. doi: 10.1017/S0033291723001654. Epub 2023 Jun 13. PMID: 37309182.
Collaborative Research Center 289 “Treatment Expectation”
The nationwide Collaborative Research Center (CRC/TRR 289) “Treatment Expectation”, funded by the German Research Foundation (DFG), has been investigating how patient expectations influence the effectiveness of medical treatments since 2020. The interdisciplinary research network spans the universities of Duisburg-Essen, Marburg, and Hamburg. Germany holds a leading international position in placebo and nocebo research. In May 2024, the Collaborative Research Center was awarded approximately €15 million by the DFG for a further four-year funding phase. The aim of this interdisciplinary collaboration is to understand the complex mechanisms of expectation effects – from the molecular to the systemic level – using state-of-the-art scientific methods. A central focus lies in identifying psychological and neurobiological differences between individual patients and conditions, and in examining how expectation effects can be used to optimize established pharmacological and other therapeutic approaches. To this end, around 100 researchers from medicine, psychology, and neuroscience are conducting extensive experimental and clinical studies. The overarching goal is to improve the tolerability of existing medications, enhance their effectiveness, and reduce side effects by harnessing the effects of positive expectations. The spokesperson of the research consortium, Prof. Dr. Ulrike Bingel from the Faculty of Medicine at the University of Duisburg-Essen, explains: “Patient expectations have a substantial influence on the course of diseases and the effectiveness of treatments. Our goal is to integrate scientifically grounded knowledge demonstrating the importance of expectation, context, and communication into conventional medical care.”
Further information on the current state of research and guidance for patients is available online: www.treatment-expectation.de/en.
Photos of Prof. Ulrike Bingel, Prof. Tobias Kube and Prof. Winfried Kief can be downloaded at: https://www.uni-frankfurt.de/182668122.
Contact:
Prof. Dr. Tobias Kube, Clinical Psychology and Psychopathology, Goethe University Frankfurt, Varrentrappstr. 40-42, 60486 Frankfurt. kube@psych.uni-frankfurt.de
Prof. Dr. Winfried Rief, Clinical Psychology and Psychopathology, Head of the Psycholoical Emergency Services, Marbug University, Gutenbergstraße 18, 35032 Marburg. riefw@staff.uni-marburg.de
Editor: Dr. Dirk Frank, Press Officer/ Deputy Press Spokesperson, PR & Communications Office, Theodor-W.-Adorno-Platz 1, 60323 Frankfurt, Tel.: +49 (0)69/798-13753, frank@pvw.uni-frankfurt.de