Publisher Health

Groundbreaking new research has uncovered a potential route to developing the first ever drug treatments for vascular dementia, that directly target a cause of the condition. The research, funded by the British Heart Foundation and published in the journal Proceedings of the National Academy of Sciences, has shed light on how high blood pressure causes changes to arteries in the brain, a process that leads to the devastating condition.
High blood pressure is a main cause of vascular dementia, a condition characterised by poor blood flow to the brain. The reduced blood supply starves brain cells of nutrients and over time they become damaged and die. Symptoms of vascular dementia include loss of energy, lack of concentration and poor memory.
It’s normal for the brain’s arteries to narrow and widen in response to changes in blood pressure. However, consistently high blood pressure causes arteries to stay narrow and restrict the brain’s blood supply. Until now, it was not known how.
The study, from researchers at the Geoffrey Jefferson Brain Research Centre at The University of Manchester, reveals that — in mice — high blood pressure disrupts messaging within artery cells in the brain. They found that this occurs when two cell structures, that normally help transmit messages that tell arteries to dilate, move further apart. This stops the messages reaching their target, which causes the arteries to remain permanently constricted, limiting blood flow to the brain.
By identifying drugs that could restore this communication, the researchers hope to soon be able to improve blood supply to affected areas of the brain and slow the progression of vascular dementia.
While the findings are yet to be confirmed in humans, the processes of blood vessel narrowing and widening are very similar in mice and humans. The researchers are now investigating drugs that could restore this signalling, which they hope, in future will lead to human studies that aim to restore healthy brain blood flow in vascular dementia.
Professor Adam Greenstein, a clinician scientist specialising in high blood pressure at the University of Manchester and one of the leaders of the research, said:
“By uncovering how high blood pressure causes arteries in the brain to remain constricted, our research reveals a new avenue for drug discovery that may help to find the first treatment for vascular dementia. Allowing blood to return as normal to damaged areas of the brain will be crucial to stopping this devastating condition in its tracks.

Engineers have developed nanoscale tattoos — dots and wires that adhere to live cells — in a breakthrough that puts researchers one step closer to tracking the health of individual cells.
The new technology allows for the first time the placement of optical elements or electronics on live cells with tattoo-like arrays that stick on cells while flexing and conforming to the cells’wet and fluid outer structure.
“If you imagine where this is all going in the future, we would like to have sensors to remotely monitor and control the state of individual cells and the environment surrounding those cells in real time,” said David Gracias, a professor of chemical and biomolecular engineering at Johns Hopkins University who led the development of the technology. “If we had technologies to track the health of isolated cells, we could maybe diagnose and treat diseases much earlier and not wait until the entire organ is damaged.”
The details are published in Nano Letters.
Gracias, who works on developing biosensor technologies that are nontoxic and noninvasive for the body, said the tattoos bridge the gap between living cells or tissue and conventional sensors and electronic materials. They’re essentially like barcodes or QR codes, he said.
“We’re talking about putting something like an electronic tattoo on a living object tens of times smaller than the head of a pin,” Gracias said. “It’s the first step towards attaching sensors and electronics on live cells.”
The structures were able to stick to soft cells for 16 hours even as the cells moved.

An antibody in single-chain fragment variable (scFv) format that binds to the powerful opioid carfentanil was shown to reverse signs of carfentanil overdose in preclinical tests conducted by scientists at Scripps Research.
Carfentanil is a variant of the synthetic opioid fentanyl, and about 100 times as potent as its chemical cousin. Along with fentanyl and other fentanyl variants, it is commonly mixed with illegal drugs such as heroin and cocaine to enhance their euphoric effects, resulting in many fatal overdoses.
In the study, published in ACS Chemical Neuroscience on August 3, 2023, the researchers developed a human antibody that binds very tightly to carfentanil, fentanyl and other fentanyl variants. In rodents, they showed that administering a solution of the antibody shortly after an overdose reverses the potentially deadly respiratory depression caused by carfentanil, the most dangerous of the variants. The results suggest that the antibody could be a more powerful, longer-lasting treatment for synthetic opioid overdose, compared to existing options.
“We expect this antibody to be a valuable new weapon for fighting the opioid crisis,” says study senior author Kim D. Janda, PhD, the Ely R. Callaway, Jr. Professor of Chemistry at Scripps Research.
The study’s first author was Lisa Eubanks, PhD, a senior staff scientist in the Janda laboratory.
Opioid drugs, whether synthetic or derived from the opium poppy, bind and activate neuronal receptors called mu-opioid receptors. These receptors are present on different types of neurons across the human nervous system, which is why opioid drugs have multiple effects like pain-relief and euphoria, but also respiratory depression — slower and shallower breathing. Respiratory depression is the immediate cause of death in the tens of thousands of fatal opioid-related overdoses that occur each year in the U.S.
Carfentanil, after fentanyl, is the next-most common synthetic opioid found in illicit drugs in the U.S. Once available legally as a tranquilizer for large animals, it was pulled from the market by the FDA in 2018 because of its potential for misuse — and its potential lethality at doses measured in micrograms. Carfentanil is so potent that the U.S. government regards it as a possible chemical warfare agent; the Janda lab’s early work on the new antibody was funded in part by a National Institutes of Health program aimed at finding antidotes to such weapons.

Researchers from the National Institutes of Natural Sciences and Nagoya City University have achieved a significant breakthrough by elucidating the structure of amyloid β (Aβ) bound to glycolipids on the surface of nerve cells. This finding shed light on the critical role of abnormal Aβ fibril formation, a major contributor to Alzheimer’s disease, and holds promise for innovative advancements in medicine and pharmacy.
Alzheimer’s disease is characterized by the abnormal aggregation of Aβ into amyloid fibrils, which accumulate in the brain. Understanding the molecular mechanism of Aβ fibril formation is crucial in the fields of medicine and pharmacy. To address this, researchers focused on the interaction of Aβ with glycolipids called GM1 gangliosides on the neuronal cell membrane.
Using solid-state nuclear magnetic resonance spectroscopy and molecular dynamics simulations, the research group revealed that Aβ adopts a “U”-shaped conformation upon binding with GM1 gangliosides on the membrane surface. This “U”-shaped Aβ structure consists of two layers, the β1 layer (distal from the membrane) and the β2 layer (closer to the membrane), arranged alternately. In contrast to previously reported Aβ amyloid fibrils, which align in a uniform direction, the Aβ assembly on membranes containing GM1 gangliosides exhibited a completely different conformation. Notably, the highly exposed β1 layer on the membrane surface was found to act as a catalyst, significantly accelerating the fibrillation of surrounding Aβ molecules. Furthermore, the anti-GM1-Aβ antibodies were specifically observed to recognize this region.
This research successfully unveiled the three-dimensional structure of Aβ, acting as a catalytic platform for amyloid fibril formation, in the presence of GM1 gangliosides on neuronal cell membranes. While various therapeutic antibodies targeting Aβ aggregates have been developed, they primarily bind to amyloid fibrils or their precursors. The distinct Aβ structure discovered in this study offers novel possibilities as the anti-GM1-Aβ antibodies are capable of recognizing and binding to this unique conformation. Consequently, this research represents the first identification of the structural entity responsible for producing amyloid fibrils in brain tissue, potentially offering insights into predicting the onset risk of Alzheimer’s disease and opening avenues for inhibiting its progression. The three-dimensional structure of Aβ molecules, as revealed in this study, provides exciting prospects for developing new therapeutic strategies against Alzheimer’s disease.

An international collaboration between researchers at the RIKEN Center for Brain Science (CBS) in Japan, the University of Tokyo, and University College London has demonstrated that self-organization of neurons as they “learn” follows a mathematical theory called the free energy principle. The principle accurately predicted how real neural networks spontaneously reorganize to distinguish incoming information, as well as how altering neural excitability can disrupt the process. The findings thus have implications for building animal-like artificial intelligences and for understanding cases of impaired learning. The study was published August 7 in Nature Communications.
When we learn to tell the difference between voices, faces, or smells, networks of neurons in our brains automatically organize themselves so that they can distinguish between the different sources of incoming information. This process involves changing the strength of connections between neurons, and is the basis of all learning in the brain. Takuya Isomura from RIKEN CBS and his international colleagues recently predicted that this type of network self-organization follows the mathematical rules that define the free energy principle. In the new study, they put this hypothesis to the test in neurons taken from the brains of rat embryos and grown in a culture dish on top of a grid of tiny electrodes.
Once you can distinguish two sensations, like voices, you will find that some of your neurons respond to one of the voices, while other neurons respond to the other voice. This is the result of neural network reorganization, which we call learning. In their culture experiment, the researchers mimicked this process by using the grid of electrodes beneath the neural network to stimulate the neurons in a specific pattern that mixed two separate hidden sources. After 100 training sessions, the neurons automatically became selective — some responding very strongly to source #1 and very weakly to source #2, and others responding in the reverse. Drugs that either raise or lower neuron excitability disrupted the learning process when added to the culture beforehand. This shows that the cultured neurons do just what neurons are thought to do in the working brain.
The free energy principle states that this type of self-organization will follow a pattern that always minimizes the free energy in the system. To determine whether this principle is the guiding force behind neural network learning, the team used the real neural data to reverse engineer a predictive model based on it. Then, they fed the data from the first 10 electrode training sessions into the model and used it to make predictions about the next 90 sessions. At each step, the model accurately predicted the responses of neurons and the strength of connectivity between neurons. This means that simply knowing the initial state of the neurons is enough to determine how the network would change over time as learning occurred.
“Our results suggest that the free-energy principle is the self-organizing principle of biological neural networks,” says Isomura. “It predicted how learning occurred upon receiving particular sensory inputs and how it was disrupted by alterations in network excitability induced by drugs.”
“Although it will take some time, ultimately, our technique will allow modelling the circuit mechanisms of psychiatric disorders and the effects of drugs such as anxiolytics and psychedelics,” says Isomura. “Generic mechanisms for acquiring the predictive models can also be used to create next-generation artificial intelligences that learn as real neural networks do.”

Today in the U.S., a child with risk factors for heart disease (high blood pressure, overweight, etc.) can wait close to a year to see a cardiologist because of high demand and limited resources. This is precious time that could be spent managing their conditions to help them avoid having a heart attack or stroke at a young age.
A new study from Northwestern University and the Ann & Robert H. Lurie Children’s Hospital of Chicago provides the firstcomprehensive look at the practice of pediatric preventive cardiology in 30 years. It found a high incidence of youth with risk factors for cardiovascular disease but a significant lack of resources and personnel to provide the timely, preventive care they need.
The scientists said the study should be viewed as a call to action for policymakers and health care systems to devote more resources, such as increased investment in pediatric preventive cardiology, more research to inform clinical care and more collaboration between programs to develop best practices.
“We’re not talking about primordial prevention — they’ve already got risk factors and are at risk for having an early heart attack or stroke,” said corresponding study author Dr. Amanda Marma Perak, assistant professor of pediatric cardiology and preventive medicine at Northwestern University Feinberg School of Medicine and a pediatric preventive cardiologist at Lurie Children’s Hospital. “It’s the difference between treating and controlling their risk over time versus letting that risk factor damage their vessels over many years to the point you’ve lost ground.”
The findings were published Aug. 7 in the journal Circulation: Cardiovascular Quality and Outcomes.
A snapshot of youth, adult cardiovascular health
In the U.S., 39% of youth between the ages of 12 and 19 are overweight or obese; 53% have abnormal lipids; 18% have prediabetes; and 15% have elevated blood pressure, previous research has found. These risk factors in childhood are closely associated with premature heart attack and stroke.

ells or B lymphocytes are an important part of the body’s immune system. When healthy B cells are infected with the Epstein-Barr virus (EBV), they undergo growth transformation, a process that immortalizes B cells, leading to their uncontrolled proliferation. The induction of immortalized B cells is the first step in the development of posttransplant lymphoproliferative disorder (PTLD), which can evolve to lymphoma and other lymphoproliferative disorders. One key feature of B cell growth transformation is the enlargement of cells and nuclei. However, the big question remains—what are the exact molecular mechanisms regulating EBV-induced B cell growth transformation?A recent study by Japanese researchers, published online in Microbiology Spectrum on 6 July 2023, has now provided the answer. By using primary B cells from healthy donors instead of cell lines, the team uncovered the genetic machinery responsible for inducing growth transformation following EBV infection. Explaining the rationale behind the study, principal investigator Prof. Takayuki Murata commented, “Insights from EBV research that uses cell lines has been limited, because cell lines are already in an immortalized state. To overcome this roadblock, we used primary B cells from healthy donors and then infected them with EBV. This allowed us to monitor the step-by-step growth transformation of B cells and analyze the mechanisms involved.”The first step involved the careful observation of primary B cells infected with wild-type EBV using electron microscopy and immunostaining. As early as two days after infection, the morphology of B cells showed significant alterations. An enlargement of the nucleolus (a region within the nucleus that produces ribosomes, the cell’s protein-producing machinery) was observed, along with an increase in the number of nucleoli. Interestingly, nucleolar enlargement was followed by an enlargement of both—the nuclei and the cells.To understand the transcriptional changes that occurred in infected B cells, RNA sequencing was performed. “Among the genes showing significantly altered expression levels, one named IMPDH2 stood out, as it had previously been linked to similar morphological changes in glioblastoma (another type of cancer). Careful analysis showed that the levels of the IMPDH2 peaked two days after infection—coinciding with the timing of nucleolar enlargement. This suggested that we were on the right path,” explained Dr. Atsuko Sugimoto from Fujita Health University School of Medicine, who was also a part of the research team.Interestingly, changes such as IMPDH2 induction and nucleolar enlargement could be seen when primary B cells were activated using inflammatory signals, even in the absence of EBV infection. Finally, the inhibition of IMPDH2 using silencer RNAs and the drug mycophenolic acid (MPA) prevented the growth transformation of primary B cells after EBV infection, producing smaller nucleoli, nuclei, and cells. This confirmed that IMPDH2 induction played a key role in the growth transformation of EBV-infected B cells.The next step involved understanding how EBV activates IMPDH2 expression. Three key viral genes—EBNA2 and LMP1—were tested because of their known role in EBV-induced B cell transformation. Interestingly, when EBV lacking EBNA2 was used for infection, IMPDH2 induction following primary EBV infection was blocked. This effect was not observed with LMP1 knockout. “This very clearly demonstrated that EBV induces IMPDH2 expression via EBNA2-dependent mechanisms. In addition, cellular transcription factor MYC was also involved in the IMPDH2 induction,” clarified Dr. Sugimoto.With several key pieces of evidence on their plate, the researchers finally set out to find the final piece of the puzzle. To highlight the clinical significance of their findings, they examined whether the drug mycophenolate mofetil (MMF) could prevent B cell transformation and PTLD. Prof. Murata elaborated, “Like MPA, which we tested in the earlier part of our study, MMF is an IMPDH2 inhibitor. More importantly, MMF is already a clinically approved immunosuppressant. That is why it was useful to test if it could be applied for the clinical prevention of PTLD.” As expected, the administration of MMF in a pre-clinical mouse xenograft model led to improved survival and reduced splenomegaly (enlargement of the spleen, indicating reduced B cell proliferation). These observations confirmed that the use of MMF can inhibit PTLD development.This study is the first to demonstrate that IMPDH2 activation and nucleolar hypertrophy are essential for EBV-induced B cell transformation and that IMPDH2 inhibition can suppress PTLD. It could lead to the adoption of MMF as an agent for the prevention of EBV-positive PTLD, providing significant relief to transplant patients.***Reference
DOI: https://doi.org/10.1128/spectrum.00440-23
About Fujita Health UniversityFujita Health University is a private university situated in Toyoake, Aichi, Japan. It was founded in 1964 and houses one of the largest teaching university hospitals in Japan in terms of the number of beds. With over 900 faculty members, the university is committed to providing various academic opportunities to students internationally. Fujita Health University has been ranked eighth among all universities and second among all private universities in Japan in the 2020 Times Higher Education (THE) World University Rankings. THE University Impact Rankings 2019 visualized university initiatives for sustainable development goals (SDGs). For the “good health and well-being” SDG, Fujita Health University was ranked second among all universities and number one among private universities in Japan. The university became the first Japanese university to host the “THE Asia Universities Summit” in June 2021. The university’s founding philosophy is “Our creativity for the people (DOKUSOU-ICHIRI),” which reflects the belief that, as with the university’s alumni and alumnae, current students also unlock their future by leveraging their creativity.Website: https://www.fujita-hu.ac.jp/en/index.html
About Professor Takayuki Murata from Fujita Health UniversityProf. Takayuki Murata is a Professor at the Department of Virology, Fujita Health University School of Medicine, Japan. He completed his PhD in Medical Sciences from Nagoya University. He is a leading expert in the fields of virology and tumor biology research, with a focus on the Epstein-Barr virus, Hepatitis B virus, and SARS-CoV-2. He is a member of the American Society for Microbiology and the Fujita Medical Society. In his long and illustrious scientific career, he published more than 100 studies and received several prestigious research grants.
Funding informationThis work was supported by grants-in-aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology (20H03493 to H.K.), the Japan Society for the Promotion of Science (22K10520, 21J40038 to A.S.), the Japan Agency for Medical Research and Development (JP20wm0325012 to T.M., T.W., Y.O., Y.S., and H.K. as well as JP21wm0325042 to A.S., Y.S., H.K., and T.M.), the Takeda Science Foundation (to T.M.), a Nihon Shinyaku Research Grant (to A.S. and T.M), and the Chemo-Sero-Therapeutic Research Institute (to H.K.).

Heart rate (HR) estimation is an essential component of health monitoring, and provides useful insights regarding the physiological and emotional state of humans. In the past decade or so, researchers have explored newer approaches for contactless HR estimation, primarily to overcome the discomfort or dermatitis associated with conventional methods that require physical contact. Non-contact HR estimation using cameras is an example of one such method. The method focuses on the blood volume pulse (BVP), that causes slight temporal changes in facial skin color captured in videos. By examining these color variations, it becomes possible to estimate HR. However, due to the small magnitude of these color changes, the accuracy of HR estimation is adversely affected by facial movements, ambient lighting variations, and noise.
To address these challenges, a team of researchers from Japan have now developed a novel method that leverages the temporal characteristics of the blood pulse. Importantly, it builds on the ability of the pulse to exhibit quasi-periodic behavior, which distinguishes it from noise artifacts. The study was led by Dr. Yoshihiro Maeda, Junior Associate Professor, from the Department of Electrical Engineering at the Tokyo University of Science and is published in Volume 11 of IEEE Access journal on 9 June 2023. Professor Takayuki Hamamoto and Kosuke Kurihara from the Tokyo University of Science and Associate Professor Daisuke Sugimura from the Department of Computer Science, Tsuda University, were also a part of this study.
The proposed method utilizes dynamic mode decomposition (DMD), a technique that analyzes spatio-temporal structures in multi-dimensional time-series signals. It also employs adaptive selection of the optimal spatio-temporal structure based on medical knowledge of HR frequencies. “Our method, unlike previous applications of DMD, effectively models and extracts the BVP signal by incorporating physics-informed DMD in a time-delay coordinate system, taking into account the nonlinearity and quasi-periodicity of the BVP dynamics,” explains Kosuke Kurihara, a Ph.D. student.
The proposed method relies solely on tracking time-series data from videos of a person’s face, eliminating the need for any attached detectors on the person’s body. In this method, the video time-series of the face, monitoring continuous changes, are converted into RGB time-series signals, which helps in extracting information of blood volume changes occurring beneath the skin. After effectively dealing with noise or misinformation that might creep into the data, the observed RGB signals are then converted to pulse wave information data.
Using the DMD method in a time-delayed coordinate system with conservative dynamics modeling, pulse waves containing major and accurate information can be extracted to estimate HR.
To demonstrate the efficacy of this method, the researchers used 67 facial videos from three publicly available datasets — namely TokyoTech Remote PPG dataset, MR-NIRP dataset, and UBFC-RPPG dataset. The results of this method were then compared with other non-contact HR estimation methods, including DistancePPG, SparsePPG, SAMC, Hierarchical, and MTTS-CAN.
Interestingly, the proposed method adaptively selects the dynamic mode that contains the most pulse wave components, based on the knowledge of the typical range of pulse wave components. As a result, the method showed a 36.5% improvement in estimation accuracy compared to conventional methods, especially in scenes with ambient light fluctuations.
“This achievement is expected to play a significant role as a fundamental technology for vital monitoring systems in the medical and fitness fields. The breakthrough contactless method holds great potential for non-contact heart rate estimation in various applications, such as remote health monitoring and physiological assessments,” concludes Dr. Maeda. The research findings provide new possibilities for enhancing healthcare technologies and improving overall patient comfort and well-being. Going ahead, further research will be needed to explore techniques that incorporate multispectral information, which can contribute to reducing noise and improving the accuracy of the method.
We wish Dr. Maeda and his team luck for their ongoing efforts towards addressing the remaining issues with this novel method.

Study reveals an important discovery in the realm of nanomachines within living systems. Prof. Sason Shaik from the Hebrew University of Jerusalem and Dr. Kshatresh Dutta Dubey from Shiv Nadar University, conducted molecular-dynamics simulations of Cytochromes P450 (CYP450s) enzymes, revealing that these enzymes exhibit unique soft-robotic properties.
Cytochromes P450 (CYP450s) are enzymes found in living organisms and play a crucial role in various biological processes, particularly in the metabolism of drugs and xenobiotics. The researchers’ simulations demonstrated that CYP450s possess a fourth dimension — the ability to sense and respond to stimuli, making them soft-robot nanomachines in “living matters.”
In the catalytic cycle of these enzymes, a molecule called a substrate binds to the enzyme. This leads to a process called oxidation. The enzyme’s structure has a confined space that allows it to act like as a sensor and a soft robot. It interacts with the substrate using weak interactions, like soft impacts. These interactions transfer energy, causing parts of the enzyme and the molecules inside it to move. This movement generates ultimately a special substance called oxoiron species, which serves the enzyme to oxidize a variety of different substances.
The key takeaway from these molecular-dynamics simulations is that the catalytic cycle of CYP450s is complex but follows a logical sequence. The enzyme’s restricted space, strategic residue placements, and channels allow it to be a sensitive sensor of the substrate, its own heme changes, and conformational shifts in the active site. This sensing-response capability creates a soft-robot with a fourth dimension of sensing, something previously unseen in regular 3D matter.
“We have discovered that CYP450s act as soft-robot machines in ‘living matters,’ displaying a remarkable sensing and response-action capability. This is an exciting revelation, and we believe that similar mechano-transduction mechanisms of soft-impact cues might be at work in other soft-robot machines in nature,” stated Prof. Sason Shaik, one of the lead researchers.
The findings open up new avenues in soft-robotics research, as 4D materials are gaining significance, driven by external triggers. These materials, such as hydrogels produced through 3D printing, resemble enzymes in their ability to sense and induce changes. The implications of this discovery extend beyond the realm of biology and chemistry, potentially revolutionizing fields like artificial intelligence design and self-evolving polymers/gels synthesis.
Dr. Kshatresh Dutta Dubey, co-researcher of the study, added, “We are entering an exciting era for chemistry, where soft-robotics and intelligent design of nanomachines can lead to unprecedented advancements. The future may witness the creation of self-evolving polymers and perpetual nanomachines capable of synthesizing new molecules at will.”
The scientists believe that the integration of the soft-robotic language and machine programming could accelerate progress in the development of 4D materials and unlock the full potential of soft-robotics.

Chronic pain is often accompanied by depression and anxiety. In an invited commentary published in JAMA Network Open, Kurt Kroenke, M.D., of Regenstrief Institute and Indiana University School of Medicine, discusses the relationship between pain, the most common symptom for which individuals visit a physician, and depression and anxiety, the two most prevalent mental health conditions worldwide. He highlights the importance of not neglecting psychological symptoms in patients experiencing pain.
“One of the reasons for the bi-directional linkage between pain and depression, as well as anxiety, is the existence of a feedback loop. Individuals with pain don’t sleep well and their resulting tiredness affects their mood, making them vulnerable to depression and anxiety. Having problems with depression or anxiety can increase susceptibility to pain.
“Also, areas in the brain that affect the pain that people experience are connected with areas that regulate mood, making physical and mental symptoms closely associated,” Dr. Kroenke said.
Noting that successfully addressing depression and anxiety is associated with improvement in pain, he observes that treating pain may not improve depression and anxiety to the same degree but does not negate the benefit of identifying and treating both physical and psychological symptoms.
“Symptoms of the body and the mind are frequent fellow travelers,” said Dr. Kroenke. “But patients seeing their primary care physician for a headache, back or muscle or leg pain or stomachache often neglect to mention the symptoms commonly associated with depression and anxiety that they are also experiencing such as fatigue, lack of motivation, nervousness and moodiness. And physicians don’t always ask about symptoms beyond the ones which brought the patient into the office.
“Un- or under-treated, these emotional symptoms can cause long-term suffering and impaired quality of life. If clinicians measure and monitor both physical and mental symptoms they will be more able and likely to treat them. But there is no blood pressure cuff, lab test or X-ray for symptoms. We don’t have a way to measure symptoms other than from what the patient tells us, yet screening and diagnosis are crucial to improving patient outcomes.”
Dr. Kroenke is one of the fathers and leaders of the growing field of symptomology and the developer of several validated and widely used scales which enable clinicians to use feedback from patients to measure type and severity of pain (PEG), depression (PHQ-9), anxiety (GAD-7) and other symptoms including cancer fatigue (FSI-3) and risk of suicide (P-4). These brief measurement tools have been translated into more than 100 languages.
Symptoms account for half of all outpatient primary care visits. In a review article published in 2014, Dr. Kroenke and colleagues reported that one in three common symptoms do not have a clear-cut disease-based explanation. That percentage is now thought to be more than one in two, he says.
The need to address both physical and psychological symptoms has long been recognized, says Dr. Kroenke, whose measurement tools are helping physicians to do so. He concludes his JAMA Network Open commentary with an illustrative quote from Ovid [born 43 B.C.], “I am no better in mind than in body; both alike are sick and I suffer double hurt.”