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Delirium is common among women with urinary tract infections (UTIs) — especially those who have experienced menopause. Investigators from Cedars-Sinai, working with laboratory mice, have been able to prevent symptoms of the condition with estrogen, which is commonly used for hormone replacement therapy. Their study was published in the peer-reviewed journal Scientific Reports.
“There has been a resurgence of interest in hormone replacement therapy, and this study, which builds on our previous work, shows that it may be a tool to mitigate delirium,” said Shouri Lahiri, MD, director of the Neurosciences Critical Care Unit and Neurocritical Care Research at Cedars-Sinai and senior author of the study. “I think it is a major step toward a clinical trial of estrogen in human patients with UTIs.”
Lahiri said that delirium — a change in mental abilities that includes lack of awareness of one’s surroundings — is a common problem in older women with UTIs.
“Even as a medical student, you know that if an older woman comes to the hospital and she’s confused, one of the first things you check is whether the patient has a UTI,” Lahiri said.
In previous studies, Lahiri’s team found a connection between delirium and an immune-regulating protein called interleukin 6 (IL-6). Events such as lung injury or UTI cause IL-6 to travel through the blood to the brain, causing symptoms such as disorientation and confusion. Estrogen is a known suppressor of IL-6, so the investigators designed experiments to test its effects on UTI-induced delirium.
The researchers compared pre- and postmenopausal mice with UTIs and observed their behavior in several types of specialized environments. They found that the mice in which menopause had been induced exhibited symptoms of delirium, such as anxiousness and confusion, while the others did not.

The move broadens access to the reformulated shots, but only a small fraction of the country’s youngest children are likely to get one of the new doses in the near future.WASHINGTON — The Food and Drug Administration on Thursday expanded eligibility for the updated coronavirus shots to children as young as 6 months old, the latest step to make the retooled doses available to more Americans.The federal government rolled out the updated boosters from Pfizer-BioNTech and Moderna in September, though the public has shown little interest in the new shots. The government expanded eligibility to children as young as 5 in October.The new action by the F.D.A. further expands access to the so-called bivalent shots, though there is unlikely to be strong demand for them among parents. Only a small fraction of the country’s youngest children have been immunized since the original vaccines were authorized for that age group in June.The move comes as coronavirus cases in the United States are on the rise. Young children have also been hit hard in recent months by respiratory syncytial virus, known as R.S.V. Cases have swamped pediatric units across the United States.“More children now have the opportunity to update their protection against Covid-19 with a bivalent Covid-19 vaccine, and we encourage parents and caregivers of those eligible to consider doing so — especially as we head into the holidays and winter months where more time will be spent indoors,” Dr. Robert M. Califf, the F.D.A. commissioner, said in a statement.For the country’s youngest children, eligibility for the updated coronavirus shots will vary depending on which vaccine and how many doses they have received.Children ages 6 months through 5 years who received Moderna’s two-dose vaccine will be eligible for the company’s updated booster two months after finishing their initial vaccination round.Pfizer’s vaccine is given as a three-dose series for children ages 6 months to 4 years. For those children, the third dose in the series will now be the updated shot instead of the original formulation.Young children who have already received all three doses in Pfizer’s series will not yet be eligible for an updated booster. But the F.D.A. said it expected that new data would be available in January concerning the retooled booster for that population, and the agency said it would assess that data “as quickly as possible.”The broadened eligibility for the updated shots still needs to be signed off on by the Centers for Disease Control and Prevention.The Biden administration has struggled to generate interest in the updated booster shots, which target both the original version of the virus and Omicron subvariants. Only about 13 percent of Americans ages 5 and up have received one of the new doses so far.The F.D.A. authorized the Pfizer and Moderna vaccines for the country’s youngest children in June, a move that came a year and a half after the vaccines were first rolled out for adults.But few young children have been immunized since then. Less than 10 percent of children ages 4 and under have received a vaccine dose so far, and even fewer have completed their full vaccination round.

About 430 million people around the world experience disabling hearing loss. In the United States, approximately 37.5 million adults report some trouble hearing. Hearing loss can happen when any part of the ear or the nerves that carry information on sounds to the brain do not work in the usual way.
For instance, damaged hair cells in the inner ear can lead to hearing loss. “These cells allow the brain to detect sounds,” said Dr. Amrita Iyer, first author of a new paper published in eLife. Iyer was a graduate student in the lab of Dr. Andrew Groves, professor and Vivian L. Smith Endowed Chair in Neuroscience and of molecular and human genetics at Baylor College of Medicine, while she was working on this project.
Hair cells are generated during normal development but this ability is progressively lost after birth as mammals mature. “When hair cells are lost in mature animals, the cells cannot be naturally regenerated, which can lead to permanent hearing loss,” Iyer explained. “In the current study, we looked closer into the possibility of promoting hair cell regeneration in mature animals using cell reprograming. Our approach involved the overexpression of various transcription factor combinations.”
Transcription factors promote the expression of certain genes and prevent the expression of others. By changing the pattern of gene expression, the researchers hoped to lead cells to a state in which they would regenerate hair cells in mature animals similarly to what happens during development.
“We compared the reprogramming efficiency of the hair cell transcription factor ATOH1 alone or in combination with two other hair cell transcription factors, GFI1 and POU4F3, in mouse non-sensory cells in the cochlea, the part of the inner ear that supports hearing,” Iyer said. “We did this at two timepoints — eight days after birth and 15 days after birth, assessing the extent of hair cell regeneration in mice.”
To study the structure of the hair cell bundles generated by reprogramming, Iyer collaborated with Dr. Yeohash Raphael’s lab at the University of Michigan to perform scanning electron microscopy imaging on the cochleae of mice conditionally overexpressing these transcription factors. The images clearly showed that the hair cell bundles were in accordance to what is observed on inner hair cells during development. Further studies showed that these cells also had some characteristics that suggested that they were capable of sensing sound.
“We found that although expressing ATOH1 with hair cell transcription factors GFI1 and POU4F3 can increase the efficiency of hair cell reprogramming in older animals compared to ATOH1 alone or GFI1 plus ATOH1, the hair cells generated by reprogramming at eight days of age — even with three hair cell transcription factors — are significantly less mature than those generated by reprogramming at postnatal day one,” Iyer said. “We suggest that reprogramming with multiple transcription factors is better able to access the hair cell differentiation gene regulatory network, but that additional interventions may be necessary to produce mature and fully functional hair cells.”
These findings are key to advancing the existing understanding of the mammalian inner ear hair cell regeneration process. From a therapeutic standpoint, transcription factor-mediated reprogramming and the underlying biology associated with its function may enable fine-tuning of current gene therapy approaches for long-term hearing loss treatment.
Other contributors to this work include Ishwar Hosamani, John D. Nguyen, Tiantian Cai, Sunita Singh, Melissa M. McGovern, Lisa Beyer, Hongyuan Zhang, Hsin-I Jen, Rizwan Yousaf, Onur Birol, Jenny J. Sun, Russell S. Ray, Yehoash Raphael and Neil Segil. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine, the University of Southern California and the University of Michigan.
The project was supported by the following grants: RO1 DC014832, R21 OD025327, DC015829 and a Hearing Restoration Project Consortium award from the Hearing Health Foundation. The project was also supported by funding from a CPRIT Core Facility Support Award (CPRIT-RP180672), NIH grants (P30 CA125123, S10 RR024574, S10OD018033, S10OD023469, S10OD025240 and P30EY002520), the R. Jamison and Betty Williams Professorship, the University of Michigan College of Engineering and NSF grant #DMR-1625671.
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Materials provided by Baylor College of Medicine. Original written by Ana María Rodríguez, Ph.D.. Note: Content may be edited for style and length.

Researchers at the University of Michigan Rogel Cancer Center and School of Dentistry found that certain drugs can change the fundamental makeup of cancer stem cells in mouse models of mucoepidermoid carcinoma — a lethal form of salivary gland cancer that currently has no treatment options. These results appeared in Clinical Cancer Research.
“We observed that when we used small molecule inhibitors of MDM2 for a short period of time, the population of cancer stem cells decreased quite a bit,” said Jacques Nor, D.D.S, M.S,. Ph.D., Donald Kerr Professor of Dentistry and lead author of this study. The team initially thought that the cancer stem cells were being selectively killed by this drug, but the study revealed something more profound. Cancer stem cells represent the small number of cells in a tumor that fuel cancer’s growth and spread.
“We found that the drug actually changes the fundamental nature of the cells to make them more vulnerable to other therapies and less able to start new tumors.”
Nor’s team also observed that the incidence of relapse in mice treated with this drug was much lower than in the mice that were not treated.
Mucoepidermoid carcinoma is the most common malignant salivary gland cancer with very limited therapeutic options. Over 3,000 people die of the disease in the United States every year, and to date there is no FDA approved drug to treat it.
“There is currently no effective therapy for this cancer. Right now, these patients are typically treated with radical surgery and radiation, and that usually is insufficient. Patients die because of tumor relapse and tumor metastasis. We need a systemic drug. This is one of the first outcomes that is showing some positive signs in terms of tumor regression or inhibiting tumor relapse,” Nor said.
Nor has been studying for years drugs that activate P53 to see if this makes cancer cells more vulnerable to therapies. In 2019, he and his team published a study in Clinical Cancer Research that showed that small molecule inhibitors work well in mouse-models of MEC, but the team still hadn’t figure out just how the drugs work. This new study moves the team one step closer to that understanding.
P53 is frequently mutated in most cancers but rarely in MEC, which made these small molecule inhibitors a good candidate to study. “This drug requires a non-mutated form of P53 to work,” said Nor. “In mucoepidermoid carcinoma, this drug works well because P53 is not mutated.” These results show that P53 is integral to MEC and suggest that therapeutic activation of p53 could present new treatment options for patients, possibilities that energize Nor and his team.
“The bottom line is we now have a drug that is in a clinical trial for patients with salivary gland cancer,” he said.
Additional authors: Christie Rodriguez-Ramirez, Zhaocheng Zhang, Kristy A Warner, Alexandra E Herzog, Andrea Mantesso, Zhixiong Zhang, Eusik Yoon, Shaomeng Wang, Max S Wicha
Funding: National Institute of Dental and Craniofacial Research (R01-DE021139), J.E. Nor; National Institute of Dental and Craniofacial Research (R01-DE23220) J.E. Nor; National Institute of Dental and Craniofacial Research (R01-DE021139S1) C.Rodriguez-Ramirez
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Materials provided by Michigan Medicine – University of Michigan. Original written by Anna Megdell. Note: Content may be edited for style and length.

For decades, doctors have treated kids with attention-deficit/hyperactivity disorder (ADHD) with methylphenidate, a stimulant drug sold as Ritalin and Concerta, making it one of the most widely prescribed medications aimed at the central nervous system. One might expect that researchers would know how methylphenidate works in the brain by now, but little is known about the drug’s mechanism of action. Now, a new study seeks to close this gap and understand how methylphenidate interacts with cognitive control networks and attentional behavior.
The new study appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier.
What researchers do know is that individuals with ADHD have lower dopamine signaling activity than neurotypical individuals in the interconnected brain networks that control attention and goal-directed behaviors. Specifically, methylphenidate is hypothesized to ameliorate ADHD symptoms by increasing dopamine levels in the nucleus accumbens (NAc), a hub for dopamine signaling.
In the new study, researchers led by Yoshifumi Mizuno, MD, PhD, Weidong Cai, PhD, and Vinod Menon, PhD, used brain imaging to explore the effects of methylphenidate on the NAc and a so-called triple network system that plays a key role in behaviors that require adaptive control of attention. The three networks include the salience, frontoparietal, and default mode networks. Aberrant activity was detected in the NAc and in multiple brain networks in children with ADHD, suggesting that dysregulation in the system may underlie ADHD symptoms, and that correcting the dysfunction might alleviate those symptoms.
“Our findings demonstrate in two independent cohorts that methylphenidate changes spontaneous neural activity in reward and cognitive control systems in children with ADHD. Medication-induced changes in cognitive control networks result in more stable sustained attention. Our findings reveal a novel brain mechanism underlying methylphenidate treatment in ADHD and inform biomarker development for evaluating treatment outcomes,” noted Dr. Menon, Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine.
The researchers used functional magnetic resonance imaging (fMRI) to measure the effects of methylphenidate on spontaneous brain activity in 27 children with ADHD and 49 typically developing controls. Children with ADHD were scanned during two different visits one to six weeks apart — once while receiving methylphenidate and once while receiving a placebo. (Typically developing children did not receive medication or placebo.) Outside the scanner, children with ADHD also performed a standardized task to assess sustained attention. Additionally, the researchers tested the replicability of methylphenidate’s effects on spontaneous brain activity in a second independent cohort.
Not surprisingly, children performed better on the attention tasks when they were medicated. And as the researchers hypothesized, they also saw greater spontaneous neural activity in the NAc and the salience and default mode networks when methylphenidate was administered. Children with ADHD who displayed enhanced changes in brain activity patterns in the default mode network with medication performed better on the attention tasks with medication. Findings were replicated across two independent cohorts, providing further evidence that methylphenidate may alleviate ADHD symptoms by its actions on the NAc and the triple network cognitive system.
Cameron Carter, MD, editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, said of the study, “The findings, which used the widely available technique of resting-state functional MRI, confirm the positive effects of methylphenidate on attention in children with ADHD and reveal the likely mechanism of action, through improved coordinated brain network activity and a likely key role for enhanced dopamine effects in the NAc region of the brain.”
The work advances researchers’ understanding of how ADHD affects cognitive control networks in the brain and how methylphenidate interacts with these networks to shift behavior. The findings could guide future work using brain imaging as a clinically useful biomarker of response to treatments.
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Losing too much weight when infected with COVID-19 has been linked to worse outcomes. Now, researchers at Karolinska Institutet in Sweden have discovered that SARS-CoV-2 infection fuels blood vessel formation in fat tissues, thus revving up the body’s thermogenic metabolism. Blocking this process by using an existing drug curbed weight loss in mice and hamsters that were infected with the virus, according to the study published in the journal Nature Metabolism.
“Our study proposes a completely new concept for treating COVID-19 associated weight loss by targeting the blood vessels in the fat tissues,” says Yihai Cao, professor at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, and the study’s corresponding author.
The researchers examined how different types of fat, including brown fat and visceral and subcutaneous white fat, reacted when exposed to SARS-CoV-2 and how it impacted weight in mice and hamsters. They found that the animals lost significant amounts of weight in four days and that this weight loss was preceded by the activation of brown fat and the browning of both types of white fat. These fat tissues also contained more microvessels and high levels of a signaling protein called vascular endothelial growth factor (VEGF), which promotes the growth of new blood vessels.
The researchers observed the same mechanisms in human tissue samples from four patients who died of COVID-19, suggesting the findings could be clinically relevant for humans.
When the researchers treated the animals with a substance that inhibits the formation of new blood vessels, a so-called antiangiogenic drug, the animals recovered most of their lost weight and their fat tissues exhibited fewer microvessels.
“Antiangiogenic drugs are currently used in the clinic to treat various types of cancers,” Yihai Cao says. “It’s possible these drugs could also be helpful in treating COVID-19-related problems such as excessive weight loss and metabolic changes, thus improving the quality of life and survival for these patients. Of course, we will need more research to validate if our preclinical findings also hold up in human trials.”
The study was funded by grants from the Swedish Research Council, the Hong Kong Centre for Cerebro-cardiovascular Health Engineering, the Swedish Cancer Foundation, NOVO Nordisk, the Swedish Childhood Cancer Fund, the Strategic Research Areas (SFO)-Stem Cell and Regenerative Medicine Foundation, the Karolinska Institutet Foundation, the National Natural Science Foundation of China and the Doctor Fund of Shandong Natural Science Foundation. The authors have not reported any conflicts of interest.
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Ribosomes, the tiny protein-producing factories within cells, are ubiquitous and look largely identical across the tree of life. Those that keep bacteria chugging along are, structurally, not much different from the ribosomes churning out proteins in our own human cells.
But even two organisms with similar ribosomes may display significant structural differences in the RNA and protein components of their mitoribosomes. Specialized ribosomes within the mitochondria (the energy producing entities within our cells), mitoribosomes help the mitochondria produce proteins that manufacture ATP, the energy currency of the cell.
Scientists in the laboratory of Sebastian Klinge wondered how mitoribosomes evolved, how they assemble within the cell, and why their structures are so much less uniform across species. To answer these questions, they used cryo-electron microscopy to generate 3D snapshots of the small subunits of yeast and human mitoribosomes as they were being assembled. Their findings, published in Nature, shed light on the fundamentals of mitoribosome assembly, and may have implications for rare diseases linked to malfunctioning mitoribosomes.
“Three dimensional pictures can tell us a lot about what steps are required, what proteins are involved in the process, and how you might be able to regulate the assembly of these large and complex machines,” says Nathan Harper, a graduate student in Klinge’s lab. “Cryo-EM allowed us to identify and isolate individual stages of the assembly pathway from a heterogeneous population of purified complexes, and we are able to see how these complexes change over time during assembly,” adds Chloe Burnside, also a graduate student in Klinge’s lab.
By observing this process in two different species — yeast and humans — the team managed to directly observe many similarities and differences in mitoribosome assembly. One key distinction: different proteins often were involved in otherwise similar acts of RNA folding. That’s likely because “there are common hurdles for these ribosomes,” Harper explains. “You can think about it like manufacturing two different bikes — a road bike and a mountain bike. You might need additional parts or tools for each one, but some key stages in production will be similar.”
The results provide unique insights into how molecular complexity and diversity arises in macromolecular complexes, and how assembly systems evolve along with the complexes themselves. A better understanding of mitoribosomes may also have implications for a range of severe diseases linked to mitoribosome dysfunction, such as Perrault syndrome. “We were able to map various disease-causing mutations onto different assembly factors’ structures, so that we could see how these mutations could affect the ribosome assembly process.”
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Researchers at the University of Copenhagen’s Faculty of Science have modified a yeast cell to sense the active substances in cannabis and get it to turn red when it does. The result paves the way for more actors to discover new medicinal substances and for a new type of drug test that can be done with a smartphone.
Yeast cells are simple organisms. They do two things in life: eat and propagate. Now, researchers at the University of Copenhagen’s Department of Plant and Environmental Sciences have equipped common baker’s yeast cells with a new function.
The researchers substituted the yeast cell’s sex drive with a sense of taste and smell that allows it to detect cannabinoids, the active substances in cannabis. Going one step further, the researchers made the yeast turn red or glow when it successfully detects cannabinoids. The study has been published in Nature Communications.
“We have made a living sensor out of the yeast cell, which can now sense cannabinoids or molecules that have the same function as cannabinoids even if they look very different than cannabinoids. Among other things, the biosensor can be used to look for new substances with the same properties as cannabinoids. This could democratize medicinal development so that pharmaceutical companies aren’t the only ones equipped to discover new substances,” says Professor Sotirios Kampranis of the Department of Plant and Environmental Sciences, who headed the research.
Turns red when sensing cannabinoids
Humans use hundreds of different GPCRs (G-protein-coupled receptors) to taste and smell. In our noses alone, 400 different GPCRs make it possible for us to detect and distinguish between the smell of roses and freshly baked bread, each of which activates different GPCRs that then signal the brain.

Gait analysis systems measure certain metrics to give their results. These results then drive clinical treatment for gait correction. However, detailed gait analysis requires expensive equipment, and a lot of space, markers, time. Measurements from markerless, video-based gait analysis systems, on the other hand, are inaccurate. To improve upon existing systems, researchers have now combined RGB camera-based pose estimation and an inertial measurement unit sensor for gait analysis. This significantly reduces errors in the process.
In people with gait disabilities (i.e., a pattern of walking — or gait — that is not normal), assessing gait speed, stride length, and joint kinematics are essential. Measurement of gait parameters over a period of time is critical to determine treatment effects, predict fall risk in elderly individuals, and plan physiotherapy treatments. In this regard, optoelectronic marker-based three-dimensional motion capture (3DMC) — a gait analysis tool — can accurately measure gait metrics. However, economic and time constraints, coupled with requirements for a large space, extensive equipment, and technical expertise make 3DMC impractical in clinical settings. Alternate methods include inertial measurement unit (IMU)-based motion capture systems and RGB camera-based methods, which can measure gait without reflective markers when equipped with depth sensors. But these have their own drawbacks. IMU-based systems require many IMU sensors to be attached to human body segments, reducing their feasibility, and compared to optoelectronic 3DMC systems, RGB camera-based methods are less accurate in their measurement of kinematic parameters such as lower limb joint angles.
Hence, improved gait analysis systems are needed.
To this end, a team of researchers comprising Dr. Masataka Yamamoto, Mr. Yuto Ishige, and Professor Hiroshi Takemura from the Faculty of Science and Technology, Tokyo University of Science, and Professor Koji Shimatani from the Prefectural University of Hiroshima, Japan, have developed a simple and accurate sensor-fusion method for accurate gait analysis. “We combined information from a small IMU sensor attached to the shoe with estimated information on the bones and joints of the lower limb, obtained by capturing the gait from a single RGB camera,” explains Dr. Yamamoto, the lead author of the study. In a recent article published in Volume 12 of Scientific Reportson October 21, 2022, the researchers have detailed this method and the results they achieved with it.
The team used single RGB camera-based pose estimation by OpenPose (OP) and an IMU sensor on the foot to measure ankle joint kinematics under various gait conditions for sixteen healthy adult men between 21 and 23 years of age who did not have any limitation of physical activity. The participants’ gait parameters and lower limb joint angles during four gait conditions with varying gait speed and foot progression angles were noted using only OP as well combined measurements from OP and the IMUs. The latter was the team’s novel proposed method. Results from these techniques were compared to gait analysis using 3DMC, the current gold standard.
The proposed combination method could measure gait parameters and lower limb joint angles in the sagittal plane (which divides the body into right and left). Moreover, the mean absolute errors of peak ankle joint angles calculated by the combination method were significantly less compared to OP alone in all the four gait conditions. This is a significant development in gait analysis. “Our method has the potential to be used not in medicine and welfare, but also to predict the decline of gait function in healthcare, for training and skill evaluation in gyms and sports facilities, and accurate projection of human movements onto an avatar by integrating with virtual reality systems,” notes Dr. Yamamoto.
With further research, this method can be adapted to clinical settings and a larger demographic.
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Gig workers, waiters, salespeople and others who rely on fluctuating income may be paying for wage volatility with their health, according to research published by the American Psychological Association.
In three studies spanning several industries in the U.S., workers who experienced more volatile pay reported worse physical health symptoms, including poor sleep quality, headaches, stomach issues and back pain. The research was published online in Journal of Applied Psychology.
“Pay volatility seems to predict worse health outcomes across a wide range of incomes,” said study author Gordon Sayre, PhD, an assistant professor of organizational behavior at Emlyon Business School in France. “Not only was pay volatility related to worse health in lower-paid tipped jobs or among freelancers in the gig economy but for higher-paid professionals working in finance, sales and marketing where commissions and performance bonuses are common.”
In one study, 85 workers in the U.S. who relied on tips (waiters, delivery drivers, maids, etc.) answered daily online surveys for two weeks about their total daily pay and health. Participants reported receiving tips on 80% of their workdays, with an average daily tip total of $36.18, accounting for a quarter of their total income on average.
Large fluctuations of daily pay over the two-week period were associated with negative physical health symptoms and poor sleep quality. That relationship was stronger when volatile pay made up a larger percentage of the participants’ total pay, the study found.
Another study included 375 participants in the U.S. who spent an average of 29 hours per week working on Amazon’s Mechanical Turk, a website where gig workers can complete various tasks for minimal amounts of pay. The participants completed weekly surveys for three weeks and the findings were similar to the study on tipped workers.
Sayre conducted a final online survey with 252 higher-income employees in finance, marketing and sales who relied on commissions or bonuses for a smaller fraction of their income. The workers completed monthly surveys for three months, and pay volatility was less harmful to health when they were less reliant on commissions or bonuses.
Mindfulness, or a focus on the present moment, has been shown to buffer against stress in other aspects of work and life. Individuals’ mindfulness was measured in this research, but it did not help reduce the physical symptoms associated with volatile pay. Pay volatility was less impactful for workers who were less dependent on those volatile forms of income, however.
Businesses should consider whether volatile forms of pay (e.g., tips, piece-rate work, performance bonuses and commissions) are necessary and ensure that more stable forms of compensation make up a larger proportion of workers’ total income, Sayre said.
Legislation also could improve the lives of millions of Americans who rely on fluctuating income, such as raising the federal tipped minimum wage of $2.13 per hour and providing greater protections to gig workers, Sayre said.
“Unions are another way that workers could secure stronger protections against volatile pay,” he added. “Raising the proportion of base pay and reducing dependence on volatile pay should help protect workers’ health in many industries.”
The study findings do not prove that volatile pay causes health symptoms, only that there is a correlation between them.