Currently, formal models of addiction focus either on the complex individual decision-making processes involved in addiction or on the social dynamics of addiction. They do not integrate these two levels, which has been identified as a key shortcoming of current formal models of addiction. To address this, we propose a nonlinear dynamical modeling framework of addiction integrating both the individual level and social level of addictive behavior. The individual level of our modeling framework is a formalization of a dual-process theory, where one type of process increases the consumption of addictive goods, and another type of process limits consumption. For our formalization, we build on a well-studied model from ecology, originally used to model periodic outbreaks of the spruce budworm population. To this model, we add the process of incentive sensitization at the individual level and at the social level, we incorporate the critical processes of selection homophily and peer influence. We show that our integrated modeling framework can be used to explain key phenomena identified in addiction literature: a gradual transition to heavy use, sudden relapse and sudden quitting, relatively stable use states over time (i.e., abstinence moderate use, and heavy use), social contagion and sudden outbreaks, clustering of users, and social aid in recovery. In addition, we demonstrate how our modeling framework can be extended to include mutualistic, competitive, and more complex interactions between different addictive behaviors. Finally, we show how our framework can lead to new insights and predictions and suggest avenues for future research. (PsycInfo Database Record (c) 2026 APA, all rights reserved)
A cornerstone of human intelligence is the ability to flexibly adjust our cognition and behavior as our goals change. For instance, achieving some goals requires efficiency, while others require caution. Different goals require us to engage different control processes, such as adjusting how attentive and cautious we are. Here, we show that performance incurs control adjustment costs when people adjust control to meet changing goals. Across four experiments, we provide evidence of these costs and validate a dynamical systems model explaining the source of these costs. Participants performed a single cognitively demanding task under varying performance goals (e.g., being fast or accurate). We modeled control allocation to include a dynamic process of adjusting from one’s current control state to a target state for a given performance goal. By incorporating inertia into this adjustment process, our model accounts for our empirical finding that people undershoot their target control state more (i.e., exhibit larger adjustment costs) when goals switch rather than remain fixed (Study 1). Further validating our model, we show that the magnitude of this cost is increased when: distances between target states are larger (Study 2), there is less time to adjust to the new goal (Study 3), and goal switches are more frequent (Study 4). Our findings characterize the costs of adjusting control to meet changing goals and show that these costs emerge directly from cognitive control dynamics. In so doing, they shed new light on the sources of and constraints on flexibility of goal-directed behavior. (PsycInfo Database Record (c) 2026 APA, all rights reserved)
Understanding how people assign subjective value to outcomes with multiple attributes, such as risk and delay, is central to understanding the structure and manifestation of economic preferences. However, multiattribute preference has been primarily studied through binary choices. The price at which a person would buy, sell, or equate each prospect offers another measure of subjective value that may diverge from multiattribute choice. In both risky and intertemporal domains, choice and price preferences exhibit systematic preference reversals, where a smaller, sooner, or safer option is chosen while a larger, later, or riskier alternative is assigned a higher price. The present study takes a deep dive into how subjective value is assigned in each case in an attempt to reconcile these diverging measurements and methods of assessing value. To explain how and why preferences change across choice and price, the domains of gains and losses, price frames of buying and selling, and varying levels of time pressure, we develop a two-step neural network–based modeling approach. First, we tested cognitive mechanisms underlying value-based judgments and decisions using a switchboard model comparison. Next, we fit and evaluated individualized joint models, where all data from an individual are modeled using parameters and mechanisms that are specific to their best fitting model structure. While mechanisms like delay discounting and risk aversion are common to both models, our results suggest that anchoring and payoff sensitivity diverged between pricing and choice. Extensive differences across elicitation procedures indicate that a common representation of value may remain elusive. (PsycInfo Database Record (c) 2026 APA, all rights reserved)
The accumulation of fluid in the belly, known as ascites, is something that women with advanced ovarian cancer may know all too well. The results of research by a team at Duke University School of Medicine now suggest that, more than causing discomfort, this fluid may protect cancer cells from a form of cell death known as ferroptosis, helping cancer cells survive and spread. The studies also indicated that a decades-old cholesterol-lowering drug, bezafibrate, may be able to disrupt that protection.
The findings, derived through lab experiments and an analysis of patient samples, do not show that bezafibrate treats ovarian cancer. But they do suggest that changing the environment that cancer depends on could make it more vulnerable to existing cancer treatment.
“Doctors have mostly viewed ascites as a symptom rather than an active driver of disease,” said Jen-Tsan Chi, PhD, a professor in the department of molecular genetics and microbiology and co-leader of the Cancer Biology Program at the Duke Cancer Institute. “We’ve learned it gives cancer a survival advantage, which fills a major gap in understanding how ovarian cancer spreads.”
Chi is senior and corresponding author of the team’s published paper in Nature Communications, titled “Ascites protects against ferroptosis and enables the peritoneal growth of ovarian cancer.” In their paper, the authors concluded, “Our findings identify ascites as a key determinant of ferroptosis resistance in metastatic OVCA and highlight its role in promoting tumor survival and dissemination within the peritoneal cavity.”
The peritoneum is a frequent site of metastasis in ovarian cancer (OVCA), the authors explained, and this is often accompanied by the accumulation of ascites in the peritoneal cavity. And while ascites is observed in other diseases such as liver cirrhosis, it’s most often associated with metastatic OVCA. The fluid occurs in 90% of those with advanced ovarian cancer. Doctors will drain ascites to ease pain, improve mobility, and make breathing easier, which offers patients relief even if it doesn’t stop the disease.
“Due to the enrichment of cellular and acellular factors, the ascitic fluid is reported to harbor a growth-promoting and immune-evading environment for cancer cells and is thought to serve as a medium for cancer cell dissemination and tumor progression and metastasis,” the team continued. However, they noted, “Despite its prevalence, ascites and its role in the peritoneal growth of OVCA remain poorly understood.”
According to the newly reported study findings, ascites also acts as a shield, helping cancer cells evade a specific form of cell death called ferroptosis. Ferroptosis is a kind of cellular rusting. It happens when iron inside a cell reacts with certain fats, causing the cell membrane to break apart. Many metastatic cancer cells—those that float freely through the abdomen looking for new places to grow—are naturally vulnerable to this kind of damage. “… we and other groups have reported that detached and metastasizing OVCA cells are especially vulnerable to ferroptosis, a form of cell death characterized by iron dependency and an irreversible accumulation of lipid hydroperoxides,” the authors wrote.
The study in Nature Communications shows how they survive anyway. For their research, the scientists bathed cancer cell lines and patient-derived tumor cells in ascites collected from patients, and observed how they responded to ferroptosis triggers. “Nothing is currently known about how ascites may influence OVCA cells’ ferroptosis,” they noted. “Given the common occurrence of ascites with peritoneal metastasis, ascites may be crucial for the peritoneal spread of OVCA.”
(From Left) Susan Murphy, Andrew Berchuck, Yasaman Setayeshpour, and Jen-Tsan Chi pose in the lab. Research accepted to Nature Communications led by Chi, professor in MGM, integrative immunology, and medicine, found that a cholesterol drug may make it harder for ovarian cancer cells to survive. In lab studies, fibrates weakened the protective effect of abdominal fluid that helps tumors resist a type of cell death, known as ferroptosis. Chi is also a professor of biomed engineering, cell biology and pharmacology and cancer biology and a member of DCI. [Mark Dolejs for Duke University School of Medicine]
The team found that the fluid protected cancer cells by changing how the cells store fats and control iron levels, effectively blocking cell death. The protection required only trace amounts. As little as 2% immersion shielded cancer cells from destruction, even though in patients these cells are entirely enveloped by the fluid.
“What surprised us was how selective this effect was,” said first author Yasaman Setayeshpour, a graduate student in molecular genetics and microbiology at Duke School of Medicine. “Ascites didn’t protect the cancer cells from other well-known types of cell death, like apoptosis or necrosis—it only blocked ferroptosis.
“To figure out why, we broke ascites down into major parts, like lipids, proteins, and small molecules, and tested what happened when each was removed. When we took the lipids out, the protective effect disappeared. That told us lipids are the key reason ascites helps these cancer cells survive,” Setayeshpour said.
The researchers also found an unexpected helper in the form of bezafibrate, an older type of cholesterol-lowering drug that is used to lower triglycerides by altering how the body processes fats. “The idea behind testing lipid-lowering drugs was to mimic what happens when lipids are removed from ascites,” Setayeshpour explained.
The studies showed that bezafibrate restored sensitivity to ferroptosis, but only when ascites was present. On its own, the drug did not trigger cell death, nor did it slow tumor growth in mice. The researchers found that the drug’s impact hinged on the cancer’s surroundings, in this case, the fat-rich fluid bathing the tumor. The studies showed that targeting this environment, using repurposed drugs like bezafibrate, could leave cancer cells more exposed to existing cancer treatments. “Given the intrinsic vulnerability of metastatic cancer cells to ferroptosis, these data suggest that ascites-mediated protection represents a critical mechanism supporting peritoneal survival,” the team noted. “Importantly, re-sensitization to ferroptosis by bezafibrate raises the possibility that therapeutic targeting of this pathway may limit peritoneal dissemination.”
Chi said the finding could have implications beyond ovarian cancer. Other cancers, including colorectal and pancreatic cancers, can also spread within the abdominal cavity. “These findings may also extend beyond ovarian cancer to other metastatic settings, including peritoneal colorectal cancer and pleural, brain, or spinal metastases,” the authors stated.
“This work shows how much the environment around a tumor matters,” Chi said. “Biological fluids like ascites don’t just give cancer cells a place to move. They actively help drive how cancer spreads.”
Recent studies have demonstrated the close association of mutations in the dehydrodolichyl diphosphate synthase (DHDDS) gene with neurodevelopmental disorders and the onset of epilepsy. This report describes a female patient harboring a de novo heterozygous variant c.110G>A (p.Arg37His) in the DHDDS gene, characterized by childhood-onset myoclonus-like movement disorder (at age 6) and late-onset epilepsy (at age 17). The movement disorder was remarkably improved through the levetiracetam+ clonazepam+ haloperidol triple therapy, and epileptic seizures were also effectively controlled. A retrospective analysis of 59 epilepsy patients with DHDDS gene variants revealed significant clinical heterogeneity in disease phenotypes caused by DHDDS mutations. Epilepsy was identified as the predominant symptom, commonly accompanied by movement disorders and varying degrees of intellectual disability. Furthermore, while pathogenic mutations in DHDDS tend to be relatively clustered, no definitive genotype-phenotype correlation has been established. This study highlights the clinical manifestations, imaging features, treatment experiences, and genetic testing results through case reports and literature review, thereby providing crucial references for the clinical diagnosis, treatment, and further research of such diseases.
Irritable bowel syndrome (IBS) is a gut-brain interaction disorder characterized by abdominal pain/abdominal discomfort accompanied by changes in bowel motility. Its pathogenesis involves the interaction of multiple factors, including abnormalities of the brain-gut axis, intestinal microbiota dysbiosis, and visceral hypersensitivity. Traditional treatment strategies mainly focus on symptomatic relief, which have limitations such as insufficient targeting and significant side effects. Neuromodulation techniques, as an emerging treatment modality, modulate the central or peripheral nervous system through electrical and electromagnetic means, targeting key pathways of the brain-gut axis. These techniques can regulate gut motility and suppress inflammatory responses, thereby alleviating IBS symptoms. Currently, several techniques are widely applied, including electroacupuncture (EA), Sacral Nerve Stimulation (SNS), transcutaneous auricular vagus nerve stimulation (taVNS), and transcutaneous electrical nerve stimulation (TENS). Multiple clinical trials have confirmed their effectiveness in relieving abdominal pain, improving bowel dysfunction, and enhancing quality of life. However, there are still issues such as significant individual differences and insufficient long-term efficacy data. Future research should focus on the development of personalized treatment plans, exploration of combination therapy strategies, and technological innovation to further enhance their clinical value.
BackgroundIndividuals with attention deficit hyperactivity disorder (ADHD) are at increased risk of premature mortality, but the mechanisms that underlie this association after young adulthood are unknown. As ADHD is associated with cardiovascular disease, modifiable cardiovascular risk factors could contribute to links between ADHD and premature mortality.AimsThis study aims to investigate whether specific cardiovascular risk factors explain the association between childhood ADHD problems and a higher risk of premature mortality.MethodsWe used the UK 1958 birth cohort, the National Child Development study (NCDS), and linked death register data to examine whether children with ADHD problems at age 7 years were at higher risk of premature mortality by age 58 and if specific modifiable cardiovascular risk factors, measured at midlife (age 44 years), mediated this association using path analysis.ResultsA total of 8,016 individuals completed both the age 7 ADHD assessment and the age 44/45 biomedical assessment. Of these individuals, 231 (3.1%) were grouped as likely having ADHD. The odds ratio (OR) for deaths (n = 251) in the ADHD group versus the non-ADHD group was 1.86 (95% CI 1.08–3.17). The risk was largely explained by cigarette smoking status at midlife and by a higher waist–hip ratio (a measure of obesity).ConclusionsChildhood ADHD problems are associated with a higher risk of premature mortality by age 58. This risk seems to be mainly explained by two potentially modifiable cardiovascular risk factors: obesity and smoking. These risks should be prioritized for preventative interventions to reduce the risk of premature mortality in those with a history of ADHD.
This study shows that brain signals can identify and amplify the voice a person wants to hear in a crowded scene. Choudhari et al. provide evidence that brain-controlled hearing can improve speech perception and clarity in noisy environments.
![From left, Duke University School of Medicine researchers Susan K. Murphy; Andrew Berchuck, MD; Yasaman Setayeshpour, PhD, and Jen-Tsan Ashley Chi, PhD, are studying how a common class of cholesterol drugs, called fibrates, can strip away a key defense used by ovarian cancer cells, making them more vulnerable to treatment. [Duke University School of Medicine/Mark Dolejs]](https://www.genengnews.com/wp-content/uploads/2026/05/Low-Res_20260311_Jen-Tsan-Ashley-Chi_MRD14-300x200.jpg)