The Trump administration has launched what officials described as the largest immigration enforcement operation ever Tuesday in the Minneapolis–St. Paul area, initiating the deployment of federal agents and officers in a crackdown tied to widespread fraud investigations allegedly involving mainly Somali residents.
Department of Homeland Security Secretary Kristi Noem participating in an immigration enforcement operation in Minnesota with U.S. Immigration and Customs Enforcement (ICE) officers on Jan. 6, 2026, that resulted in the arrest of Tomas Espin Tapia, a fugitive wanted for murder and sexual assault in Ecuador. (DHS)DHS
Homeland Security Secretary Kristi Noem was on the ground early Tuesday as the sweep started, adding to the number of top federal officials focused on the state as federal investigations expand this week.
The Department of Homeland Security has made more than 1,000 arrests of illegal immigrants, many with criminal convictions, in Minnesota, including 150 in Minneapolis Monday, the agency reported.
“We have the largest immigration operation ever taking place right now,” acting U.S. Immigration and Customs Enforcement (ICE) Director Todd Lyons told Newsmax on Tuesday.
Federal agents and officers were going door to door at businesses in the area suspected of being involved in illegal hiring and fraud, Lyons said.
“We’re not leaving until the problem is solved,” DHS wrote on X Tuesday.
DHS and ICE did not return requests to confirm how many agents and officers were involved in the operations.
According to Noem, Minnesota authorities are not allowing immigration officers to access state detention centers to detain illegal immigrants with pending deportation orders. A large number of federal officers was needed after a lack of local support, Noem indicated in a social media post Tuesday.
“You won’t steal from Americans or break our laws and get away with it,” Noem said.
Included in Tuesday’s arrests was Tomas Espin Tapia, a fugitive wanted for murder in Ecuador, DHS reported.
Tapia illegally entered the U.S. in October 2022 and was released into the country by the Biden administration, according to the agency.
Tapia’s criminal history also includes sexual assault in Connecticut and previous convictions in Ecuador for robbery and extortion.
Mong Cheng, a criminal illegal immigrant from Laos who was convicted of homicide, vehicle theft, possession of stolen property, assault, and arson, was also among those arrested Tuesday, DHS reported.
Immigrant rights groups and elected officials in the Twin Cities area reported an increase in sightings of federal agents, especially around St. Paul.
Minnesota Gov. Tim Walz blasted the immigration operation, calling it “ridiculous.”
“Nobody is fooled into thinking this bafoonery [sic] is a reasonable use of taxpayer dollars,” Walz wrote on X. “It should not take 50 ICE agents to arrest one guy in a library.”
Walz dropped his reelection bid Monday as federal agencies expanded investigations into alleged systemwide social services fraud in the state.
The former vice presidential candidate said he needed time to concentrate on combating fraud.
A federal immigration officer shot and killed a person whom Homeland Security described as a "violent rioter," while local Democratic lawmakers said she was a "legal observer," after DHS said she attempted to run over an agent. The incident comes as ICE officers in Minneapolis conduct targeted operations to deport criminal illegal aliens, and Democrats ramp up rhetoric and pressure campaigns on the ground against these agents.
DHS Assistant Secretary Tricia McLaughlin described the incident in an X post in the early afternoon:
Today, ICE officers in Minneapolis were conducting targeted operations when rioters began blocking ICE officers and one of these violent rioters weaponized her vehicle, attempting to run over our law enforcement officers in an attempt to kill them—an act of domestic terrorism.
An ICE officer, fearing for his life, the lives of his fellow law enforcement and the safety of the public, fired defensive shots.
He used his training and saved his own life and that of his fellow officers.
The alleged perpetrator was hit and is deceased. The ICE officers who were hurt are expected to make full recoveries.
This is the direct consequence of constant attacks and demonization of our officers by sanctuary politicians who fuel and encourage rampant assaults on our law enforcement. These men and women who are simply enforcing the law on the books are facing 1,300% increase in assaults against them and an 8,000% increase in death threats.
This is an evolving situation, and we will give the public more information as soon as it becomes available.
Today, ICE officers in Minneapolis were conducting targeted operations when rioters began blocking ICE officers and one of these violent rioters weaponized her vehicle, attempting to run over our law enforcement officers in an attempt to kill them—an act of domestic terrorism.…
Video of the deadly shooting has surfaced on X, showing an ICE agent asking the woman, who was blocking the street with an SUV, to step out of the vehicle. She did not comply and instead accelerated toward another agent, at which point the agent fired multiple rounds into the vehicle, striking the woman, who died moments later.
The office of Senator Tina Smith, a Democrat of Minnesota, and Representative Ilhan Omar, another Democrat whose congressional district includes the scene of the shooting, said the woman was a "legal observer."
Gov. Tim Walz's office said the shooting occurred in a residential neighborhood in South Minneapolis. He asked people in the community to remain calm.
The New York Times noted, "Hundreds of people gathered at the scene in protest of the presence of immigration agents. The shooting took place in a middle-class residential neighborhood in Minneapolis, about a mile from where George Floyd was killed by police in 2020."
"DHS correctly identifies the causal link between Democrat rhetoric and domestic terrorism. These politicians painted targets on federal agents, and a violent extremist acted on their orders. The officer responded with the only currency the mob respects. Force. When you attempt to murder the enforcers of our sovereignty, you invite your own destruction. The blood is on the hands of every sanctuary city official who encouraged this insurrection. We stand with ICE and the rule of law," X user Saggezza Eterna said.
Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at NYU Grossman School of Medicine in New York City.
I’m getting an interesting question from many doctors from different specialties, and also from more primary care people. How do I work clinically and ethically with chatbots and artificial intelligence? They’re not asking about making appointments or handling data behind the scenes. They want to know, in dealing with patients, how do I do this and do this right?
Are people doing it? At least one survey I found said that 70% of the physician respondents said they were using chatbots to help them in their clinical decision-making.
Let me say first that I’m not sure that the chatbot world is ready for use clinically. At best, what I think it can be right now is a supplement, almost like a curbside consult to get another opinion.
The databases the chatbots have available to them about many health issues are not accurate. The best ones are usually firewalled, and some are proprietary. The chatbots pick up all kinds of things floating around on the internet that are vetted or not vetted, true or not, and gurgle them back when asked a question. It’s not that you can’t look as an ethical physician, but you have to be careful.
Remember, too, just like with a curbside consult where you’re getting informal advice from another doctor, you are liable. You are responsible, ultimately, for the diagnosis and recommendation of treatment, not the company that made the chatbot.
That’s the overall picture. I would say it’s generally useful as a supplement or an adjuvant, but not as a substitute. It shouldn’t be used that way.
There are a couple of ethical rules. First, get informed consent if you’re going to use it. Be transparent with your patients about how it’s going be used.
Second, make sure that the information is private. Many of these AI chatbot companies don’t have privacy. They weren’t intended to be used clinically when they formed them, so you have to be sure that anything you share with the chatbot in the way of personal information is kept private.
Overall, I think it’s still early days for, if you will, AI MD. Yes, there’s information that helps. It’s great for reminders. It’s great for bringing up things that you might have overlooked or forgotten in making a diagnosis.
No, it can’t be the final word to rely on because that’s still a doctor’s job still and that’s your responsibility. If we’re going to move forward with this world, which I think we are, then consent and privacy are absolutely the ethical norms that have to be in place.
Welcome toImpact Factor, your weekly dose of commentary on a new medical study. I’m Dr F. Perry Wilson from the Yale School of Medicine.
From a lifestyle perspective, the time period between Thanksgiving and New Year’s is, let’s face it, rough. There’s the food, the parties, the cold weather keeping you indoors, and of course, the alcohol. It’s no wonder many of us wake up January 1st thinking “ok, something’s gotta change here.”
Is “Dry January” the answer?
Dry January was officially started by Alcohol Change UK in 2013, but it has grown dramatically from just 4000 registered participants in the inaugural year to millions (both officially and unofficially) today.
I get why it is so attractive. The new year always brings a renewed focus on health, and there’s something that seems... approachable about taking a month off from alcohol. It’s not forever; if anything, you’re sort of proving to yourself that you can do it. And the social nature of it helps. You have friends who are doing it. The social media feeds are filled with #DryJanuary hashtags.
But… does it actually do anything? Are there clear, physiologic benefits to a month (a mere month) of withholding alcohol? Or is it just a fad? Or worse, does participating in Dry January make you drink more in February or the rest of the year?
Pour yourself a cold glass of… milk and we’ll dig in.
Let’s dive into the Dry January literature to figure out if this is all hype or something that might be worth your time here in 2026.
First, I need to get something out of the way which will color how we interpret these data moving forward. People who do Dry January are a very particular sort.
Broadly speaking, they are much more likely to be female. They have higher incomes and are more likely to be college-educated. They also drink more alcohol than the average person. They are “health-conscious hazardous drinkers,” and though some may meet the official criteria for alcohol use disorder, few would refer to themselves as alcoholics.
We need to keep this in mind when we look at the effects of Dry January. Because, as you’ll see, there are a lot of potential benefits but also some risk, including withdrawal (which can be fatal) in particularly heavy drinkers.
Of course, you won’t see any benefits if you don’t actually do it, but success rates are surprisingly high. About two-thirds of people in the UK and 80% of those in the Dutch version of Dry January called “IkPas” made it through the month without drinking.
Interestingly, analyses of social media show much worse success rates. An analysis of Twitter posts about Dry January found that only 12.7% indicated success, while 66% indicated some kind of failure. But you don’t need me to remind you that social media is not real life.
So, assuming you can successfully navigate the month of January without alcohol, will it make a difference?
The data are actually fairly impressive across several domains.
Let’s start with the liver. In 2017, researchers enrolled 64 heavy drinkers in a 4-week abstinence program. At baseline and at the end of the month, they measured the liver stiffness (using a noninvasive FibroScan device). The effects were pretty dramatic — 80% of those who abstained from drinking saw an improvement in liver stiffness — on average around a 15% reduction. In fact, the results were so impressive that the authors concluded that the FibroScan device may overestimate liver stiffness during active drinking because it was hard to imagine why improvement would occur so rapidly.
But I think this might be real, not necessarily in terms of improving liver fibrosis — that probably does take more than a month — but in terms of improving liver inflammation. This small study showed significant improvements in liver enzymes after 4 weeks of abstinence, for example.
Of course, alcohol is not only bad for the liver. One oft-overlooked fact about alcohol intake is that it has a lot of calories, 7 calories per gram actually, making it more calorie-dense than carbs or protein and only slightly less calorie-dense than fat. Participants in Dry January tended to lose a bit of weight — around 3 pounds over the month. It’s not a GLP-1, but it’s not bad.
Some studies have shown even more dramatic biochemical changes after a month without alcohol. This study in BMJ Open compared 94 Dry January participants to 47 who kept drinking. The abstinent group had a 25% improvement in insulin resistance and a 7% reduction in systolic blood pressure. Maybe more surprising, those who held off the sauce had a 42% reduction in VEGF levels and a 74% reduction in EGF levels — these are both biomarkers that have implications for cancer risk.
To be honest, it was hard for me to find a physiological metric that doesn’t improve during Dry January. But that didn’t answer my biggest question, which is what happens when Dry January ends?
According to data from the UK, there are some lasting changes. Researchers looked at Dry January participants in August to see how their relationship with alcohol had changed. Overall, it was positive. In August, they had reduced their drinking days per week from 4.3 to 3.3. They drank less alcohol when they did drink, and their days of being drunk decreased from 3.4 to 2.1 per month. So, far from a rebound effect or even a return to pre-Dry January baseline, we see some measurable changes down the road.
We can speculate about why this might be. It may simply be that Dry January proves to individuals that they don’t need alcohol. They can navigate social situations or stressors without it. This is really about self-efficacy. But there is power in proving to yourself that you can do something, and clearly some of the habits built in January may carry throughout the whole year.
Because it’s Dry January, I’m going to devote all my columns this month to alcohol, in some form or another. Next week, we’ll look at the still mysterious ability of the GLP-1 weight loss drugs to curb alcohol intake and the implications that has for our health in the future.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator. His science communication work can be found in the Huffington Post, on NPR, and here on Medscape. He posts at@fperrywilsonand his book, How Medicine Works and When It Doesn’t, is available now.
Many clinicians will understandably dismiss a patient’s report of a vivid, frightening dream about falling ill as a byproduct of anxiety. However, a growing body of neurobiological research suggests these nocturnal narratives may be more than mere coincidence. Emerging evidence indicates that some dreams may serve as harbingers of disease, detecting physiologic changes before conventional diagnostics — or even symptoms — emerge.
Unlike typical dreams that fade upon waking, “prodromal dreams” stay with people and involve vivid, often disturbing imagery in which they discover a specific illness. Anecdotal examples from the International Association for the Study of Dreams include a woman who dreamt of her aunt, who had died of breast cancer, warning her that she too had the disease — later confirmed by mammogram.
Now, new neuroscientific models and clinical studies are beginning to provide biological plausibility for how the sleeping brain might detect early pathology.
A 2025 hypothesis and theory paper in Frontiers in Psychiatry, for example, proposes that some prodromal dreams emerge from interoceptive predictive processing during REM sleep. During REM, limbic and paralimbic regions involved in interoception compress high-dimensional visceral and autonomic inputs into low-dimensional summaries. When these summaries diverge from the brain’s predictions, a “prediction error” is generated. Because REM operates in a hallucinatory, hyper-associative mode with reduced external input, the brain’s attempt to explain that error is rendered as vivid, often threat-laden or metaphorical dream imagery that can foreshadow emerging pathology.
Abidemi Otaiku, MD
“In neurodegenerative conditions, such as Parkinson’s disease and Alzheimer’s disease, it is possible that changes to brain networks involved in dream generation and emotional tone may cause changes to dreaming years or decades before other symptoms of the disease emerge,” Abidemi Otaiku, MD, clinical research fellow at UK Dementia Research Institute, Imperial College London, London, England, told Medscape News Europe.
Early Warning in Disease
Research is revealing a possible connection between dreams and neurodegeneration in Parkinson’s disease, where dream-related symptoms can emerge years before motor dysfunction. Isolated REM sleep behavior disorder (iRBD) — in which people physically act out their dreams while having no overt neurologic disease — often emerges years before motor symptoms appear, according to a 2025 review in the Journal of Sleep Research. The predictive power of this phenomenon is sobering: a 2019 meta-analysis tracking nearly 4000 patients with iRBD found that about one third had developed Parkinson’s disease or dementia with Lewy bodies after an average of 5 years, with statistical modeling estimating this proportion would exceed 90% by 14 years. A smaller subset may develop multiple system atrophy.
These clinical observations now have a biological correlate. A 2025 Brain Communications study used advanced MRI to detect excess iron accumulation in the substantia nigra — a small but critical movement hub — in people with early Parkinson’s disease. Those with dream enactment showed iron levels intermediate between healthy control individuals and patients with Parkinson’s disease, and iron deposition increased measurably over 4 years. This suggests that dream enactment can coincide with subtle, yet detectable, brain changes that precede clinical diagnosis.
The genetic architecture of this subtype is equally revealing. A 2025 international genetics study comparing patients Parkinson’s disease with and without RBD uncovered distinct patterns at two pivotal genes: SNCA and LRRK2. This genetic fingerprint points to an alpha-synuclein-related subtype in which dream enactment may be woven into the disease pathway from its earliest stages. A 2023 review in Cell Death and Disease additionally reports that when RBD accompanies Parkinson’s disease, the disease typically follows a more aggressive trajectory, with faster progression and higher rates of cognitive decline, hallucinations, depression, and anxiety.
Otaiku’s own research includes a study that found frequent and distressing dreams are associated with an increased risk for Parkinson’s disease if the dreams occurred within 5 years prior to diagnosis. “My work has mostly been about nightmares as a prodromal sign in neurodegenerative diseases,” Otaiku said. “I think nightmares could be used alongside other prodromal symptoms like loss of smell, depression, and dream enactment to facilitate early detection.”
When Patients Report Prodromal Dreams
If a patient reports having prodromal dreams or aggressive nightmares, what should clinicians do? A sleep study may be warranted to differentiate prodromal dreaming from other sleep disorders. Nightmares and dream enactment are treatable, and evaluation can uncover conditions such as RBD, obstructive sleep apnea, or medication effects.
Anthony Bloxham, PhD
Some patients may report upsetting dreams to their physician and express a desire to stop them. “It is possible to wake yourself up from a dream, and there are those who may do so during a distressing one,” explained Anthony Bloxham, PhD, lecturer in psychology and member of the Sleep Research Group at Nottingham Trent University, Nottingham, England. “Lucid dreaming is all about recognizing when you are dreaming, and then maybe taking more active control of the dream as it unfolds.”
However, in the case of a prodromal dream, waking up may be counterproductive because important details may be lost. “Confronting whatever is bothering you in the dream, understanding it, and trying to change it into something positive or more pleasant seems a more problem-solving focused approach than simply trying to escape,” Bloxham told Medscape News Europe.
If a patient expresses fear or discomfort about their dreams, reassurance is important. Ensure the patient understands that a dream is not necessarily indicative of a diagnosis, but that you would like to gather more information.
Brigitte Holzinger, PhD
“My advice would be to keep the topic light,” said Brigitte Holzinger, PhD, professor and scientific director of the postgraduate sleep coaching program at the Medical University of Vienna, Vienna, Austria. “Call it an experiment — ask if the patient would be interested in participating,” she told Medscape News Europe. Ask the patient to keep a dream journal, noting details as soon as they wake up. Even an incidental part of a dream may be a valuable clue.
Finally, a full medical workup is warranted if there is enough evidence to suggest a suspected illness.
Otaiku, Bloxham, and Holzinger reported no relevant financial relationships.
The Alzheimer's Association announced today that it has earned Joint Accreditation status to provide interprofessional continuing education from Joint Accreditation for Interprofessional Continuing Education™. The national credential allows the Association to train entire health care teams — including physicians, nurses, social workers, pharmacists and others — through a single, unified accreditation process.
The accreditation marks a significant milestone, expanding the Association's ability to deliver high-quality education in brain health, early detection and diagnosis, and dementia care, while preparing the health care workforce for emerging treatments and innovations.
"Joint Accreditation is a major step forward for our mission," said Katie Evans, chief programs and mission engagement officer, Alzheimer's Association. "Brain health and dementia care require a team approach — and now we can train those teams together using the highest national standards. This strengthens care today and prepares communities for the breakthroughs ahead."
Joint Accreditation, founded in 2009 by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE) and the American Nurses Credentialing Center (ANCC), sets standards for interprofessional continuing education. Jointly accredited providers certify that activities are developed by and for health care teams, with an emphasis on integrity, independence, and measurable impact on health care quality and patient safety.
The designation enables organizations to plan and deliver education that brings physicians, nurses, pharmacists and other health professionals together to learn with, from and about each other. This approach reflects how real-world care is delivered and supports better collaboration, stronger clinical decision-making, and improved outcomes for people and families.
"Interprofessional education is critical because brain health and dementia care require a team approach," Evans said. "This designation significantly expands our reach. We can now support busy frontline professionals with practical, case-based education that helps them work together more effectively in dementia care and brain health."
With its new accreditation, the Alzheimer's Association plans to expand its portfolio of interprofessional education offerings, including live conferences, virtual programs, online training and quality-improvement-focused education. These offerings will help health systems, health plans and community partners build workforce capacity in brain health, early detection, diagnosis, care coordination and treatment navigation.
"The Alzheimer's Association is proud to earn joint accreditation and to share our expertise with health professionals," Evans said. "This recognition strengthens our ability to support the professionals caring for millions of Americans and to advance a future where everyone can protect their brain health and access high-quality dementia care. We can't wait to get started."
The Alzheimer's Association joins a growing list of organizations offering jointly accredited continuing education, including medical societies, health systems, universities and other leading providers of continuing education.
In support of improving patient care, the Alzheimer's Association is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.
About the Alzheimer's Association The Alzheimer's Association is a worldwide voluntary health organization dedicated to Alzheimer's care, support and research. Our mission is to lead the way to end Alzheimer's and all other dementia — by accelerating global research, driving risk reduction and early detection, and maximizing quality care and support.
Patients with a history of GLP-1 receptor agonist treatment had a significantly lower risk of developing colorectal cancer (CRC) as compared with those who took aspirin, according to a retrospective study reported here.
A history of GLP-1 receptor agonist treatment was associated with a 36% reduction in the odds of developing CRC versus aspirin, and this increased to 42% among high-risk individuals. A clear trend in favor of GLP-1 agonists persisted across all prespecified subgroups, including by age, body mass index (BMI), atherosclerosis and diabetes status, and different types of GLP-1 agonists.
"The large population size [more than 280,000 patients] of this study and the favorable safety profile of GLP-1 receptor agonists versus aspirin could underscore a potential public health impact," said Jones. "These findings warrant prospective validation in randomized clinical trials."
The study is thought provoking, given the longstanding interest in aspirin and nonsteroidal anti-inflammatory drugs for CRC prevention and the recognition of aspirin's side effects, creating a challenge for use in a broad patient population, said ASCO discussant Joel Saltzman, MD, of the Cleveland Clinic.
"It will certainly be interesting over the upcoming years to see how these drugs fit in [CRC prevention] and what we can learn from the development of cancer and how it really ties into obesity as perhaps a cause of cancer," said Saltzman.
During a discussion that followed, Jones hinted at the possibility of additional data suggesting that the potential cancer-reducing benefits of GLP-1 agonists may extend across multiple types of cancer. Noting that he has submitted abstracts for presentation at the ASCO annual meeting later this year, Jones said he did not want to reveal too much about the research at this point.
"It could be widespread," Jones said of GLP-1 agonists' impact on cancer prevention.
Jones also responded to a recent meta-analysis of randomized trials of GLP-1 agonists, which showed "little or no effect" of the drugs on the risk of obesity-related cancers.
"Most of those randomized controlled trials were not actually designed to evaluate cancer as a primary outcome," he said. "That's one of the limitations of the meta-analysis. In addition, most of the studies had relatively short follow-up, only 1 or 2 years. I don't think that is long enough to detect long-latency effects, including both cancer prevention and cancer risk."
Aspirin for CRC prevention has been investigated extensively, but modest efficacy and bleeding risks have limited widespread use. Interest in GLP-1 agonists' CRC prevention potential has increased with evidence that the drugs regulate the PI3K/AKT/mTOR signaling pathway, but the issue has remained largely unexplored, said Jones.
To compare CRC prevention with GLP-1 agonists or aspirin, the investigators queried the TriNetX database, which encompasses 150 million patients in 106 health organizations. They identified 149,115 patients with a history of exposure to GLP-1 agonists and 3,011,724 with a history of aspirin use. After propensity matching, the analysis involved two groups with 140,828 patients each. The primary endpoint was CRC incidence.
The study population had a median age of 58, two-thirds of patients were white, and two-thirds were women. Median follow-up was about 6 years in the GLP-1 group and 5 years for the aspirin users.
The results showed that GLP-1 agonist use was associated with a CRC hazard of 0.643 versus the aspirin group (95% CI 0.531-0.778). Among high-risk patients -- those with mutations associated with CRC, family history, or high-risk comorbidities -- the hazard ratio decreased to 0.579 in the GLP-1 agonist group.
Subgroup analysis consistently favored GLP-1 agonists, including for all age groups (lowest hazard in the youngest patients, 0.583), normal or high BMI, history of atherosclerosis, and history of diabetes (lower hazard in non-diabetic patients, 0.588). Across four types of GLP-1 agonists, the CRC hazard ranged from 0.436 with liraglutide (Victoza, Saxenda) to 0.711 with tirzepatide (Mounjaro, Zepbound) and achieved statistical significance for all except tirzepatide.
GLP-1 agonists were associated with fewer episodes of gastrointestinal bleeding (2.0% vs 2.1%, HR 0.852, P=0.018), gastric ulcers (0.5% vs 0.55%, HR 0.815, P=0.038), and acute kidney injury (1.15% vs 2.8%, HR 0.369). Patients treated with GLP-1 agonists had higher rates of diarrhea (6.8% vs 5.4%, HR 1.131, P=0.0001) and abdominal pain (19.0% vs 16.3%, HR 1.055, P=0.0001). Rates of nausea and vomiting were similar with GLP-1 agonists (10.5%) and aspirin (9.7%, HR 0.98).
Disclosures
Jones reported no relevant financial disclosures.
Saltzman has disclosed relationships with Pfizer and Seagen.
