Sen. Scott: How To Rescue America From the Spread of Socialism

 Zohran Mamdani is right that our political system has failed the American people. The rise of his brand of socialism in America is terrifying, but it shouldn’t shock anyone who has watched Washington catastrophically fail to lead with policies that work for the American people.

Every two years, establishment politicians beg for votes with the same empty promises: to hold government accountable, lower prices and fight for the American Dream. We have watched this cycle repeat for decades, and things have only gotten worse.

Instead of holding government accountable, politicians in Washington have dug Americans into a $40 trillion debt grave by massively expanding the federal government.

While promising to lower prices, Congress has approved massive government spending, causing prices and interest rates to skyrocket.

In the name of protecting the American people, the federal government has crept into every part of our lives, crushed opportunity and choked the American Dream nearly to death with countless regulations.

We have all seen this play out and are furious about it, but young Americans are understandably on the verge of revolt. The American Dream that existed for their parents and grandparents is out of reach for them. Washington’s failures have left them feeling cheated and disillusioned with our political system, and stuck in a world where they can’t afford to buy a house, have decent health care or start a family. Their anger is real, but socialism will not solve any of their problems.

Socialists promise steady wages and health care, but they end up controlling where you work, how much money you make and where you can travel. The government becomes the one that can decide if you live in a house or a one-bedroom apartment, how much food your children need or whether your elderly mother can have surgery. If you think I'm exaggerating, there are plenty of Cuban and Venezuelan socialism survivors in my state of Florida who would beg to differ.

So, if socialism isn’t the answer, how do we reignite the American Dream? Simple: listen to the American people and make government work for the things that are most important to them. In other words, blow up the status quo in Washington to lower prices, fuel private sector job creation, and return to the American freedom that gave me and the generations before me the chance to succeed.

That means doing three things: drastically reduce government spending to balance the federal budget, shred the massive regulatory regime that has grown out of control in Washington, and make job creation the number one priority through tax cuts, smart investment and good policy.

Washington’s obsession with spending has become so reckless that we are now running muti-trillion-dollar annual deficits. These deficits are fueling a $40 trillion debt that costs more than a trillion dollars in interest annually. That’s a trillion dollars that provides zero return for American families. It cannot be spent on national security, Social Security, roads, or Medicare.

To save the programs Americans depend on most, we must reduce government spending in all the places it doesn’t provide a real return for taxpayers and finally balance the federal budget. We cannot tax our way out of this problem. If Congress doesn’t end its spending addiction, critical programs will soon see enormous cuts or cease to exist entirely, interest rates will remain high—and so will prices.

To make sure that workers keep more of their paychecks and can afford loans for cars, homes and businesses, we must balance the budget.

Next, Congress must take a sledgehammer to federal government’s regulations. As governor of Florida, I slashed 5,000 burdensome regulations, taking permitting times from months to days, eliminating stupid regulatory hurdles that had no impact on safety, and cutting costs to start and grow a business. Our economy boomed and businesses created 1.7 million new private sector jobs in just eight years.

Finally, if we cut spending and balance the budget, while slashing back the regulatory burden of the federal government, we can fuel the economic boom needed to grow private sector jobs, revitalize our great nation and save the American Dream.

Jobs. Jobs. Jobs. That should be the number one priority of the federal government.

The dream we know today is broken, but it’s not dead yet. That’s why I’ve launched a project to rescue the American Dream. It starts with pointing out all the ways that big government and bad policy have betrayed the average American. From there, we can map the way back to the kind of country that made it possible for a poor kid like me who grew up in public housing to become a CEO, a governor and a senator.

If we want to spare the next generation the misery of socialism, we need to show them the opportunities freedom offers when Washington actually works for them and lets them live the American Dream.

Let’s get to work.

Rick Scott is a Republican U.S. senator from Florida and a former two-term governor of the state.

https://www.newsweek.com/sen-scott-how-to-rescue-america-from-the-spread-of-socialism-opinion-12462031

Polymarket Processor Reported Fraud Surge as Compliance Team Raised Concerns

In February, a company handling debit card transactions for Polymarket's U.S. betting platform reported that fraudsters were flooding the app and trying to steal at least $10 million. According to ChainCatcher, users linked stolen debit cards to Polymarket U.S. accounts, placed bets, and attempted to withdraw funds to clean cards or accounts they controlled.

The processor at one point rejected more than 80% of deposits as fraudulent, far above the industry standard of about 1%. Polymarket employees raised concerns to Chief Executive Shayne Coplan, and people familiar with the matter said the compliance team was shocked by Coplan's response: keep growing and pay any fine if regulators find out.

https://www.binance.com/en/square/post/09-20-2026-polymarket-processor-reported-fraud-surge-as-compliance-team-raised-concerns-368562307757137

2 Survival Wins in NSCLC With Bispecific Seeking Worldwide Status

 The investigational bispecific antibody ivonescimab significantly improved overall survival (OS) in PD-L1-positive advanced non-small cell lung cancer (NSCLC) compared with single-agent pembrolizumab (Keytruda), an updated analysis of the randomized HARMONi-2 trial showed.

Median OS -- the key secondary endpoint of the trial -- improved from 22.6 months with pembrolizumab to 30.8 months with ivonescimab. The survival curves began to separate at 12 months and steadily swung in favor of ivonescimab, with no narrowing of the gap. A consistent benefit was observed across subgroups, irrespective of PD-L1 expression cutoff, age, or tumor histology.

Previously reported results from the study showed superior progression-free survival (PFS) with ivonescimab, bolstering a case for a first-line indication, said Caicun Zhou, MD, PhD, of Shanghai East Hospital and Tongji University School of Medicine in Shanghai, at the World Conference on Lung Cancer (WCLC) in Seoul, South Korea.

"With longer follow-up, ivonescimab maintained a favorable and manageable safety profile with no new safety signals," said Zhou. "These findings support ivonescimab as a first-line treatment for PD-L1-positive non-small cell lung cancer. A global phase III trial of ivonescimab versus pembrolizumab in PD-L1-high metastatic NSCLC is ongoing to provide a potential chemo-free regimen for patients worldwide."

Not Ready for Prime Time ... Yet

HARMONi-2 was conducted entirely in China, and PD-L1 expression was ascertained by means of an assay currently available only in China, noted invited discussant Mariana Brandão, MD, PhD, of Institut Jules Bordet in Brussels. Moreover, the pembrolizumab monotherapy control arm is not a global standard for the population.

"What we saw was, indeed, an improvement in overall survival among the PD-L1-positive population, which is not only statistically significant but also clinically relevant," said Brandão. "Of course the control arm ... is not what most of us are using in clinical practice. In these patients, we prefer to use anti-PD-1 plus chemotherapy."

Closer inspection of the subgroup analysis showed that the results were driven primarily by the PD-L1-high subgroup (tumor proportion score [TPS] ≥50%) and, surprisingly, patients with squamous histology, who usually have a worse prognosis, she pointed out. Data on concomitant genomic alterations would have been informative, and the trial included relatively few non-smokers and patients with liver metastases, though both groups benefited from ivonescimab.

"Am I changing my clinical practice tomorrow for this PD-L1-high non-small cell lung cancer subset, replacing anti-PD-1 with ivonescimab?" asked Brandão. "The answer is no. This was an underpowered subgroup analysis of a secondary endpoint, and we know that ivonescimab, although well tolerated, has an increased toxicity compared to pembrolizumab. Also, we don't have any other predictive biomarkers."

"Am I excited by these data?" she continued. "Absolutely. I think this is really interesting, and of course, now we have to wait for the phase III global HARMONi-7 trial that is being conducted specifically in the PD-L1-high population. We also have to compare this to the other results that we already have in this space."

In a separate presentation, ivonescimab picked up another OS win in an updated analysis of the global phase III HARMONi trial, involving patients with EGFR-mutated NSCLC and resistance to EGFR inhibitors.

At last year's WCLC, the HARMONi trial showed a statistically significant improvement in PFS with ivonescimab plus chemotherapy versus pembrolizumab and chemotherapy. At that time, the second primary endpoint of OS trended in favor of the ivonescimab arm but did not achieve statistical significance.

The updated analysis showed a median OS of 16.8 months with ivonescimab-chemotherapy and 14 months with pembrolizumab-chemotherapy, representing a 24% reduction in the survival hazard (95% CI 0.61-0.95, P=0.0151), reported Antonio Passaro, MD, PhD, of the European Institute of Oncology in Milan.

A first-in-class therapy, ivonescimab pairs a PD-1 inhibitor and a VEGF inhibitor. The drug is approved in China but nowhere else in the world, and the bispecific has been studied most extensively in Chinese patients. Studies such as HARMONi-7 and HARMONi are evaluating ivonescimab in different populations to demonstrate broader applicability for treating PD-L1-positive NSCLC.

HARMONi-2 Details

HARMONi-2 included 398 patients with locally advanced/metastatic NSCLC, a PD-L1 TPS ≥1%, and no prior systemic therapy. Patients were randomized to ivonescimab or pembrolizumab and treated for as long as 2 years in the absence of progression or unacceptable toxicity.

The OS analysis showed an 8-month difference in favor of ivonescimab, translating into a 27% reduction in the survival hazard (95% CI 0.57-0.95, P=0.009). Landmark OS analyses favored ivonescimab at 24 months (57.9% vs 48%) and 36 months (45% vs 33.1%). For context, Zhou referred to the China-based KEYNOTE-042 study, which showed 2- and 3-year OS rates of 43.8% and 28.1%, respectively, in a population treated with pembrolizumab alone.

As Brandão pointed out, the overall benefit was driven by statistically significant advantages for ivonescimab in two subgroups: patients with PD-L1 TPS ≥50% (median OS not reached vs 23.2 months, HR 0.58, 95% CI 0.38-0.89) and squamous histology (30.5 vs 19.3 months, HR 0.65, 95% CI 0.45-0.95).

OS also favored ivonescimab in the PD-L1 TPS 1-49% population, but the difference did not achieve statistical significance (28.5 vs 22.1 months, HR 0.85, 95% CI 0.61-1.18). The same was true of patients with non-squamous tumors (33.6 vs 25.6 months, HR 0.79, 95% CI 0.55-1.14).

Twice as many patients in the ivonescimab arm developed grade ≥3 treatment-related adverse events (TRAEs, 41.6% vs 21.6%), but TRAE-related discontinuation rates were similar (4.1% vs 5%).

Disclosures

The HARMONi-2 trial was supported by Akeso Biopharma.

The HARMONi trial was supported by Akeso Biopharma and Summit Therapeutics.

Zhou disclosed relationships with Eli Lilly, Sanofi, Boehringer Ingelheim, Roche, MSD, Qilu Pharmaceutical, Jiangsu Hengrui Pharmaceuticals, Innovent Biologics, CStone Pharmaceuticals, Luye Pharma, Top Alliance Biosciences, Amoy Diagnostics, Allist Pharmaceuticals, and Dizal Pharma.

Passaro disclosed relationships with AbbVie, ArriVent BioPharma, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, Eli Lilly, Janssen, Johnson & Johnson, Gilead, GSK, MSD, Novartis, Pfizer, Roche/Genentech, Mundipharma, Summit Therapeutics, eCancer, Medscape, Takeda, PeerVoice, PeerView, and touchONCOLOGY.

Brandão disclosed relationships with AstraZeneca, Boehringer Ingelheim, Johnson & Johnson, Pierre Fabre, Daiichi Sankyo, Amgen, Pfizer, MSD, Bristol Myers Squibb, Janssen, Takeda, Merus, Roche/Genentech, Sanofi, and Revolution Medicines.

Primary Source

World Conference on Lung Cancer

Source Reference: Zhou C, et al "Overall survival analysis from HARMONi-2: Ivonescimab vs pembrolizumab as first-line treatment for PD-L1-positive NSCLC" WCLC 2026; Abstract OA14-01.

Secondary Source

World Conference on Lung Cancer

Source Reference: Passaro A, et al "Ivonescimab-chemo versus placebo-chemo in EGFR-TKI-resistant, EGFR-mutated NSCLC (HARMONi): Updated overall survival analysis" WCLC 2026; Abstract OA14.05.

https://www.medpagetoday.com/meetingcoverage/iaslc/123041

Study Assesses Who's at Risk for Young-Onset MASLD Cirrhosis

 

• A quarter of patients with cirrhosis caused by metabolic dysfunction-associated steatotic liver disease (MASLD) presented before the age of 50 with distinct risk profiles, data from a prospective study showed.
• In models adjusting for demographic and metabolic factors, a high genetic risk score and type 2 diabetes were independently associated with early-onset MASLD cirrhosis.
• Reliance on age-dependent first-line liver fibrosis tools can miss cases, the researchers suggested.

A quarter of patients with cirrhosis from metabolic dysfunction-associated steatotic liver disease (MASLD) presented before the age of 50 and had distinct features, including inherited genetic risk factors and type 2 diabetes, according to data from a prospective multicenter study.

In multivariable models adjusting for demographic and metabolic factors, a high genetic risk score (OR 2.33, 95% CI 1.26-4.23, P=0.006) and type 2 diabetes (OR 3.74, 95% CI 2.08-6.82, P<0.001) were independently associated with cirrhosis in MASLD patients under the age of 50, reported Rohit Loomba, MD, of the University of California San Diego, and colleagues in Clinical Gastroenterology and Hepatology.

The prevalence of cirrhosis increased for patients with both low and high genetic risk scores if they also had type 2 diabetes: from 2.0% to 9.5% and from 6.2% to 10.7%, respectively.

"Our findings show that younger adults who develop cirrhosis from MASLD are not simply experiencing the same disease earlier," said Loomba in a press release. "They appear to have a unique combination of genetic susceptibility and metabolic risk factors that accelerate progression to advanced liver disease."

Loomba and team noted that while high genetic risk and type 2 diabetes independently identified younger adults at increased risk of MASLD cirrhosis, reliance on age-dependent first-line liver fibrosis tools like the Fibrosis-4 (FIB-4) index can miss cases.

A normal FIB-4 score is <1.3 for adults under age 65. However, about 30% of patients with early MASLD cirrhosis in this study had a FIB-4 score <1.3, "suggesting this population may be at higher risk of misclassification with current clinical care pathways," the authors wrote.

"In our cohort, a FIB-4 cut-point of 1.0 identified 82.7% of cases ... supporting direct referral for fibrosis assessment in these patients irrespective of FIB-4," they added.

In the press release, co-author Veeral Ajmera, MD, also of the University of California San Diego, noted that since current screening tools like FIB-4 incorporate age, "they miss almost a third of patients with early-onset MASLD cirrhosis. This study helps us identify which patients are at greatest risk and need a more accurate assessment of their liver disease."

The study included 2,395 patients with biopsy-confirmed MASLD enrolled in the national Nonalcoholic Steatohepatitis Clinical Research Network. Of these participants, 9.8% had cirrhosis. Median age was 58.4 years, 71.4% were women, 85% were white, 50% had a body mass index ≥30, and 66% had type 2 diabetes.

The cutoff for early MASLD cirrhosis (the lowest quartile of age) was less than 50 years, with 53 participants presenting with cirrhosis before age 50 and 181 presenting at 50 or older. Only 6% reported alcohol consumption two or more times per month, with no difference between early and non-early MASLD cirrhosis groups.

All study participants underwent a standardized clinical evaluation and biochemical testing. Genetic risk scores were calculated by adding up the number of alleles across three single-nucleotide polymorphisms -- PNPLA3, HSD17B13, and TM6SF2 -- which were selected based on their association with cirrhosis in multiple studies. Scores ranged from 0 to 6 (low 0 to 3, high 4 to 6).

Compared with non-cirrhotic MASLD participants under age 50, those with cirrhosis more often had a body mass index of at least 35, higher alkaline phosphatase levels, and lower alanine aminotransferase levels.

Loomba and colleagues said future work should validate age-aware screening thresholds, refine genetic risk, and evaluate targeted interventions in younger patients with genetically high-risk MASLD.

Disclosures

Funding for this research was provided by National Institute of Diabetes and Digestive and Kidney Diseases grants and a National Center for Advancing Translational Sciences grant.

Loomba reported relationships with Aardvark Therapeutics, Altimmune, Alnylam/Regeneron, Amgen, Arrowhead Pharmaceuticals, AstraZeneca, Bristol Myers Squibb, CohBar, Eli Lilly, Galmed, Gilead, Glympse Bio, HighTide Therapeutics, Inipharm, Intercept, Inventiva, Ionis, Janssen, Madrigal, Metacrine, NGM Biopharmaceuticals, Novartis, Novo Nordisk, Merck, Pfizer, Sagimet, Theratechnologies, 89bio, Terns Pharmaceuticals, Viking Therapeutics, Boehringer Ingelheim, Galectin Therapeutics, Hanmi, Sonic Incytes, and LipoNexus.

A co-author reported relationships with Madrigal, Zydus, Insitro, Biomea Fusion, Eccogene, Chugai, GSK, Altimmune, Akero, Boehringer Ingelheim, Exact Sciences, Avant Sante, and Heligenics.

Primary Source

Clinical Gastroenterology and Hepatology

Source Reference: Ajmera V, et al "Risk factors and definition of younger-onset metabolic dysfunction-associated steatotic liver disease (MASLD) cirrhosis" Clin Gastroenterol Hepatol 2026; DOI: 10.1016/j.cgh.2026.08.033.

https://www.medpagetoday.com/gastroenterology/generalhepatology/123050

Study 'Challenges' Standard of Prolonged Antibiotics for Orthopedic Infections

 

• The standard of care for orthopedic infection usually includes at least 4 weeks of postoperative systemic antibiotic treatment.
• A noninferiority trial showed that rates of definite treatment failure at 12 months were similar between patients who received short- or long-duration postoperative systemic antibiotics.
• At 6 weeks of follow-up, 17.2% of those in the short-duration group and 45.2% of those in the long-duration group reported symptoms that were potentially linked to antibiotic treatment.

Giving no more than a week's worth of systemic antibiotics was as effective as a standard multi-week course for preventing treatment failure in patients who underwent surgery for orthopedic infection paired with implant of a local antibiotic carrier, an open-label noninferiority trial showed.

Among 475 patients included in the primary analysis, definite treatment failure at 12 months occurred in 11.1% of those randomized to 7 or fewer days of postoperative systemic antibiotics versus 14.1% of those who received 4 or more weeks of treatment, with that difference meeting the trial's noninferiority margin of 10 percentage points.

At a 6-week follow-up visit, 17.2% of those in the short-duration antibiotic group and 45.2% of those in the long-duration antibiotic group reported symptoms that were potentially linked to antibiotic treatment, reported Martin McNally, MD, of Oxford University Hospitals in England, and colleagues in the New England Journal of Medicine.

"This trial challenges the standard of care for orthopedic infection," the authors wrote. "Treatment with local antibiotics delivered by a carrier implanted during surgery allows patients and clinicians to consider a shorter duration of systemic antibiotic regimen after surgery."

Although the results appear to support that combination approach, McNally and team cautioned that "a substantial amount of high-quality data is needed before local therapy is adopted as the primary approach in clinical practice."

The management of bone and joint infections usually includes a combination of surgical debridement and extended administration of systemic antibiotic therapy. Local antibiotics delivered by an implanted licensed carrier are increasingly being used along with systemic antibiotics in the treatment of orthopedic infections.

"Theoretical advantages of local antibiotics include delivery of very high antibiotic concentrations locally, limited systemic absorption of antibiotics and potentially fewer side effects, and improved antimicrobial stewardship," the authors noted. "However, local therapy may be associated with an increased risk of hypercalcemia, renal impairment, or local problems with wound leakage or fracture of an antibiotic-loaded spacer."

The Short or Long Antibiotic Regimes in Orthopaedics (SOLARIO) trial included adults who were undergoing curative surgery for an orthopedic infection. All patients had a licensed local-antibiotic carrier implanted during surgery and received broad-spectrum antibiotic systemic therapy perioperatively.

The trial didn't include patients who had antibiotic powder sprinkled into operative sites, those with irrigation devices, or patients who received intraosseous infusions. Their exclusion means the SOLARIO results "should not be used to support the use of these techniques for delivery of local antibiotics," McNally and team cautioned.

The 25-site trial ran from February 2019 through August 2023. The choice of local and systemic antibiotics was made by infectious disease specialists at the individual trial sites. The study's primary endpoint, definite treatment failure within 12 months of surgery, was defined as a surgical-site sinus tract or purulence, infection, newly elevated biomarkers during aspiration or reoperation, or death from infection at the original surgical site.

Median ages at surgery in the short- and long-duration groups were 57 and 59 years, respectively, and 28.7% and 29.4% of patients were women. The median Charlson Comorbidity Index score in both groups was 2. The most frequent surgery indication in both groups was debridement for osteomyelitis or fracture-related infection, in 35.6% and 34.9%, respectively, and Staphylococcus aureus was the most frequent infecting organism (33.9% and 35.3%).

The median duration of systemic antibiotic therapy was 6 days among the short-duration patients and 42 days in the long-duration group.

Patients in the short-duration group stayed a mean 11.9 days in the hospital compared with 14.8 days for those in the long-duration group. Serious adverse events occurred in 17.1% and 19.9%, respectively. Overall survival rates at 12 months were 97.9% among the short-duration patients and 96.3% among the long-duration patients.

SOLARIO's clinical results could also have financial effects. "Direct costs will likely be lower with the short duration than with the long duration," McNally and colleagues noted, "given that the short-duration group used fewer systemic antibiotics and had a shorter length of hospital stay and lower number of events with an indication for treatment."

Study limitations included the trial's open-label design, as well as the potential for selection bias, since clinicians may not have recruited patients with a high risk of treatment failure. The trial also wasn't designed to evaluate specific local antibiotics.

Disclosures

The study was supported by the European Bone and Joint Infection Society, the National Institute for Health Research, and the British Medical Association.

McNally disclosed relationships with Bonesupport AB and Peptilogics. Colleagues disclosed relationships with multiple organizations.

Primary Source

New England Journal of Medicine

Source Reference: McNally M, et al "Short or long antibiotic regimens in orthopedics" N Engl J Med 2026; DOI: 10.1056/NEJMoa2506756.

https://www.medpagetoday.com/orthopedics/orthopedics/123069

People Fear AI Will 'Kill All Humans.' But What if It Can Save Our Patients?

 The New York Times reported this week that "The Trump administration is accelerating efforts to make artificial intelligence an integral part of medical care in the United States, throwing the resources and support of the federal government into projects that deploy A.I. agents to diagnose and prescribe treatments to patients."

Depending on what news you've read recently, this could excite you or terrify you. I've previously written about my excitement about artificial intelligence (AI), but each day I am growing more worried that the way AI is being portrayed to the public is going to prevent patients from trying any drug, treatment, or tool that involves AI.

When CEOs of AI companies and developers are warning that the technology could "kill all humans," why should we expect anything but skepticism from patients and the clinicians who use AI tools?

It appears AI has a branding problem. To calm those fears and enable AI to support healthcare, the medical community needs to lead the way. We'll need to define what AI is, and what it is not; acknowledge AI will disrupt peoples' lives, sometimes in negative ways; admit there are risks to human welfare and create systems for accountability; and help patients sort the tools that pose a threat from those that help.

Put simply: healthcare executives and clinicians need to be vocal and lead.

What Is AI Anyway?

AI is everywhere. Or is it?

The algorithm that helps a radiologist flag a pulmonary nodule? We call that AI.

The ambient tool that drafts a note while I talk to a patient, so I am not charting at midnight? AI.

The system that flags a sepsis trajectory earlier than a busy resident? AI.

The frontier models now raising alarms about autonomous cyberattacks and engineered pathogens? Also AI.

It's one phrase, but these technological advancements should not be grouped in the same category. In fact, it's a major problem when we put them all in the same AI bucket.

To those of us who work with these tools, the distinctions are obvious. A narrow model trained to detect diabetic retinopathy has about as much in common with a self-directing frontier system as a blood pressure cuff has with a nuclear reactor.

But the public doesn't see it that way. To my patients, their families, voters, and maybe even to the regulators who ultimately will shape what we can and cannot do with AI, the distinctions are really blurry. Everything is now called "AI." That's a problem because it means they believe all these tools, many of which are life-saving or sustaining, are something to be feared, slowed, or completely disbanded.

AI can improve care, catch what tired humans miss, ease crushing workforce shortages, and maybe even cure cancer. But if patients, if society, rejects AI out of fear because they do not understand the nuance, the promise of the technology will never be realized.

The Growing Backlash Against AI

The backlash against AI has been swift and fierce. So fierce that the top companies have acknowledged it might be time to slow down progress.

An NBC poll published in early September found 70% of Americans are worried about AI. Young, old, wealthy, or poor, Americans have deep reservations about the technology. They are worried AI will kill them at worst or take their jobs at best.

It is no surprise, then, that clinicians are consistently more optimistic about AI than patients. A recent global index found roughly 79% of health professionals are hopeful it could improve outcomes. Only about 59% of patients agreed. More than half worried about losing the human touch in their care. A separate national study in JAMA Network Open found that patient trust in health systems to use AI responsibly was low.

Here is the part that should give healthcare professionals pause: the trust deficit had less to do with how much someone understood AI than with how much they trusted the healthcare system in the first place. Read that again. Comfort with medical AI is not a knowledge gap we can close with a pithy little explainer video.

It comes because people do not trust the system in general. Combine low trust in the healthcare community with zero trust in the people who run data centers and you can easily see the problem we are facing.

Distrust Threatens Investment

AI in medicine may hold promise, but Americans are forming their opinions of healthcare's future use of the technology far outside of exam rooms. They are listening to economists, politicians, AI company defectors, national security officials, and even their children's teachers who are banning it from classrooms. Even if none of it is about healthcare specifically, it all shares the label. And guilt by association is a powerful force.

The question I keep coming back to is this: has "AI" become such a broad and increasingly troubling brand that it could begin to thwart the implementation, investment, and adoption of some of its most useful medical applications?

I believe that is a real risk. If patients grow wary of anything labeled AI, they may decline tools that would genuinely help them, or lose confidence in the clinicians who use them. If that skepticism hardens, health systems may quietly slow rollouts or walk back projected savings. If the public mood sours enough to invite heavy-handed regulation aimed at frontier systems, narrow clinical tools could get swept up in the same net. Investors, reading all of this, may grow more cautious about the very applications most likely to help at the bedside.

There are legitimate concerns about AI, but we need to separate the tools that work from those that do not -- or those that may pose a threat.

That distinction exists in the technology. But it does not yet exist in Americans' minds.

So, What's the Prescription?

First, we need better words. "AI" is now nearly useless as a category. In medicine, we should name things plainly:

• Clinical decision support
• Ambient documentation
• Image analysis

We should also be honest about what each tool does, what it does not do, and who stays accountable when it is used. Patients will be reassured not by technical wizardry, but by human oversight and clear lines of responsibility.

Second, we should separate our story from Silicon Valley's. Medicine's use of these tools is relatively narrow, increasingly regulated (although gaps exist), and validated against outcomes. That is a fundamentally different enterprise than the race toward ever more capable general-purpose systems. We should stop letting the two be described in the same breath.

Third, we must keep earning trust the old-fashioned way. As the data show, it is the trust in us, not the sophistication of the tools, that patients are really evaluating.

The technology may be remarkable. But if we let "AI" become a scary word, some of the most useful applications in medicine could stall.

N. Adam Brown is a practicing emergency physician, entrepreneur, and healthcare executive. He is the founder of ABIG Health, a healthcare growth strategy firm, and a professor at the University of North Carolina's Kenan-Flagler Business School.

https://www.medpagetoday.com/opinion/prescriptionsforabrokensystem/123022