Two separate federal policy decisions within days of each other are simultaneously boosting the pipeline of foreign-born physicians through travel-ban policy changes while straining the pipeline of some domestic clinical workers through student loan caps.
The Department of Homeland Security quietly changed its travel-ban policy to no longer subject physicians to the processing hold. The department confirmed to TheNew York Times that it will resume processing visas and work permits for medical physicians — freeing them from the visa renewal limbo they have faced for months.
At the same time this change could alleviate stressors on the foreign-born physician pipeline at U.S. hospitals, a new rule could hinder the domestic pipeline of clinical workers. The Department of Education finalized a rule April 30 implementing sweeping changes to federal student loans, limiting how much some healthcare students can borrow. Industry leaders argue the rule could restrict access to education and worsen workforce shortages in nursing, physician assistant and physical therapy programs.
The visa reversal addresses an immediate problem. The U.S. Citizenship and Immigration Services updated its website to indicate physicians are no longer subject to a processing hold imposed under travel restrictions, which froze decisions on visa extensions, work permits and green cards for citizens of 39 countries. While the ban did not apply to visa holders already in the U.S., USCIS paused visa renewals and updates for individuals from those countries. The pause affected more than 10,000 physician H-1B visa holders and 17,000 J-1 holders, as well as thousands of nurses, lab technicians and other healthcare workers. Many physicians were placed on administrative leave by hospitals while awaiting renewal.
The Department of Education rule moves in the other direction. The agency released final regulations April 30 implementing the student loan provisions of the Working Families Tax Cuts Act, which President Donald Trump signed into law July 4. The act caps federal loans for graduate and professional students, creating a $20,500 annual borrowing limit for graduate students and a $50,000 annual limit for professional students. The rule establishes a formal definition for “graduate student” and “professional student,” which determines eligibility for higher federal loan limits. Under the rule’s framework, some healthcare fields — including physician assistant programs and certain advanced practice nursing pathways — are treated as graduate programs rather than professional ones. Students in those programs will be placed in the lower borrowing tier, limiting annual federal loans to $20,500 beginning July 1.
Healthcare professional groups protested the exclusion of major fields throughout the public comment period and after it was finalized. The American Nurses Association said the rule “will be felt in real communities, for example, in rural areas where nurse practitioners, midwives and nurse anesthesiologists are often the only providers of core care services.” The American Academy of Physician Associates and the PA Education Association said they will challenge the rule in court.
The two policies describe two different theories of how the U.S. clinical workforce should be supplied. The visa reversal reflects a near-term operational reality, while the loan caps reflect a longer-term policy choice that the federal student loan program should not finance graduate borrowing to the extent it has been — even in fields where industry groups say shortages are documented and worsening.
For health system leaders, the changes signal an opportunity for a stronger pipeline of foreign-trained physicians, though that pipeline remains tethered to immigration policy that has shifted multiple times over the past year. The systems best-positioned for what comes next may be the ones building durable internal pipelines — residency partnerships with nursing and PA schools, employer-sponsored tuition support for graduate-level licensure, in-house upskilling programs — rather than relying on either federal lever to hold steady.
Lithiumcarbonate has been the gold standard for the treatment ofbipolar disordersince the 1950s. For nearly two decades, researchers have also wondered if this old, cheap drug might slow neurodegeneration as well.
From observational studies in people treated with lithium for psychiatric illness to epidemiological data of the drug in drinking water, research has long tied the substance to lower dementia rates. A 2025 Nature paper even hinted at a potential role for lithium in Alzheimer’s disease (AD) by suggesting the disorder may begin with a fundamental lithium deficiency in the brain. But the data still weren’t strong enough to justify a larger clinical trial to measure the substance’s neuroprotective qualities.
Researchers had hoped that results from a pilot project — the first prospective randomized controlled trial to study the effects of lithium on memory and brain aging — would finally settle the question. However, findings published earlier this year were mixed.
The trial missed every one of its six primary endpoints, which spanned cognition, brain volume, and a plasma biomarker. Still, there was one glimmer: Verbal memory declined at roughly half the rate in older adults who received low-dose lithium compared to those who received a placebo. While those results were promising, the data fell short of statistical significance.
Ariel Gildengers, MD
“Our results were encouraging but not definitive,” lead investigator Ariel Gildengers, MD, professor of psychiatry at the University of Pittsburgh School of Medicine, told Medscape Medical News. “What lithium appears to do — if the signal holds up — is slow deterioration.”
Researchers say the findings can inform future trials, while outside experts have questioned whether the signal they observed holds up at all. The field had hoped for answers. Instead, it seems that there are just more questions.
A Neuroprotective Effect?
More than a decade ago, Gildengers observed signals of better brain health among older bipolar patients on long-term lithium. Those findings raised a question: Might lithium’s apparent neuroprotective effects extend beyond mood disorders, and could they be tested in people with mild cognitive impairment (MCI) who had no psychiatric diagnosis?
To find out, Gildengers designed the Lithium as a Treatment to Prevent Impairment of Cognition in Elders (LATTICE) trial in adults aged 60 and older with MCI. They randomized 41 patients to lithium (mean age, 72.9 years; 56% female) and 39 to placebo (mean age, 71.2 years; 56% female). Participants received treatment for 2 years, with a mean daily dose of approximately 195 mg of lithium carbonate — roughly one-fifth the standard psychiatric dose — producing serum levels around 0.17 mEq/L.
When researchers analyzed the data, they found no meaningful group differences in cortical gray matter, visuospatial memory, a composite cognitive score, and plasma levels of brain-derived neurotrophic factor (BDNF).
Of the six coprimary outcomes, only verbal memory showed a nominally significant treatment-by-time interaction. Scores on the California Verbal Learning Test-II declined 1.42 points per year in the placebo group vs 0.73 in the lithium group (P = .05), though this did not meet the study’s prespecified significance threshold of P < .01. Hippocampal volume trended favorably (P = .09) but also did not reach significance.
The trial did confirm that low-dose lithium was safe and well tolerated, with serious adverse events in 29% of the lithium group vs 23% on placebo.
“This does not mean lithium improves memory or reverses cognitive impairment,” Gildengers said. “At best, it may slow decline under certain conditions.”
Questioning Signal Strength
But Lon Schneider, MD, who wasn’t part of LATTICE, has a hard time looking past the six missed primary outcomes.
“The positive evidence is still lacking. This kind of profile could come out if you used a wholly inactive ingredient,” Schneider, a professor of psychiatry, neurology, and gerontology at the University of Southern California Keck School of Medicine, Los Angeles, told Medscape Medical News.
And the verbal memory finding, he added, is statistically fragile. “If you did the study again with a different group of 80 people, there’s roughly a 50% chance you just wouldn’t see this effect.”
The study also had a number of methodological problems, said Orestes Forlenza, MD, PhD, a professor of psychiatry at the University of São Paulo, Brazil. Among them, the inclusion of nonamnestic MCI patients, a low proportion of amyloid-positive participants, and a low lithium dose.
“I think the results were not as good as expected,” Forlenza told Medscape Medical News. The null BDNF finding was particularly surprising, he added, given that lithium has increased the factor in virtually every prior experimental model tested, including in a study he led in patients with amnestic MCI.
For that trial, Forlenza and colleagues followed 61 patients over 4 years, using roughly double the serum lithium levels that LATTICE achieved. The findings showed what LATTICE did not: that lithium was reaching the brain and was associated with an approximately 50% inhibition of glycogen synthase kinase-3 beta — the enzyme whose inhibition by lithium is considered central to its proposed neuroprotective mechanism. The study also tracked cerebrospinal fluid (CSF) biomarkers of AD pathology over 36 months.
In addition, Forlenza found a significant increase in CSF amyloid-beta 42 that suggested improved amyloid clearance, though an earlier reduction in phosphorylated tau at 12 months did not persist at 36 months. Those changes indicated the drug was acting on both molecular hallmarks of AD, providing evidence of disease modification, not just symptom management.
Designing the Next Study
Gildengers said he is planning a larger trial informed by what they learned from LATTICE, especially the need to enroll participants based on blood biomarkers of AD pathology. “If we were designing this study today, we would enroll participants based on amyloid status from the start,” he said.
When LATTICE was conceived nearly a decade ago, blood-based AD biomarkers like plasma p-tau217 had not yet been identified. Participants were enrolled based on clinical symptoms alone. Only about a quarter turned out to be amyloid-positive. About one-fifth had nonamnestic MCI, a subtype less commonly linked to AD progression.
If lithium’s mechanism of action is specific to AD biology, testing it in a mostly non-AD population dilutes the signal, Forlenza said.
“You actually need Alzheimer’s disease pathology to find the effect from lithium. It doesn’t work if you don’t have these pathophysiological abnormalities in your patient population,” he noted.
In LATTICE’s exploratory analyses of amyloid-positive completers, lithium effect sizes were larger: Hedges g was 0.74 for verbal memory and 0.82 for hippocampal volume, compared with 0.32 and 0.09, respectively, in amyloid-negative completers. Effect sizes in this range are considered medium to large, meaning lithium’s apparent benefit was concentrated almost entirely in participants who had AD pathology, and largely absent in those who did not.
The study wasn’t powered to compare results based on amyloid positivity, but the results are informative for the next trial design, Gildengers noted.
Other Challenges to Address
The next trial may also need to consider a different lithium formulation. Findings from a 2025 Nature study revealed that amyloid plaques carry a negative charge that attracts free lithium ions, trapping them before they reach neurons. The lithium carbonate used in LATTICE dissociates rapidly in the bloodstream, making its lithium ions particularly vulnerable to this sequestration.
But lithium orotate, the formulation used in the Nature study, remains bound to its carrier longer, allowing the delivery of lithium directly to neurons, said study investigator Bruce Yankner, MD, PhD, a professor of genetics and neurology at Harvard Medical School, Boston.
“Lithium carbonate was a reasonable choice when LATTICE was initiated in 2018,” Yankner told Medscape Medical News. “In our 2025 study, however, lithium carbonate was the least active of all the lithium salts tested.”
Another consideration might be to do a dose-ranging study before launching a larger trial, Forlenza suggested. This step would measure central nervous system penetration to establish if enough lithium is reaching the brain to engage its molecular targets.
But there’s an even greater challenge in lithium studies: funding. Because lithium is generic, no company stands to profit from proving it works. The entire burden falls on public funding.
“We really need a multicentric study, as we would do with any new pharmaceutical compound,” Forlenza said. “But who will pay for that?”
Clinical Takeaways
One thing Gildengers, Schneider, and Forlenza agree on is that the research to date does not support the drug’s clinical use beyond its approved indication, which does not include MCI or dementia.
“Patients should not self-medicate with over-the-counter lithium supplements. Lithium is a potent medication that requires careful dosing and close monitoring of kidney and thyroid function,” Gildengers said.
That warning comes as the lithium orotate supplement market continues to expand — valued at an estimated $411 million in 2024 and projected to nearly double by 2032. The supplements, sold online without prescription, are marketed for mood support, cognitive clarity, and brain health.
A 2025 survey published in the Canadian Journal of Psychiatry found that among 211 adults self-reporting use of over-the-counter lithium supplements, cognitive improvement was the most commonly experienced benefit, and side effects and withdrawal symptoms were more prevalent than anticipated.
Forlenza cautioned that the evidence does not yet support self-medication. “People take some experimental evidence and epidemiological data, and they decide it’s good to take lithium,” Forlenza said. “But it’s too early. We don’t have enough consistent evidence.”
The study was supported primarily by the National Institute on Aging (R01 AG055389). Gildengers reported receiving honoraria for invited lectures, according to the study’s published disclosures. Schneider, Forlenza, and Yankner reported no financial relationships relevant to this article.
Deep inside the gut, a high-fat diet might be doing more than just driving metabolic shifts — it could be opening a literal gateway to the brain. While researchers have long understood that there’s cross talk between the gut and the brain — even labeling it the gut-brain axis — the paths connecting the two are still being mapped out.
One striking new theory comes from research in mice suggesting that when the intestinal barrier fails, live bacteria can escape the gut and “hitchhike” along the vagus nerve, the massive neural highway connecting the digestive system to the cranium. The study, published in PLOS Biology, adds to a mounting pile of evidence that gut dysfunction could be a hidden driver of conditions such as Alzheimer’s disease, Parkinson’s disease, and autism spectrum disorder.
“The question is, do the bacteria actually cause these diseases?” said study author Arash Grakoui, PhD, professor of medicine, microbiology, and immunology at Emory University in Atlanta.
Mapping the Microbial Migration
To see how these bugs move, researchers put mice on a short-term, high-fat diet. Within days, the regimen flipped the mice’s microbiome and triggered intestinal permeability — the “leaky gut” effect. Using bacterial cultures, the team tracked microbes as they migrated from the leaky intestines to the vagus nerve, eventually landing in the brain. While the bacteria arrived in the brain, the counts remained low, staying well below the levels seen in acute infections such as meningitis.
“It’s not like the bacteria get in the bloodstream and then somehow get to other organs,” Grakoui said. “We didn’t find bacteria in any of the organs that we looked at, nor in the blood.”
To prove the path wasn’t a fluke, the team cleared the mice’s natural flora with antibiotics and introduced a “barcoded” bacterial DNA strain. Days later, that exact strain showed up in the animals’ vagus nerves and brains. When they severed the right side of the vagus nerve, significantly fewer bacteria made the trip. The team also noted similar gut-barrier compromises in mouse models of Alzheimer’s and Parkinson’s.
The team spent nearly 7 years on the project, employing obsessive decontamination protocols — including head-to-toe personal protective equipment and bleach scrubs — to ensure no outside DNA skewed the results.
While the “vagus hitchhike” is now well documented, the how remains a mystery.
“The bacteria we’ve found in the brain are varied enough that it’s unlikely they are doing something specific like ‘swimming’ using flagella,” said study author David S. Weiss, PhD, professor at the Emory University School of Medicine. “It seems more plausible that it’s in part a host mechanism.” One example may be traveling up from nerve endings alongside nerve signals.
Brian J. Balin, PhD, director of the Center for Chronic Disorders of Aging at PCOM, called the work “impressive” but noted that the next step is high-resolution mapping.
“The fact that they did culturing, in general, that’s a good thing, but it doesn’t give us the specificity of where in the brain the bacteria may be going,” Balin said.
Plugging the Leak: Map for Treatment
The silver lining is that the damage appears to be reversible. When the mice went back to standard chow for 14 days, their gut permeability tightened, and brain bacterial counts dropped.
This link suggests a massive shift in how we might treat currently incurable neurologic disorders — moving the target from the brain down to the gut.
“The gut is the leaky pipe, and then your house is flooding, and that’s your brain,” Weiss said. “It wouldn’t be effective to take out bucket after bucket of water — you really want to stop the leaking pipe.”
The findings dovetail with other advances, like research into alpha-synuclein — a protein linked to Parkinson’s disease that may also use the vagus nerve as a backdoor to the brain.
“Organisms could actually get into our brains and potentially initiate or exacerbate a damage response,” Balin said. “Some organisms could be initiators of inflammation, and then others may take advantage of what’s been triggered to enter the brain.”
Ideally, this could lead to a suite of diagnostic tests — using blood, feces, or even saliva — to catch this damage before neurologic symptoms appear.
More research is needed to change clinical practice, but the findings have already influenced the researchers’ lunches.
“Everyone who works on this project eats better than they did before starting,” Weiss said. “There’s a lot more yogurt being consumed and a lot less fast food.”
The United States carried out strikes against the port city of Bandar Abbas and Qeshm Island in southern Iran, Fox News correspondent Jennifer Griffin reported on Thursday, citing a senior official. On the other hand, the source alleged the attacks did not mean the ceasefire with Iran was ending.
In the meantime, Iranian and Israeli media reported that the US and Iran exchanged fire in the Strait of Hormuz, indicating a possible resumption of hostilities between the two nations. Additionally, there were reports of fresh blasts in Bandar Abbas, Minab, and Qeshm.
US officials have not publicly commented on the latest development.
Iran fired at a US ship after it attacked an Iranian oil tanker in the Strait of Hormuz, Islamic Republic of Iran Broadcasting (IRIB) said on Thursday, citing a military source. The report came shortly after explosions thunderedin several locations in southern Iran.
According to Iranian media, the incident reportedly occurred while US warships were attempting to enforce Washington's naval blockade of Iran. Meanwhile, Israel Hayom newspaper quoted an Israeli official confirming that the exchange of fire between the US and Iran took place, with an Iranian vessel firing missiles at a US ship blocking a tanker from exiting the strait, prompting a response from the Americans.
“We continued to execute well across our business in the first quarter, delivering triple-digit revenue growth combined with strong gross margin and lower operating expenses. We were also pleased to see statistically significant and clinically meaningful benefit from the TULSA Procedure beginning to readout from the randomized post-market CAPTAIN clinical trial comparing it to robotic radical prostatectomy, the current standard of care,” said Arun Menawat, Profound’s CEO and Chairman. “These and other anticipated tailwinds, including the expansion of payer coverage for the TULSA Procedure, give us confidence that we are moving closer to a pivotal inflection point in our growth trajectory. Nevertheless, it continues to be difficult for the investment community to accurately predict our revenues in the short-term. Accordingly, we are setting what we believe is a reasonable bar for our total annual revenue in 2026.”
The Company projects total revenue for full-year 2026 to be approximately $25 million, which represents 56% growth compared to its prior year revenue. The Company also expects full year 2026 gross margin to be 70% or higher.
