Soft robotic, wearable device improves walking for individual with Parkinson's

 Freezing is one of the most common and debilitating symptoms of Parkinson's disease, a neurodegenerative disorder that affects more than 9 million people worldwide. When individuals with Parkinson's disease freeze, they suddenly lose the ability to move their feet, often mid-stride, resulting in a series of staccato stutter steps that get shorter until the person stops altogether. These episodes are one of the biggest contributors to falls among people living with Parkinson's disease.

Today, freezing is treated with a range of pharmacological, surgical or behavioral therapies, none of which are particularly effective.

What if there were a way to stop freezing altogether?

Researchers from the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS) and the Boston University Sargent College of Health & Rehabilitation Sciences have used a soft, wearable robot to help a person living with Parkinson's walk without freezing. The robotic garment, worn around the hips and thighs, gives a gentle push to the hips as the leg swings, helping the patient achieve a longer stride.

The device completely eliminated the participant's freezing while walking indoors, allowing them to walk faster and further than they could without the garment's help.

"We found that just a small amount of mechanical assistance from our soft robotic apparel delivered instantaneous effects and consistently improved walking across a range of conditions for the individual in our study," said Conor Walsh, the Paul A. Maeder Professor of Engineering and Applied Sciences at SEAS and co-corresponding author of the study.

The research demonstrates the potential of soft robotics to treat this frustrating and potentially dangerous symptom of Parkinson's disease and could allow people living with the disease to regain not only their mobility but their independence.

The research is published in Nature Medicine.

For over a decade, Walsh's Biodesign Lab at SEAS has been developing assistive and rehabilitative robotic technologies to improve mobility for individuals' post-stroke and those living with ALS or other diseases that impact mobility. Some of that technology, specifically an exosuit for post-stroke gait retraining, was licensed and commercialized by ReWalk Robotics.

Researchers at SEAS and the BU's Sargent College of Health & Rehabilitation Sciences used a soft, wearable robot to help a person living with Parkinson's walk without freezing. The robotic garment, worn around the hips and thighs, gives a gentle push to the hips as the leg swings, helping the patient achieve a longer stride. The research demonstrates the potential of soft robotics to treat a potentially dangerous symptom of Parkinson's disease and could allow people living with the disease to regain their mobility and independence. Credit: Harvard SEAS

"Leveraging soft wearable robots to prevent freezing of gait in patients with Parkinson's required a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists and apparel designers," said Walsh, whose team collaborated closely with that of Terry Ellis, Professor and Physical Therapy Department Chair and Director of the Center for Neurorehabilitation at Boston University.

The team spent six months working with a 73-year-old man with Parkinson's disease, who—despite using both surgical and pharmacologic treatments—endured substantial and incapacitating freezing episodes more than 10 times a day, causing him to fall frequently. These episodes prevented him from walking around his community and forced him to rely on a scooter to get around outside.

In previous research, Walsh and his team leveraged human-in-the-loop optimization to demonstrate that a soft, wearable device could be used to augment hip flexion and assist in swinging the leg forward to provide an efficient approach to reduce energy expenditure during walking in healthy individuals.

Here, the researchers used the same approach but to address freezing. The wearable device uses cable-driven actuators and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the gait and generate assistive forces in tandem with muscle movement.

The effect was instantaneous. Without any special training, the patient was able to walk without any freezing indoors and with only occasional episodes outdoors. He was also able to walk and talk without freezing, a rarity without the device.

"Our team was really excited to see the impact of the technology on the participant's walking," said Jinsoo Kim, former Ph.D. student at SEAS and co-lead author on the study.

During the study visits, the participant told researchers, "The suit helps me take longer steps and when it is not active, I notice I drag my feet much more. It has really helped me, and I feel it is a positive step forward. It could help me to walk longer and maintain the quality of my life."

"Our study participants who volunteer their time are real partners," said Walsh. "Because mobility is difficult, it was a real challenge for this individual to even come into the lab, but we benefited so much from his perspective and feedback."

The device could also be used to better understand the mechanisms of gait freezing, which is poorly understood.

"Because we don't really understand freezing, we don't really know why this approach works so well," said Ellis. "But this work suggests the potential benefits of a 'bottom-up' rather than 'top-down' solution to treating gait freezing. We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control."

The research was co-authored by Jinsoo Kim, Franchino Porciuncula, Hee Doo Yang, Nicholas Wendel, Teresa Baker and Andrew Chin. Asa Eckert-Erdheim and Dorothy Orzel also contributed to the design of the technology, as well as Ada Huang, and Sarah Sullivan managed the clinical research.

More information: Soft robotic apparel to avert freezing of gait in Parkinson's disease, Nature Medicine (2024). DOI: 10.1038/s41591-023-02731-8

https://medicalxpress.com/news/2024-01-soft-robotic-wearable-device-individual.html

Novel compound protects against infection by virus that causes COVID-19: preliminary studies

 Compounds that obstruct the "landing gear" of a range of harmful viruses can successfully protect against infection by the virus that causes COVID-19, a study led by Dana-Farber Cancer Institute scientists shows. Based on the findings, researchers have launched a human clinical trial of one such compound made by chemically stabilizing a key coronavirus peptide.

If the compound, called a stapled lipopeptide, proves effective as a nasal spray in the trial, it could be the basis for a new drug modality to prevent or treat COVID-19, say the authors of the study, posted online Jan. 4 in the journal Nature Communications.

Because such compounds foil a mechanism many viruses use to enter and infect cells, stapled lipopeptides may also be effective against dangerous and potentially deadly viruses such as RSV, Ebola, and Nipah, as the authors demonstrate in their study.

"Although vaccines, monoclonal antibodies, and small molecule drugs have played a crucial role in protecting people from life-threatening COVID-19 infection, there remains a critical gap in the treatment arsenal," said Loren Walensky, MD, Ph.D., Physician and Principal Investigator, Linde Program in Cancer Chemical Biology at Dana-Farber/Boston Children's Cancer and Blood Disorders Center.

He led the research with Gregory Bird, Ph.D., of Dana-Farber, and Robert Davey, Ph.D., of Boston University's National Emerging Infectious Diseases Laboratories (NEIDL).

"The constant evolution of the virus and the emergence of new variants has markedly decreased the effectiveness of immune-based approaches, requiring periodic reformulation of vaccines. What has been missing are fast-acting, easy-to-administer, and resistance-proof agents that can be used before or after exposure to the virus to prevent infection or reduce symptoms directly. Our study is an encouraging indication that stapled lipopeptides offer that potential," Walensky added.

"It was exciting to see how these peptides, which work by jamming the gears of the virus infection machine, moved quickly from a basic idea on paper to being effective with the viruses and in real disease models," said Robert Davey, Ph.D., Professor, Microbiology at Boston University's NEIDL.

"This was a great collaboration that started in the very first days of the pandemic when we wanted to work out a treatment for SARS-CoV-2 using the great biocontainment resources we have at Boston University. Our two labs worked very well together, and this is something we will continue to do in the future on other viruses that I work on, like Ebola."

Unlike mRNA vaccines, which are a form of immune-based therapy that provides delayed protection and also requires periodic administration due to viral mutation and/or waning immunity, the stapled lipopeptides developed by Walensky's lab act directly on SARS-CoV-2, the coronavirus responsible for COVID-19, interfering with its ability to infect healthy cells.

Because this approach does not use the immune system as an intermediary, it is especially promising for people with weakened immune systems, either due to their disease or treatment with immunosuppressive agents, such as chemotherapy.

Walensky's lab has pioneered developing and applying stapled peptides for nearly 20 years. These unique agents consist of natural peptides—a stretch of amino acids in a defined sequence—whose bioactive structure is chemically stabilized by an installed "staple" and, in this case, further linked to a lipid, which is believed to help concentrate the stapled peptide at the site of viral infection—the membrane surface of the otherwise healthy cell.

The new study shows that stapled lipopeptides are exceptionally stable, resisting extremes of temperature and chemical conditions, an important feature for persistence both inside and outside the body. The design strategy not only prevents peptide degradation in the body upon administration but also remedies prior challenges with shipment and storage, such as the required cold chain for COVID-19 vaccines.

In 2010, Walensky's lab first developed double-stapled peptides that target the same key step in the process by which the human immunodeficiency virus (HIV) binds to and then infects human cells, causing AIDS.

The stapled peptides mimicked the virus's "landing gear," a bundle of six coils or "helices" of the virus that comes together, enabling the virus to fuse with the host cell's membrane.

The therapeutic approach, known as fusion inhibition, prevents the virus from entering the cell to off-load its nucleic acid blueprint, otherwise turning it into a virus-producing factory. The stapled peptide, which mimics one of the coiled regions, disrupts the formation of the fusion apparatus, halting infection at its source.

In 2014, Walensky's team developed analogous stapled peptides targeting this same feature of the RSV virus, which can cause severe respiratory illness and even respiratory failure in the elderly and very young alike. They showed that administering the stapled peptide as a nose drop could prevent RSV infection in mice and also prevent the spread of established nasal infection from migrating to the lungs.

When the COVID-19 pandemic broke out in early 2020, Walensky's lab promptly converted one of the coiled motifs of the SARS-CoV-2 six-helix bundle into a stapled peptide in an effort to develop a therapeutic for pre- and post-exposure prophylaxis.

"Remarkably, the viral peptide sequence that we use to block the fusion apparatus is 100% identical between SARS-CoV-2 and SARS1, which emerged as a deadly respiratory virus in 2003," notes Walensky. He points out that, in contrast to the viral sequences that frequently mutate to evade immune-based therapies, the virus's fusion sequences are rarely altered due to the critical role of six-helix bundle assembly in promoting viral infection.

In cooperation with researchers experts in highly pathogenic viruses at the NEIDL, Walensky's team began developing dozens of stapled peptide fusion inhibitors for anti-viral testing, altering the location of the staple and the linker between the staple and the lipid to determine which version worked best against the broadest spectrum of SARS-CoV-2 variants.

Ironically, as the virus evolved to evade vaccines and monoclonal antibodies, the more effective the stapled lipopeptides became, owing to the essential nature of the fusion mechanism they target.

Then, in partnership with the laboratory of Richard Bowen, DVM, Ph.D., of Colorado State University and the newly formed Red Queen Therapeutics of Cambridge, Massachusetts, that licensed the Dana-Farber technology, the Walensky lab began testing the inhibitors in hamsters. The studies evaluated a lead-stapled lipopeptide as a preventive and therapeutic agent. The animals were randomly selected to receive an inhibitor before and/or after nasal inoculation with SARS-CoV-2.

The results were very encouraging, Walensky remarks. The animals in each group that received the inhibitor maintained their weight, an indication that they remained well despite viral exposure. Examination of their noses showed a relative drop in viral titers compared to the untreated control group, and evaluation of their lung tissue found that the animals were significantly protected from severe pneumonia, a common complication of COVID-19.

"Similar to what we saw with RSV, nasal treatment with a stapled peptide fusion inhibitor—even if given after inoculation with SARS-CoV-2—prevented the infection from adversely affecting the lungs and causing severe disease," Walensky comments.

A second set of studies explored whether the inhibitors could help reduce transmission of the virus from one hamster to another. Again, the results were encouraging. "Animals that weren't treated consistently lost weight. Those that received treatment, either before or after exposure to an infected hamster, preserved their weight," Walensky notes. Correspondingly, viral loads in the noses and lungs of treated animals were lower than in untreated animals.

The fact that many viruses with pandemic potential rely on the six-helix bundle to enter and infect cells suggests that stapled lipopeptides developed by Walensky's lab can be adapted to block or reduce infection by other viruses "on demand."

"Red Queen Therapeutics was founded on the conviction that this novel technology from the Walensky lab would be broadly applicable in successfully combating viral threats, using a pre- and post-exposure prophylaxis paradigm, and COVID presents a proving ground as well as an important opportunity in its own right," said Ron Moss, M.D., CEO of Red Queen Therapeutics. "We are excited to validate data in this publication with our human trials in SARS-CoV-2 now under way and anticipate having data to share later this quarter," he added.

"This approach has the potential to fill an important gap in our arsenal against COVID-19 and other viruses that cause severe respiratory and hemorrhagic diseases," Walensky said.

"Imagine being able to protect yourself from COVID-19 or other disruptive respiratory viruses with a simple nasal spray that you could use to avoid infection at a large gathering or after exposure to a close contact who turns out to test positive for SARS-CoV-2. That is the promise this work holds, not only for otherwise healthy individuals, but especially for immunocompromised patients who remain most at risk of severe infection."

More information: Gregory H. Bird et al, A stapled lipopeptide platform for preventing and treating highly pathogenic viruses of pandemic potential, Nature Communications (2024). DOI: 10.1038/s41467-023-44361-1

https://medicalxpress.com/news/2024-01-compound-infection-virus-covid-preliminary.html

'Why vaccines don't work as well in some older adults'

 An important aspect to aging is how the immune system changes over time. Such changes have consequences, and they contribute to the greater risk for severe infections and other diseases such as cancer in the aging population. Researchers at The Jackson Laboratory (JAX) and UConn Health are rigorously investigating why vaccines don't work as well in some older adults

Streptococcus pneumoniae is a dangerous bacterial pathogen that causes diseases such as pneumonia, meningitis and sepsis. Infants and older adults are at greatest risk for pneumococcal infections, and case-fatality rates increase with age for reasons still not well understood.

Fortunately, several vaccines developed against the polysaccharides found on the surface of S. pneumoniae, including PPSV23 (Pneumovax), are generally effective in older adults, though not as protective as in younger adults. Combining (conjugating) the polysaccharide with a protein, such as a nontoxic variant of a diphtheria toxin, can induce additional adaptive immune activation, resulting in better protection.

The strategy was used to develop a new class of FDA-approved conjugated vaccines (e.g., PCV13, Prevnar). Despite these advances, responses to pneumococcal vaccines still decline with age. Moreover, it remains unclear which of these two vaccines are preferable in subpopulations of older adults.

To address these gaps in knowledge, a team led by JAX Associate Professor Duygu Ucar, Ph.D., UConn Health Professor and Director of UConn Center on Aging George Kuchel, M.D., C.M., and Jacques Banchereau, Ph.D. (Immunoledge, Montclair, NJ), recruited and vaccinated a cohort of 39 pneumococcal vaccine-naïve healthy adults, all aged 60 or above, to thoroughly compare pre- and post-vaccine immune characteristics.

Their findings, presented in "Distinct baseline immune characteristics associated with responses to conjugated and unconjugated pneumococcal polysaccharide vaccines in older adults," published in Nature Immunology, identify the biological traits underlying variable responses to the two different vaccines. Importantly, they also reveal distinct baseline (i.e., pre-vaccination) predictors that have the potential to affect vaccination strategies and lead to interventions that are more effective, by virtue of being more specific.

"Understanding who will respond strongly to which vaccine will provide us opportunities to stratify the population for improved vaccine efficacy at the population level, as well as understanding whether we can modulate the immune characteristics of individuals prior to vaccination to improve outcomes at the individual level," says Ucar.

All participants received a single dose of PPSV23 or PCV13 from May to early fall. Blood was drawn before vaccination, then one, 10, 28 and 60 days after to provide longitudinal data. Following vaccination, the researchers developed measures to quantify vaccine responses and rank donors with respect to responsiveness within the cohort. While overall responses to both vaccines were comparable, there were clear differences in baseline immune phenotypes, separating the strong and weak responders.

The baseline abundance of two specific T cell types, Th1 and Th17 cells, played an important role in PCV13 responses. Th1 cells produce molecular signals to activate early innate immune responses to pathogens, while Th17 cells also contribute to the defense response by producing a different group of inflammatory signaling molecules.

For PCV13 vaccine responses, higher levels of Th1 cells showed a positive association and higher levels of Th17 cells a negative association. Thus, a pre-vaccination Th1/ Th17 ratio can be predictive of PCV13 response strength. Interestingly, women have a higher frequency of Th1 and lower frequency of Th1 7 cells compared to men and responded more strongly to the PCV13 vaccine.

From the pre-vaccination gene expression data, the researchers uncovered a gene module that included cytotoxic genes that was associated with reduced PCV13 responses, called the CYTOX signature. Single cell profiling linked this gene expression signature to mature CD16+ natural killer (NK) cells.

The abundance of mature CD16+ NK cells in blood was associated with responses to PCV13, where weak responders had more CD16+ NK cells than strong responders. The CYTOX signature was not associated with responses to the alternative PPSV23 vaccine, however—another, distinct gene set predicted responses to PPSV23.

"Our study offers a reminder that 'one size fits all' approaches do not work well for older patients," says Kuchel. "Moreover, if our findings can be replicated in other populations, they may offer remarkable opportunities for implementing care models for older adults involving Precision Gerontology that are more effective by virtue of being more precise, ultimately matching individuals with those vaccines that work best for them."

A surprising aspect of the study is that the baseline predictors for the two available classes of pneumococcal vaccines are quite distinct and independent from each other, despite both vaccines using the same bacterial polysaccharides to provoke the protective immune response.

Importantly, however, the paper shows that responses to the two vaccines can be predicted in older adults based on specific pre-vaccination characteristics, and the findings imply that individuals can be readily stratified based on which vaccine is likely to work best for them. For example, older adults with low CYTOX/CD16+ NK cell levels will likely respond well to the PCV13 vaccine, while those with high CYTOX would more likely benefit from the PPSV23 vaccine.

Overall, the results have important implications for more precise vaccination strategies for pneumococcal vaccines, and potentially for other vaccines as well, to better protect older adults from infection and disease.

More information: Sathyabaarathi Ravichandran et al, Distinct baseline immune characteristics associated with responses to conjugated and unconjugated pneumococcal polysaccharide vaccines in older adults, Nature Immunology (2024). DOI: 10.1038/s41590-023-01717-5

https://medicalxpress.com/news/2024-01-vaccines-dont-older-adults.html

ICE deported < 5% of all migrants encountered in 2023 – far fewer than sent back under Trump

 Immigration and Customs Enforcement (ICE) deported over 142,000 people in 2023 – less than 5% of all 3.2 million migrants encountered at US borders.

In its 2023 annual report released last week, ICE readily noted its number of expulsions was double those of the previous year, but under Joe Biden’s presidency the agency is deporting far fewer people than it did under Donald Trump.

For example, in the immigration agency’s 2018 financial year, ICE removed 265,000 individuals from the US, representing over 30% of the 680,000 migrants encountered at the border that year, according to Customs and Border Protection’s figures.

During the fist year Biden was in office, statistics from CBP show border encounters almost tripled from 647,000 to 1.95 million.  

That same year Biden issued new guidelines about how ICE should carry out immigration enforcement, which resulted in just 59,000 removals for the year, the lowest number of deportations in the last six years.

ICE’s latest figures show its agents deported 142,580 immigrants to about 180 countries from the US in the last fiscal year, including more than 44,000 from the interior and more than 98,000 from the border, the report said.

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ICE deported 142,000 people in 2023 .Los Angeles Times via Getty Images

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Under Joe Biden’s presidency, ICE is deporting far fewer people than it did under Donald Trump.Getty Images

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Some of the people deported had criminal convictions or pending criminal charges, ICE’s 2023 annual report shows.REUTERS

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During the fist year Biden was in office, statistics from CBP show border encounters almost tripled from 647,000 to 1.95 million.

It also highlighted how ICE removed more noncitizens in 2023 than in 2022, when 72,000 people were deported by the agency.

“Among those removed, 108 were foreign fugitives wanted by their governments for crimes including homicide, rape, kidnapping, drug trafficking, assault, and sex offenses,” the report stated.

According to ICE, 139 “known or suspected terrorists” and 3,406 “known or suspected gang members” were also among the deportees.

Additionally, more than 60,000 noncitizens were expelled prior to May 12 last year under the Title 42 public health order.

“ICE continues to disrupt transnational criminal organizations, remove threats to national security and public safety, uphold the integrity of US immigration laws, and collaborate with colleagues across government and law enforcement in pursuit of our mission to keep US communities safe,” ICE Deputy Director Patrick J. Lechleitner said in a statement.

ICE is not the only branch of the Department of Homeland Security which deports people, and many who are initally stopped by border patrol are ejected from the country or sent back to their point of origin by CBP.

Full figures for the number of people deported from the US were not immediately available, but between October and May, the DHS said it had deported over 300,000 people, a number which included those sent by ICE.

As well as deporting people, ICE also monitors migrants who are in the US pursuing asylum applications or on parole.

The 2023 report showed the true scale of that operation, revealing at the end of the year the agency had 37,000 in custody waiting to be removed from the US, and that another 6.2 million people who were non-detained.

That figure has almost doubled since 2020 when ICE were looking after 3.3m active cases in total. 

During CBP’s fiscal 2023, which runs from Ocotber 1 to Septemeber 30, more than 3,201,000 encounters with migrants were reported along the US-Mexico border, according to data from US Customs and Border Protection. 

Nearly 2.5 million people were apprehended illegally crossing the Mexico-US border in that year — a record-breaking tally — but the Department of Homeland Securty also estimates another 670,000 “gotaways” managed to evaded authorities and get across the border unchecked.

The border crisis also shows no sign of slowing down with more than 276,000 asylum seekers hoping to cross from Mexico in December, the highest number for a single month in history, according to the preliminary data obtained by Fox News.

https://nypost.com/2024/01/05/news/ice-is-deporting-far-fewer-people-under-bidens-presidency-than-it-did-under-trump-report/

Sorry, but the ‘drugs from Canada’ don’t work

 “Drugs from Canada” is a policy that won’t work. And a political soundbite that won’t die.

As H.L. Mencken presciently said, “For every complex problem there is an answer that is clear, simple and wrong.”

That’s exceedingly true in the debate over whether states should be allowed to import drugs from Canada en masse. On Friday, the Food and Drug Administration granted conditional approval for a Florida plan to do just that.

But let’s set aside the rhetoric and look at the facts:

First, how much would all the added risk to the safety and effectiveness of medicines from importation save US consumers? Hardly anything.

The Congressional Budget Office ran the numbers and found that importing drugs would cut costs by a paltry 0.01%.

If that sounds surprising, it’s probably because importation advocates exaggerate the savings patients can expect.

Outside of a few specialty drugs, most generic drugs approved by the FDA for sale in the United States cost about the same here (or less) as they do in Canada — and about 90% of the drugs prescribed in America are generics.

Second, the population math is upside down.

According to Mary Durette, a spokeswoman for Health Canada, Canada’s version of the FDA, “Canada’s drug supply is too small to meet the demands of both American and Canadian consumers.”

Florida has a population of almost 22 million. The strain on the Canadian medicine supply would likely lead to shortages and increased costs for Canadian patients.

If Canada filled 10% of US prescriptions, its own drug supply would run out in less than eight months.

In 2019, I testified before the Florida legislature on lawmakers’ desire to import Canadian drugs.

“Has anyone discussed this idea with Health Canada?” I asked.

The answer? “No.” Of course not.

Call me the Cassandra of Canadian drug importation.

Indeed, Canada is already facing a serious problem with drug shortages.

There are close to 1,800 drugs in short supply, per Canada’s health ministry.

And in a recent survey of more than 1,700 pharmacists, 79% said they believed the frequency of drug shortages had “greatly increased” over the past three to five years.

Meanwhile, the Florida Plan would undoubtedly send many Americans to existing scam “drugs from Canada” websites.

One FDA operation found 85% of “Canadian” drugs actually originated in 27 different countries.

And more than a third of those drugs were potentially counterfeit.

“Drugs from Canada” does not always mean “the same medicines Canadians get.”

Canadian regulators have warned Americans that importation could be risky.

One official at Health Canada supply said the regulator “does not assure that products being sold to US citizens are safe, effective and of high quality and does not intend to do so in the future.”

Relying on caveat emptor makes for bad health-care policy.

It’s also crucial to recognize that Health Canada and the FDA make regulatory decisions independent of each other — and the approval processes are not identical.

Imported drugs would not receive the same kind FDA scrutiny and certification for safety, quality and effectiveness as American-made drugs.

Should prisoners and people on Medicare and Medicaid, who’d be given the drugs imported by states like Florida, be Guiana pigs for this ill-considered scheme?

Headlines notwithstanding, the Florida plan’s approval is conditioned on several difficult next steps.

Per the FDA, “Before drugs can be imported, Florida’s Agency for Health Care Administration must:

• Submit additional drug-specific information for the FDA’s review and approval.
• Ensure the drugs Florida seeks to import have been tested for, among other things, authenticity and compliance with the FDA-approved drugs’ specifications and standards.
• Relabel the drugs to be consistent with the FDA-approved labeling.

These requirements are not easy tasks to accomplish and aren’t foregone conclusions.

As for the political ramifications, the Florida plan will only add to the already existing confusion and general bloviation over ways to address better access to medicines.

Alas, there are no simple answers.

But drug importation is no longer a pipe dream. It’s now a pipe bomb.

Peter J. Pitts, a former FDA associate commissioner, is president of the Center for Medicine in the Public Interest.

https://nypost.com/2024/01/05/opinion/sorry-but-the-drugs-from-canada-dont-work/