Gabapentin’s Side Effects May Lead to ‘Prescribing Cascade’

By Pat Anson

Over the years, we’ve published many warnings about gabapentin (Neurontin), a nerve medication that is widely prescribed off-label for pain conditions it was never intended to treat. 

Common side effects from gabapentin include brain fog, dizziness, weight gain, headache, fatigue, and anxiety. The drug has also been linked to a higher risk of dementia.  

According to a new study, those side effects may lead to a “prescribing cascade” in which physicians mistakenly prescribe unnecessary medications to a patient that cause even more side effects. 

The problem is not limited to gabapentin, but includes other gabapentinoids such as pregabalin (Lyrica). Both medications may cause edema – fluid retention and swelling in the legs and feet –  leading doctors to suspect congestive heart failure and prescribe diuretics that can cause kidney injury, light headedness, and falls. 

Researchers with the VA Health Care System and the University of California, San Francisco (UCSF) analyzed the medical records of 120 older veterans, most of whom were male and  long-term users of five or more medications. All had taken gabapentinoids and diuretics, which are often prescribed for edema.  

Although none of the veterans had fluid buildup in the year before they started taking gabapentinoids, only 4 doctors suspected the drugs may be the culprit and just one discontinued the medication.

The vast majority of physicians – 69 in all – never suspected or downplayed the possibility that gabapentinoids may be causing the edema. Since fluid retention is a symptom of congestive heart failure and poor blood circulation, the veterans were put on loop diuretics such as Lasix.

Within two months, 28 veterans had side effects from the new drugs, including poor kidney function, dizziness, and blurred vision, along with low levels of sodium or potassium, which can disrupt critical body functions. Six patients had symptoms so severe they were hospitalized or taken to an emergency department. 

“Gabapentinoids may be prescribed at unnecessarily high doses or for conditions that they may not help,” said Matthew Growdon, MD, an Assistant Professor of Medicine at UCSF and first author of the study in JAMA Network Open. “In these cases, doctors should consider not prescribing these drugs — or giving lower doses to lessen the risk of prescribing cascades and other side effects.” 

One veteran in his 60’s was put on a heavy dose of gabapentin for neuropathy that was induced by chemotherapy for lung cancer. He developed edema and was switched to pregabalin. When the fluid retention didn’t stop, he was put on a diuretic. Within two days he developed light headedness and felt off-balance, and the diuretic was stopped.

Another patient in his 60’s was prescribed gabapentin twice a day for back pain, an off-label use. After two months he had edema and was put on a diuretic. Soon after, he experienced a fall, went to the ER, and was given IV pain medication. The diuretic and polypharmacy are believed to have contributed to the man falling.

The cases highlight how a prescribing cascade with multiple drugs can have serious consequences. 

Gabapentin is often prescribed off-label for migraine, fibromyalgia, cancer pain, postoperative pain, and many other pain conditions for which it is not FDA-approved. Off-label prescribing is legal, but has reached extreme levels for gabapentin. Studies estimate the drug is prescribed off-label up to 95% of the time. 

“Gabapentinoids are non-opioids, and prescribers associate them with a relatively favorable safety profile,” says senior author Michael Steinman, MD, a Professor of Medicine at UCSF.  “Patients taking them should regularly check in with their doctor to assess whether this is the best treatment for them and consider other options, including non-drug alternatives that might be more appropriate.” 

In 2024, gabapentin was the fifth most prescribed drug in the U.S., with prescriptions nearly tripling since 2010. The number of patients prescribed gabapentin reached 15.5 million in 2024, up from 5.8 million in 2010.

Lupus May Be Caused by Common Virus

By Graham Taylor and Heather Long

Around 5 million people worldwide live with the autoimmune condition lupus. This condition can cause a range of symptoms, including tiredness, fever, joint pain and a characteristic butterfly-shaped rash across the cheeks and nose.

For some people, these symptoms are mild and only flare-up occassionally. But for others, the disease is more severe – with constant symptoms

Although researchers know that lupus is caused by the immune system mistakenly attacking the body’s own tissues and organs, it isn’t entirely clear what triggers this response. But a new study suggests a common virus may play a key role in lupus.

There are two main forms of lupus. Discoid lupus primarily affects the skin, while systemic lupus erythematosus – the most common form of lupus – is more severe and affects the organs.

The immune system’s B cells play a key role in systemic lupus. B cells normally produce proteins called antibodies to target pathogens such as viruses and bacteria. But in people with systemic lupus, some B cells produce antibodies, called autoantibodies, that instead bind to and damage their own organs.

What causes B cells to produce autoantibodies in people with systemic lupus is poorly understood. But this recent study suggests that the trigger may be a common virus.

EBV Infection

Epstein-Barr virus (EBV) infects most people worldwide. Infection with EBV most commonly occurs in childhood, when it usually goes unnoticed. But if a person becomes infected by EBV in adolescence, it can cause infectious mononucleosis (better known as glandular fever).

EBV is a type of herpes virus. These are complex viruses that are able to escape the body’s immune response by hiding inside certain cells.

In these cells, herpes viruses switch off their genes and go silent – like submarines diving beneath the waves to hide from the enemy. This allows herpes viruses to persist throughout a person’s lifetime – occasionally reawakening to spread to new people.

Interestingly, EBV has evolved to hide within the immune system itself, infecting and persisting in a very small number of B cells.

This strategy has proven highly successful for EBV. Over 90% of adults around the world are infected with EBV – meaning the virus is hiding in their immune system’s B cells.

EPSTEIN-BARR (ebv) VIRUS

While most people experience no adverse consequences from their infection, EBV has been linked to certain diseases.

For instance, EBV was the first virus shown to cause cancer. Subsequent research has linked EBV to several different types of cancer – including certain lymphomas and 10% of stomach cancers. Each year, about 200,000 people develop an EBV-associated cancer.

More recently, large epidemiological studies have linked EBV with multiple sclerosis, which is an autoimmune condition. Studies have shown that people with multiple sclerosis are almost always infected with EBV.

Previous research has also suggested that EBV may be involved in systemic lupus. But this new study provides insight into the specific mechanism involved.

To conduct their study, the researchers developed a sensitive test to analyse the genetic material in thousands of B cells isolated from the blood of people with systemic lupus and healthy donors as a control.

They found that EBV was present in around 25 times more B cells in systemic lupus patients compared to participants who didn’t have the condition. In systemic lupus patients, EBV was present in around one in 400 B cells – while in healthy controls it was only present in around one in 10,000 B cells.

This is an interesting finding – though the researchers acknowledge it could potentially be caused by the medicines patients with systemic lupus take to control their illness. These decrease the activity of the immune system which reduces the symptoms of systemic lupus. But these medicines also reduce the immune system’s ability to control EBV infection.

How EBV Causes Autoimmunity

The most important finding from the research was that many of the EBV-infected B cells from systemic lupus patients made autoantibodies that bound to specific proteins. These same proteins are often targeted by autoantibodies in people with systemic lupus. In contrast, EBV-infected B cells from healthy donors did not make these autoantibodies.

To understand the mechanisms involved, the researchers then studied the expression of EBV genes in the infected B cells. Although EBV was generally shown to be in its silent state, some EBV-infected B cells from systemic lupus patients produced the viral protein EBNA2, which reprogrammed the B cells to become more inflammatory. These activated B cells were better able to stimulate responses from other immune cells, including non-EBV infected B cells and T cells.

Together, these observations suggest that EBV may initiate systemic lupus by infecting and reprogramming dormant B cells to become activated. These cells produce autoantibodies that could potentially contribute to the development of systemic lupus. They also appear to recruit additional immune cells able to produce stronger autoimmune responses that are more likely to play a role in systemic lupus development.

These new findings raise the possibility that targeting EBV could form the basis of a new therapy to treat people with systemic lupus. But given these infected B cells also recruit additional immune cells, a broader therapeutic strategy may be needed.

Additional research will also be needed to confirm whether EBV is indeed an essential trigger for the development of systemic lupus. If this is confirmed, preventing EBV infections through vaccination could prevent systemic lupus developing.

Currently there are a number of potential EBV vaccines in development – and two candidates are being tested in large clinical trials. A key requirement for any effective EBV vaccine will be its ability to generate long-term protection against infection. This is because EBV is already widespread in the population. If vaccination only delays infection until later in life, then this could lead to many cases of glandular fever.

The results of these trials are eagerly anticipated, given the potential impact an effective vaccine could have to reduce the numbers of people worldwide that develop lupus, other autoimmune conditions, or cancers caused by EBV.

Graham Taylor, PhD, is an Associate Professor in Viral and Tumour Immunology at the University of Birmingham. The main focus of Graham’s work is to increase our knowledge of the immune system in health and disease and how best to harness the immune system to treat cancer. His research helped lead to a therapeutic cancer vaccine that has undergone testing in several clinical trials. 

Heather Long, PhD, is an Associate Professor in the Department of Immunology and Immunotherapy, at the University of Birmingham. She leads a research team in the fields of viral and cancer immunology, with a long-term focus on understanding T cell control of viruses and virus-associated cancers.

This article originally appeared in The Conversation and is republished with permission.

New Autism Guidance on CDC Website Angers Health Experts

By Arthur Allen, KFF Health News

The rewriting of a page on the CDC’s website to assert the false claim that vaccines may cause autism sparked a torrent of anger and anguish from doctors, scientists, and parents who say Health and Human Services Secretary Robert F. Kennedy Jr. is wrecking the credibility of an agency they’ve long relied on for unbiased scientific evidence.

Many scientists and public health officials fear that the Centers for Disease Control and Prevention’s website, which now baselessly claims that health authorities previously ignored evidence of a vaccine-autism link, foreshadows a larger, dangerous attack on childhood vaccination.

“This isn’t over,” said Helen Tager-Flusberg, a professor emerita of psychology and brain science at Boston University. She noted that Kennedy hired several longtime anti-vaccine activists and researchers to review vaccine safety at the CDC. Their study is due soon, she said.

“They’re massaging the data, and the outcome is going to be, ‘We will show you that vaccines do cause autism,’” said Tager-Flusberg, who leads an advocacy group of more than 320 autism scientists concerned about Kennedy’s actions.

Kennedy’s handpicked vaccine advisory committee is set to meet next month to discuss whether to abandon recommendations that babies receive a dose of the hepatitis B vaccine within hours of birth and make other changes to the CDC-approved vaccination schedule. 

Kennedy has claimed — falsely, scientists say — that vaccine ingredients cause conditions like asthma and peanut allergies, in addition to autism.

The revised CDC webpage will be used to support efforts to ditch most childhood vaccines, predicts Angela Rasmussen, a virologist at the University of Saskatchewan and co-editor-in-chief of the journal Vaccine. 

“It will be cited as evidence, even though it’s completely invented,” she said.

The website was altered by HHS, according to one CDC official who spoke on condition of anonymity. The CDC’s developmental disability group was not asked for input on the website changes, said Abigail Tighe, executive director of the National Public Health Coalition, a group that includes current and former staffers at the CDC and HHS.

FROM CDC WEBSITE

Scientists ridiculed the site’s declaration that studies “have not ruled out the possibility that infant vaccines cause autism.” While upward of 25 large studies have shown no link between vaccines and autism, it is scientifically impossible to prove a negative, said David Mandell, director of the Center for Autism Research at Children’s Hospital of Philadelphia.

The webpage’s new statement that “studies supporting a link have been ignored by health authorities” apparently refers to work by vaccine opponent David Geier and his father, Mark, who died in March, Mandell said. 

Their research has been widely repudiated and even ridiculed. David Geier is one of the outside experts Kennedy hired to review safety data at the CDC.

Asked for evidence that scientists had suppressed studies showing a link, HHS spokesperson Andrew Nixon pointed to older reports, some of which called for more study of a possible link. Asked for a specific study showing a link, Nixon did not respond.

‘Using CDC to Spread Lies’

Infectious disease experts, pediatricians, and public health officials condemned the alteration of the CDC website. Although Kennedy has made no secret of his disdain for established science, the change came as a gut punch because the CDC has always dealt in unbiased scientific information, they said.

Kennedy and his “nihilistic Dark Age compatriots have transformed the CDC into an organ of anti-vaccine propaganda,” said Amesh Adalja, a senior scholar at the Johns Hopkins Center for Health Security.

“On the one hand, it’s not surprising,” said Sean O’Leary, a professor of pediatrics and infectious disease at the University of Colorado. “On the other hand, it’s an inflection point, where they are clearly using the CDC as an apparatus to spread lies.”

“The CDC website has been lobotomized,” Atul Gawande, an author and a surgeon at Brigham and Women’s Hospital, told KFF Health News.

CDC “is now a zombie organization,” said Demetre Daskalakis, former director of the National Center for Immunization and Respiratory Diseases at the CDC. The agency has lost about a third of its staff this year. Entire divisions have been gutted and its leadership fired or forced to resign.

Kennedy has been “going from evidence-based decision-making to decision-based evidence making,” Daniel Jernigan, former director of the CDC’s National Center for Emerging and Zoonotic Infectious Diseases, said at a news briefing Nov. 19. With Kennedy and his team, terminology including “radical transparency” and “gold-standard science” has been “turned on its head,” he said.

Sen. Cassidy Goes Quiet

The new webpage seemed to openly taunt Sen. Bill Cassidy (R-La.), a physician who chairs the Senate Health, Education, Labor, and Pensions Committee. Cassidy cast the tie-breaking vote in committee for Kennedy’s confirmation after saying he had secured an agreement that the longtime anti-vaccine activist wouldn’t make significant changes to the CDC’s vaccine policy once in office.

The agreement included a promise, he said, that the CDC would not remove statements on its website stating that vaccines do not cause autism.

The new autism page is still headed with the statement “Vaccines do not cause Autism,” but with an asterisk linked to a notice that the phrase was retained on the site only “due to an agreement” with Cassidy. The rest of the page contradicts the header.

“What Kennedy has done to the CDC’s website and to the American people makes Sen. Cassidy into a total and absolute fool,” said Mark Rosenberg, a former CDC official and assistant surgeon general.

On Nov. 19 at the Capitol, before the edits were made to the CDC website, Cassidy answered several unrelated questions from reporters but ended the conversation when he was asked about the possibility Kennedy’s Advisory Committee on Immunization Practices might recommend against a newborn dose of the hepatitis B vaccine.

“I got to go in,” he said, before walking into a hearing room without responding.

Cassidy has expressed dismay about the vaccine advisory committee’s actions but has avoided criticizing Kennedy directly or acknowledging that the secretary has breached commitments he made before his confirmation vote. Cassidy has said Kennedy also promised to maintain the childhood immunization schedule before being confirmed.

The senator criticized the CDC website edits in a Nov. 20 post on X, although he did not mention Kennedy.

“What parents need to hear right now is vaccines for measles, polio, hepatitis B and other childhood diseases are safe and effective and will not cause autism,” he said in the post. “Any statement to the contrary is wrong, irresponsible, and actively makes Americans sicker.”

Leading autism research and support groups, including the Autism Science Foundation, the Autism Society of America, and the Autism Self Advocacy Network, issued statements condemning the website.

“The CDC’s web page used to be about how vaccines do not cause autism. Yesterday, they changed it,” ASAN said in a statement. “It says that there is some proof that vaccines might cause autism. It says that people in charge of public health have been ignoring this proof. These are lies.”

What the Research Shows

Parents often notice symptoms of autism in a child’s second year, which happens to follow multiple vaccinations. “That is the natural history of autism symptoms,” said Tager-Flusberg. “But in their minds, they had the perfect child who suddenly has been taken from them, and they are looking for an external reason.”

When speculation about a link between autism and the measles, mumps, and rubella vaccine or vaccines containing the mercury-based preservative thimerosal surfaced around 2000, “scientists didn’t dismiss them out of hand,” said Tager-Flusberg, who has researched autism since the 1970s. “We were shocked, and we felt the important thing to do was to figure out how to quickly investigate.”

Since then, studies have clearly established that autism occurs as a result of genetics or fetal development. Although knowledge gaps persist, studies have shown that premature birth, older parents, viral infections, and the use of certain drugs during pregnancy — though not Tylenol, evidence so far indicates — are linked to increased autism risk.

But other than the reams of data showing the health risks of smoking, there are few examples of science more definitive than the many worldwide studies that “have failed to demonstrate that vaccines cause autism,” said Bruce Gellin, former director of the National Vaccine Program Office.

The edits to the CDC website and other actions by Kennedy’s HHS will shake confidence in vaccines and lead to more disease, said Jesse Goodman, a former FDA chief scientist and now a professor at Georgetown University.

This opinion was echoed by Alison Singer, the mother of an autistic adult and a co-founder of the Autism Science Foundation. “If you’re a new mom and not aware of the last 30 years of research, you might say, ‘The government says we need to study whether vaccines cause autism. Maybe I’ll wait and not vaccinate until we know,’” she said.

The CDC website misleads parents, puts children at risk, and draws resources away from promising leads, said Paul Offit, director of the Vaccine Education Center at the Children’s Hospital of Philadelphia. “Kennedy thinks he’s helping children with autism, but he’s doing the opposite.”

Many critics say their only hope is that cracks in President Donald Trump’s governing coalition could lead to a turn away from Kennedy, whose team has reportedly tangled with some White House officials as well as Republican senators.

Polling has also shown that much of the American public distrusts Kennedy and does not consider him a health authority, and Trump’s own approval rating has sunk dramatically since he returned to the White House.

But anti-vaccine activists applauded the revised CDC webpage. 

“Finally, the CDC is beginning to acknowledge the truth about this condition that affects millions,” Mary Holland, CEO of Children’s Health Defense, the advocacy group Kennedy founded and led before entering politics, told Fox News Digital.

“The truth is there is no evidence, no science behind the claim vaccines do not cause autism.”

Céline Gounder, Amanda Seitz, and Amy Maxmen contributed to this report. KFF Health News is a national newsroom that produces in-depth journalism about health issues.

Chronic Pain Raises Risk of High Blood Pressure

By Pat Anson

Having untreated or poorly treated chronic pain is known to raise the risk of serious health problems, including high cholesterol, elevated pulse, arteriosclerosis, and heart attack..

So it should come as no surprise that chronic pain also increases the risk of high blood pressure, according to a new study by the American Heart Association, which found that the extent and location of the pain may determine the level of risk. 

Someone with chronic widespread body pain, for example, has a 74% higher risk of developing high blood pressure; while chronic headaches are associated with a 22% higher risk and chronic back pain has a 16% higher risk.

“The more widespread their pain, the higher their risk of developing high blood pressure,” said Jill Pell, MD, Professor of Public Health at the University of Glasgow in the UK and lead author of the study published in the journal Hypertension.

“Part of the explanation for this finding was that having chronic pain made people more likely to have depression, and then having depression made people more likely to develop high blood pressure. This suggests that early detection and treatment of depression, among people with pain, may help to reduce their risk of developing high blood pressure.”

Pell and her colleagues analyzed over 13 years of health data from more than 200,000 adults enrolled in the UK Biobank Project. Participants completed a baseline questionnaire that asked if they had experienced pain in the last month that interfered with their usual activities. 

They also noted if the pain was in their head, face, neck/shoulder, back, stomach/abdomen, hip, knee, or all over their body. If they reported pain, they indicated whether pain persisted for more than three months.

Depression was measured based on participants’ responses to questions about the frequency of a depressed mood, disinterest in activities, restlessness or lethargy. Inflammation was measured with blood tests for C-reactive protein (CRP).

At the end of the study period, nearly 10% of all participants developed high blood pressure, which is considered a blood pressure measurement higher than 130/80 mm Hg or 140/90 mm Hg.

Compared to people with no pain, people with short-term acute pain had a 10% greater risk of high blood pressure, while those with chronic localized pain had a 20% higher risk.

When comparing sites of pain, there was a wide variation in risk levels:

• 74% higher risk for chronic widespread pain

• 43% higher risk for chronic abdominal pain

• 22% higher risk for chronic headaches

• 19% higher risk for chronic neck or shoulder pain

• 17% higher risk for chronic hip pain

• 16% higher risk for chronic back pain

Depression and inflammation accounted for 11.7% of the association between chronic pain and high blood pressure.

The findings highlight the need for good pain management to prevent or reduce the risk of hypertension and other health problems.

“When providing care for people with pain, health care workers need to be aware that they are at higher risk of developing high blood pressure, either directly or via depression. Recognizing pain could help detect and treat these additional conditions early,” Pell said.

Pain Relievers Can Cause High Blood Pressure

Another consideration is the need for further studies on the role of pain medicine in high blood pressure. Ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs) may increase blood pressure and worsen pre-existing hypertension. They can also interfere with the effectiveness of some blood pressure medications. 

The effect is more pronounced with some NSAIDs over others. Aspirin, for example, appears to have less effect on blood pressure than naproxen, which can cause the body to retain salt and water, leading to fluid buildup and hypertension. 

Opioids can cause both low and high blood pressure, depending on the dose and duration of use. Sudden discontinuation of long-term opioid use is associated with increased blood pressure

“Chronic pain needs to be managed within the context of the patients’ blood pressure, especially in consideration of the use of pain medication that may adversely affect blood pressure,” said Daniel Jones, MD, Dean and Professor Emeritus at the University of Mississippi School of Medicine.

One limitation of the study is that participants were middle- and older-aged adults who were mainly white and of British origin – therefore the findings may not apply to people from other racial or ethnic groups, or who live in other countries.

Other contributing factors is that participants reporting pain were more likely to be women, have an unhealthy lifestyle, larger waists, higher body mass index (BMI), more long-term health problems, and live in areas with higher unemployment, lower home and car ownership, and more overcrowding.

Eli Lilly Will Use AI to Speed Up New Drug Development

By Crystal Lindell

Eil Lilly is hoping its next major pharmaceutical breakthrough comes via artificial intelligence (AI). The company recently announced a partnership with NVIDIA, which makes high-performance computer chips that are essential for AI.

Lilly said the two companies “will work to build the most powerful supercomputer owned and operated by a pharmaceutical company.”

That supercomputer will power what Lilly calls “an AI factory” that will be used to run millions of experiments so it can test potential medicines, speed up drug development, and improve clinical trials. 

“Lilly is shifting from using AI as a tool to embracing it as a scientific collaborator," said Thomas Fuchs, Senior VP and Chief AI Officer at Lilly.

"By embedding intelligence into every layer of our workflows, we're opening the door to a new kind of enterprise: one that learns, adapts and improves with every data point. This isn't just about speed, but rather interrogating biology at scale, deepening our understanding of disease and translating that knowledge into meaningful advances for people.”

Lilly hopes to leverage the supercomputer to shorten drug development from years to months, which would help get new medicines to people faster.

For example, with advanced medical imaging, scientists can get a clearer view of how diseases progress, so they can develop new biomarkers for more personalized care.

"The AI industrial revolution will have its most profound impact on medicine, transforming how we understand biology," said Kimberly Powell, Vice President of Health Care at NVIDIA. "Modern AI factories are becoming the new instrument of science — enabling the shift from trial-and-error discovery to a more intentional design of medicines.”

One of the advantages of using AI in drug development is that it reduces the need for testing new medicines on animals, which has long been a sore point for animal rights activists.

"We are getting to the point where we don't actually need to do that (animal testing) anymore,"  Patrick Smith, President of Drug Development at Certara, told Reuters.

Analysts say AI-driven approaches to drug development could cut costs and timelines in half, which could lead to lower drug prices. It currently takes over a decade and $2 billion to bring a new drug to market.

NVIDIA and Lilly did not disclose financial terms of the deal. Lilly said some of NVIDIA’s equipment has already arrived at its Indianapolis data center. Lilly expects the supercomputer to be online by January.

When It Comes to Physical Activity, Resilience Outweighs Chronic Pain

By Pat Anson

It’s not uncommon for someone with chronic pain to reduce their physical activity and become more sedentary. Believing that movement will make pain worse can even lead to kinesiophobia – an irrational fear of physical activity.

But some people with chronic pain are able to remain physically active and cope with their pain – what’s known as pain resilience. Is that because they have less pain or more resilience?

A new study, published in PLOS One, suggests that resilience predicts physical activity more than pain does, and that boosting resilience should be a part of pain management. 

Researchers at the University of Portsmouth in the UK surveyed 172 adult volunteers suffering from mild-to-moderate chronic pain. Their goal was to understand how pain resilience affects the relationship between pain and movement.  

Participants were asked about their pain levels, what kind of physical activities they engaged in, and if they agreed or disagreed with a series of statements such as:

• “I am afraid that I might injure myself accidentally.”

• “My pain would probably be relieved if I were to exercise.”

• “When faced with pain I avoid negative thoughts.”  

• “When faced with pain I get back out there.”

Based on their answers, participants were given scores that ranked their resilience and kinesiophobia levels, which were then compared to their physical activity.

Researchers found that pain resilience predicts physical activity more strongly than pain intensity.

“We suspected resilience plays a major role, and this study helped confirm that,” said lead author Nils Niederstrasser, PhD, Senior Lecturer in Psychology at the University of Portsmouth.

“What we found is that it's not how much pain you're in that determines whether you stay physically active -- it's how you think about and respond to that pain, indicating that how individuals respond to and think about pain matters more than their actual pain sensitivity.”

Niederstrasser and his colleagues believe that treatments focused on building resilience could help chronic pain patients become more physically active. 

“People with greater resilience can maintain a positive attitude and push through discomfort, and this psychological factor is a better predictor of physical activity than pain intensity itself,” said Niederstrasser. “This is a significant shift from historically focusing on negative factors like fear of movement, to understanding the power of positive psychological resilience in managing chronic pain." 

This research builds on another study by Niederstrasser, which found that regular exercise and weight management can reduce pain levels, and may help prevent acute pain from becoming chronic.

Previous studies have found that being physically active boosts pain tolerance, and that light or moderate activities can have a protective effect against certain types of pain.  

Where Pain Research Is Headed and Why I’m Hopeful

By Dr. Lynn Webster

If you live with pain, you’ve probably heard promises that “something better is coming.” At this month’s Pain Therapeutics Summit in San Diego, you could see that promise taking shape. For two days, clinicians, scientists, companies and advocates compared notes on what’s working, what’s not, and what’s next.

Threaded through much of it was the National Institutes of Health’s Helping to End Addiction Long-Term (HEAL) Initiative -- an NIH-wide push launched in 2018 to accelerate better pain care and reduce opioid-related harms.

HEAL exists because of the opioid crisis; Congress gave NIH an initial $500 million in fiscal year 2018 to jump-start a coordinated research plan, and the NIH has since invested several billion dollars to keep the effort moving. In other words, HEAL is a rare silver lining: a tragedy spurring a sustained, practical response.

(The HEAL Initiative was not directly hit by any funding cuts in 2025. However, the Trump administration has proposed cutting the NIH budget by 40% next year, which could potentially impact HEAL funding.)

Since its launch, HEAL has grown into a national engine for discovery. NIH reports a cumulative investment approaching $4 billion, supporting more than 2,000 projects across all 50 states, and helping advance 40-plus new drugs and devices to FDA investigational status.

This is a sign that the pipeline is broader and closer to patients than it has been in years. Think of HEAL as scaffolding: trial networks, shared data standards, and coordinated teams that help good ideas climb faster from lab to bedside.

A decade ago, analgesic research often looked like isolated bets. Today, it feels more like a coordinated campaign. That doesn’t guarantee success, but it raises the odds that something useful will reach doctors and patients.

Just as important, what’s coming isn’t a single “miracle drug” but a wider toolkit. You’ll see more non-opioid medicines designed around the biology of different pain types; safer use of existing tools that can lower the need for higher doses when opioids are used; devices and neuromodulation approaches that calm overactive nerves or brain circuits; smarter drug delivery systems that make treatments last longer or act locally at lower doses; and digital health that captures how people actually live -- including their sleep, activity, and pain flares -- so that care decisions track real life, not just clinic visits.

The studies themselves are changing, too. Many people don’t have just one pain condition; they have overlapping problems. Newer trials are beginning to mirror that reality and to focus on outcomes you can actually experience -- walking farther, sleeping better, and participating more in life -- rather than only chasing a number on a pain scale.

Researchers are also building better signposts, such as biomarkers and other objective measures, to predict who will benefit from which therapy and who may be at risk of long-term pain after injury or surgery.

Signposts aren’t a substitute for what people tell us about their pain. In research and development, objective measures help compare treatments and identify who is most likely to benefit. Once a therapy reaches the clinic, those measures become guides, not verdicts, and should be read alongside the patient’s narrative so that care reflects how the person actually lives and feels.

HEAL has made these shifts a priority by funding large, practical datasets and endpoints that regulators and payers can use.

Here’s the clear-eyed part: many of the drugs and devices discussed at meetings like this will not make it past the investigational stage. That’s how science works. But when trials are well designed and data are shared, today’s misses can more quickly lead to tomorrow’s wins -- and the lessons won’t vanish into a file drawer.

Some analgesic candidates will cross the finish line, and even modest gains -- better sleep, fewer flares, less brain fog, or an extra hour of activity -- can change a life. Across millions of people, small wins add up to something transformative.

What does this mean if you’re living with pain right now? Expect more choices and more personalization. Conversations with your clinician may start to include options that didn’t exist a few years ago, and you may hear about clinical studies built around everyday life rather than rigid clinic schedules. If a trial is a good fit, participating in one will help move the field forward.

Most of all, there’s a reason for hope that is grounded in real progress, not hype.

None of this happened by accident. The NIH HEAL Initiative has been the engine behind much of it -- steady funding, coordination, and a focus on solutions that reach the bedside. Keeping that engine running is how promising ideas become practical relief.

Lynn R. Webster, MD, is a pain and addiction medicine specialist and serves as Executive Vice President of Scientific Affairs at Dr. Vince Clinical Research, where he consults with pharmaceutical companies.

Dr. Webster is the author of the forthcoming book, “Deconstructing Toxic Narratives -- Data, Disparities, and a New Path Forward in the Opioid Crisis,” to be published by Springer Nature. Dr. Webster is not a member of any political or religious organization.

Two-Thirds of Chronic Pain Patients Eat Comfort Foods to Help Them Cope

By Pat Anson

A slice of apple pie or a bowl of ice cream are comfort foods to many people, giving us a mood boost (not to mention a sugar rush) during times of stress, loneliness or anxiety.

For many people with chronic pain, comfort foods are also a way to cope and distract during pain flare-ups. A small study in Australia recently found that over two-thirds of people with chronic pain eat to feel better.

“People who live with pain every day need to find ways of coping. We think about medication, physiotherapy or heat packs as pain management strategies, but we don’t usually think about food in the same way. Yet two-thirds of our sample said they turned to food at least once a fortnight when pain flared,” says lead author Toby Newton-John, PhD, a clinical psychologist and Head of the Graduate School of Health at the University of Technology Sydney (UTS).

“Managing daily pain is incredibly tough, and medication often only goes so far. It’s understandable that people reach for something that feels good.”

The study, Eating to Feel Better: The Role of Comfort Eating in Chronic Pain, was recently published in the Journal of Clinical Psychology in Medical Settings.

Newton-John and his colleagues surveyed 141 adults with chronic pain, asking why they turn to food during pain flares. Given a choice of nine possible answers (and being allowed to select more than one) the results show that over half (51.8%) ate comfort foods to “give myself a pleasant experience,” followed by “distract myself” (49.6%) and “reduce my emotions” (39%).

“That was the somewhat unexpected finding,” Burton said in a press release. “Comfort eating wasn’t just for the purpose of distraction or numbing negative feelings, although those were important too. For many, eating comfort foods provided a nice experience in their day and something to look forward to. If you’re living with pain all the time, that moment of pleasure becomes a pretty powerful motivator.”

To be clear, not everyone in pain eats for distraction or pleasure. Nearly one in five (18.4%) said they tend to eat less when in pain, and a fair number said they eat as usual (11.3%), whether they’re in pain or not.

The frequency of comfort eating ran the gamut from multiple times a day (14.2%) to several times a week (19.9%), to never (18.4%).

The survey did not ask participants what foods they ate, but researchers believe pain can trigger cravings for certain foods.  

“There may also be a biological explanation. Research shows high-calorie foods can have a mild pain-relieving effect. Even in animal studies, rats in pain will seek out sugar. It seems it’s not just psychological. It's possible that there is a real analgesic property to these foods as well,” said co-author Amy Burton, PhD, a lecturer in Clinical Psychology at the UTS Graduate School of Health.

But eating for comfort comes at a cost. Nearly two thirds of participants in the study were obese (29.8%) or overweight (37.6%).  Newton-John warns that food-driven relief can become part of a vicious cycle.

“Short-term, high-calorie food makes people feel better. It reduces pain symptoms and enhances pain tolerance. Long-term, it can fuel weight gain and inflammation, which increases pressure on joints and makes pain worse; and that can trap people in a spiral that’s very hard to break,” he said.

Pain management programs usually focus on medication, physical therapy, and cognitive behavioral therapy. This research suggests a need to integrate diet and nutritional advice into pain management programs.

“We usually teach skills like relaxation, stretching exercises or how to pace activities, but we rarely talk about food in this context,” Newton-John says. “This work shows we need to help people recognise if they’re using food as a pain-management tool and give them alternatives.”

Previous studies have shown that healthy eating can reduce the severity of chronic pain. Regular consumption of vegetables, fruit, lean meat, fish, legumes/beans, and low-fat dairy products can lower pain levels and improve physical function, especially for women.

High fiber diets also reduce the risk of obesity, diabetes and cardiovascular disease, while promoting the growth of healthy bacteria in the gastrointestinal system to slow the progression of arthritis and reduce joint pain.

Magic Mushrooms May Relieve Chronic Pain and Depression

By Crystal Lindell

A new study shows that psilocybin, the active ingredient in what’s colloquially called magic mushrooms, could help relieve chronic pain and depression by targeting specific parts of the brain — at least in mice.

Psilocybin is a naturally occurring alkaloid with psychoactive properties that’s been used for pain relief for thousands of years. In the United States, however, it is classified as an illegal Schedule One controlled substance. 

Researchers at the Perelman School of Medicine at the University of Pennsylvania tested psilocybin on laboratory mice with chronic nerve injury and inflammatory pain.

They found that a single dose reduced both pain, anxiety and depression in the mice, judging by their behavior. The benefits lasted almost two weeks.

Unlike many pharmaceuticals, researchers say psilocybin gently activates specific nerves in the brain, called serotonin receptors.

“Unlike other drugs that fully turn these signals on or off, psilocybin acts more like a dimmer switch, turning it to just the right level,” lead author Joseph Cichon, MD, an assistant professor of Anesthesiology and Critical Care at Penn, said in a press release.

”This new study offers hope. These findings open the door to developing new, non-opioid, non-addictive therapies as psilocybin and related psychedelics are not considered addictive.”

To pinpoint where the effects originated, researchers injected psilocin — the active metabolite that the body rapidly converts from psilocybin — into different parts of the mice’s central nervous system. The team then used advanced fluorescent microscopy, a technique that uses glowing dyes to detect nerve activity, to see which neurons are activated and firing.

When psilocin was injected directly into the prefrontal cortex of the brains of the mice, it provided the same pain relief and mood improvements as when psilocybin was given to the whole body. But when researchers injected psilocin into the spinal cords of the mice, they found that it didn’t have the same calming effect.

“Psilocybin may offer meaningful relief for patients by bypassing the site of injury altogether and instead modulating brain circuits that process pain, while lifting the ones that help you feel better, giving you relief from both pain and low mood at the same time,” said Cichon.

Researchers hope their findings, published in the journal Nature Neuroscience, could help spur advancements in treatments for other conditions, such as addiction or post-traumatic stress disorder.

Cichon says more research is needed to determine the effectiveness of psilocybin.

“In my anesthesiology practice, I often see that both pain and mood symptoms can worsen following surgery due to the physiological and psychological stress imposed by the procedure,” he said. “While psilocybin shows promise as a treatment for both pain and depression, it remains uncertain whether such therapies would be safe, effective, or feasible in the context of surgery and anesthesia.”

The Penn team plans further studies to investigate dosing strategies, long-term effects, and the ability of the brain to re-wire itself through the use of psilocybin.

“While these findings are encouraging, we don’t know how long-lived psilocybin’s effects are or how multiple doses might be needed to adjust brain pathways involved in chronic pain for a longer lasting solution,” said co-author Stephen Wisser, a PhD student in Cichon’s lab.

While the DEA considers psilocybin an illegal substance with no accepted medical use, Oregon and Colorado have legalized it for supervised therapeutic use. Several cities in California, Michigan, Minnesota, Washington and Maine have also decriminalized it. And efforts are underway to change psilocybin’s federal status. 

The Food and Drug Administration has granted a breakthrough therapy designation to psilocybin to expedite research and drug development. Over 60 scientific studies have shown the ability of psilocybin and other psychedelics to reduce pain from fibromyalgia, cluster headache, complex regional pain syndrome (CRPS) and other conditions.

How Much Is Your Pain Worth?

By Crystal Lindell

How much pain would you be willing to endure if someone paid you?

That’s the question an international team of researchers posed in an unusual new study looking for an alternative to the 1-10 pain scale.

In a series of experiments, they offered 330 healthy volunteers in Switzerland money to undergo mild electric shocks, heat pain or no pain at all. Someone opting for a painful stimulus was paid about $20, while those who opted for having no pain received only $10.

The idea behind putting a price on pain was to see if the responses would be a better way to measure pain than the subjective and much criticized pain scale, which has been used for decades to have patients self-evaluate their pain levels.

“We’ve all been asked to rate our pain from one to ten—but one person’s three might be another’s five, and those numbers can shift with experience. Our research proposes a better way: turning pain into money — not to commodify suffering, but to create a scale we can all share,” explained lead author Carlos Alós-Ferrer, PhD, a Professor of Economics at Lancaster University Management School in the UK. 

The study findings, published in the journal Social Science & Medicine, suggest that people’s willingness to accept money in exchange for pain is a more reliable way to measure discomfort than self-reported methods.

Researchers say their economic incentives “greatly outperformed” traditional pain scales. It helped them distinguish more clearly between different levels of pain; detect the effects of pain relief more consistently; and allowed for more meaningful comparisons between people.

Interestingly, no participant chose to avoid pain completely. Everyone had a price for pain if it was high enough.  

Different people put different prices on the same pain, but they had an easier time rating their pain than they did when using the 1-10 pain scale.

“As a result, measurements are more precise and the shift from low to high levels of pain is clearly reflected in the monetary scale,” Alós-Ferrer said. “This makes it useful for clinical trials to study the effectiveness of painkillers and treatments, because participants are randomly assigned to different groups.”

I believe if a money-incentivized pain scale is used only for research studies, it might be useful. Afterall, there is definitely a need for more accurate pain measurements in research, as well as treatment.

However, my concern is that it could be misused in a clinical setting, just like the pain scale is. Researchers said “inaccurate pain measurements can lead to inadequate pain management,” and pointed to emergency medical situations and quality of life issues for people with chronic pain.

However, in most cases, the reason pain is not adequately treated has nothing to do with the pain scale. It’s because doctors tend to dismiss people’s pain and then withhold one of the most effective treatments: opioids.

I’ve written before about why I don’t like the 1-10 pain scale, which doctors tend to ignore even if you say your pain is a 10. But I don’t think replacing it with a question about how much money you’d need to endure more pain is the answer.

Rather, the best solution I’ve seen from a patient perspective — at least when it comes to chronic pain — is a scale that asks how pain is impacting daily life activities, known as the Quality of Life Scale, (QOLS).

It's a reverse of the traditional pain scale, in that 0 is the worst pain, while 10 means you're doing pretty well.

It features descriptions like:

0: Stay in bed all day. Feel hopeless and helpless about life.

1: Stay in bed at least half the day. Have no contact with the outside world.

All the way up to:

10: Go to work/volunteer each day. Normal daily activities each day. Have a social life outside of work. Take an active part in family life.

While QOLS probably isn’t ideal for studies on acute pain, it is a great way to communicate pain levels between patient and doctor. In fact, I’d say it’s significantly better than trying to assign a monetary value to pain.

Because as anyone with severe chronic pain will tell you, there’s not enough money in the world to make me want to endure my pain even one second longer than I need to.

Many Older Adults With Chronic Pain and Poor Health Can Regain Wellness

By Pat Anson

“You’re not getting older, you’re getting better.”

There’s some truth behind that cliché about growing old, according a novel study in Canada that found many older adults in poor health -- due to chronic pain and other chronic conditions -- can fully recover within just a few years.

“This isn’t just a story of resilience — it’s a roadmap for how we can help more older adults recover and thrive,” says first author Mabel Ho, PhD, a researcher at the Factor-Inwentash Faculty of Social Work at the University of Toronto. “Our findings highlight the powerful role of modifiable lifestyle and psychosocial factors in shaping healthy aging trajectories.”

Ho and her colleagues followed 8,332 respondents who were 60 years of age or older and in poor physical or mental health. Nearly one in five (18.7%) had chronic pain so severe it was considered disabling, while others had chronic illnesses such as diabetes, heart disease, hypertension, arthritis and osteoporosis.

Not surprisingly, many of the participants also felt depressed, unhappy, slept poorly, and led isolated lives with few social connections.

Their baseline health status at the start of the study was then compared to their physical and mental health after 3 years, to assess whether they had achieved “optimal well-being” – meaning they had no disabling pain, discomfort or limitations on daily activities, as well as good mental health, happiness and life satisfaction.

The research findings, published in PLOS One, show that nearly one in four older adults regained optimal well-being within just three years.

The researchers then sought to identify what factors increased the likelihood that older adults could recover their physical and mental health. Those who reported strong psychological and emotional wellness at the outset of the study were over five times more likely to achieve the high bar of “optimal well-being” when compared to those who struggled with their mental health.

Other factors significantly associated with recovery include a healthy body weight, regular physical activity, good sleep, not smoking, and participating in social activities.

“It’s incredibly encouraging to see that with the right supports and lifestyle, many older adults can reclaim full health, happiness, and independence -- even after serious health challenges,” says Ho.

The study suggests that age-related policies and programs should prioritize physical and mental wellness, to help show that recovery is not only possible for older adults, but common.

“Too often, the focus in aging research and geriatric practice is on decline and disability,” says senior author Esme Fuller-Thomson, PhD, Director of the Institute for Life Course & Aging at the University of Toronto. “Our findings disrupt that narrative. Older adults can and do bounce back—and we need to build systems that support recovery.”

By the end of the study, over 19% of those who had chronic disabling pain had achieved optimal well-being, while nearly 10% of those whose daily activities were limited progressed to no limitations. Over 12% of those who rated their physical health as poor to fair at the start of the study achieved a full recovery.   

Other factors strongly associated with optimal well being were higher education, home ownership, higher income, marriage, and having someone to show love and affection.

“We want this study to reshape how society views aging,” added Ho. “With the right environment, resources, and supports, older adults don’t just survive after struggling with health or well-being issues— they thrive.”

The study did not evaluate what medications or therapies helped older adults recover their health.

Childhood Trauma Raises Risk of Chronic Pain and Other Health Problems in Adults

By Crystal Lindell

A new study has found links between childhood trauma, chronic pain and several health problems in adults, according to research published in JAMA Network Open. 

Many previous studies have found that adverse childhood experiences (ACEs) increase the risk of chronic pain in adulthood. This study goes further, finding links between ACEs and severe pain, poor mental health, back and hearing problems, gastrointestinal issues, and hypertension at age 50.

However, it remains unclear how much of that association may be causation and how much is simple correlation. There is also a very real concern that the study will add to the stigma that chronic pain patients already face in the medical community. 

The research, which was conducted by a team of scientists at the University of Aberdeen, followed over 16,000 participants in the UK who were enrolled in the National Child Development Study.  All were born during one week in 1958 in England, Scotland or Wales, and were interviewed when they turned 50.

Researchers asked about their current health and whether they experienced any childhood trauma, such as abuse, neglect, bullying, divorce and financial stress, or if they had witnessed substance abuse, criminal activity or mental illness in their family.

While most studies report associations between ACEs and a single health outcome, researchers say this is the first research to look at a broad range of health outcomes.

They found that mental health problems and severe pain in adults had the strongest connections to childhood trauma. Men and women who experienced childhood adversity were more likely to suffer from depression, anxiety, and chronic pain at 50. 

Women who had an ACE were also more likely to have digestive problems, asthma or bronchitis compared to women who did not experience childhood trauma.

It’s important to note that the “higher risk” was often marginal, at best. For example, while 8.7% of men who experienced childhood trauma had severe pain at 50, that compares to 4.88% of men with severe pain at 50 who did not have an ACE. That’s just a 4% difference.

The same is true for women. Researchers found that 11.22% of women with childhood trauma had severe pain at 50, compared to 7.53% of women with no history of ACE. Again, just a 4% difference. Most researchers look for at least a 5% difference before calling an outcome “statistically significant.”

Little or no association was found between ACEs and migraine, hay fever or rhinitis, eyesight problems, or skin problems. 

Researchers found that the more trauma experienced, the greater the impact on health at age 50. People who experienced four or more types of childhood adversity had the highest risk of developing health problems as adults. Abuse, neglect, and family conflict had the most wide-ranging consequences. Just one adverse childhood event was found to increase the risk of dying before age 50.

The research was partly funded by Versus Arthritis, the UK’s largest charity supporting people with arthritis.

"This important research highlights the strong relationship between early childhood adversity and severe pain in adulthood. Findings suggest that our earliest experiences may be driving the health inequalities we know exist for people living with chronic pain,” Deborah Alsina, CEO of Versus Arthritis, said in a press release.

"Tackling childhood adversity is vital if our governments are serious about reducing the burden of chronic pain for the next generation."

Early Intervention and Prevention

Researchers say the study highlights the importance of preventing childhood trauma and providing early support to at-risk families.

"Going forward, screening for ACEs in primary care settings, and targeted interventions for at-risk individuals, may help reduce the burden of chronic pain, mental ill-health, and other poor health outcomes,” said lead author Gary Macfarlane, PhD, Chair of Epidemiology at the University of Aberdeen.

"While 'broad spectrum' interventions remain important to ameliorate the impact of ACEs, a targeted approach, considering types of ACE, could address specific vulnerabilities — particularly mental ill-health and severe pain.”

That’s an important goal, but for adults already suffering from health issues that could be linked to childhood trauma, that doesn’t offer much help. 

In the real world, studies like this are very often used to dismiss the health problems people suffer. That's especially true for chronic pain. 

Patients are often told their pain was caused by childhood trauma, and doctors use that as an excuse to invalidate their symptoms and withhold treatments like opioid pain medication. This gets especially frustrating when a history of childhood trauma is then used to claim that a patient is more likely to abuse opioids. 

Many doctors seem to believe that if childhood trauma is the direct cause of a health issue, then the only real treatment is mental health services. This can contribute to the stereotype that chronic pain is “all in your head” or that patients are “just looking for attention.”

There is also the question of causation vs correlation. For example, many health conditions are hereditary, including those that cause chronic pain, like arthritis and Ehlers-Danlos Syndrome.

Parents who grew up with those health problems may be more likely to have negative experiences with their children. Chronic pain drains time, money and energy, which then impacts someone's ability to be a present parent. So a parent with chronic pain may be more likely to neglect their child, not out of malice but out of necessity, as they deal with their own health issues. 

Then when the child grows up and has chronic pain, it seems like it could be related to childhood trauma when it may be actually be a case of simple genetics. 

While it is important to find better ways to respond to children who have experienced trauma, it’s also important that such research is not used to dismiss adults dealing with health issues. For many adults, the current trauma of living with chronic pain is more pressing than what they experienced in childhood. 

Chronic Pain Surged in U.S. After Pandemic

By Pat Anson

Rates of chronic pain and disabling pain surged in the United States after the Covid pandemic, reaching the highest levels ever recorded, according to a new study.

In 2019, about 20.5% of Americans (50 million people) had chronic pain and 7.5% had high-impact pain, which is pain strong enough to limit daily life and work activity.

Pain prevalence remained stable during the pandemic, and by some measures even declined, but in 2023 the chronic pain rate surged to 24.3% of Americans, while high-impact pain rose to 8.9% of the population.

That brought the total number of people who have chronic pain to 60 million, with 21 million having high-impact pain.

“We found that chronic pain, already a widespread health problem, reached an all-time high prevalence in the post-pandemic era, necessitating urgent attention and interventions to address and alleviate this growing health crisis,” wrote co-authors Anna Zajacova, PhD, at Western University in Ontario and Hanna Grol-Prokopczyk, PhD, at the University of Buffalo..

The study is based on results from the 2019, 2021 and 2023 National Health Interview Surveys (NHIS), a federal survey conducted every two years. A preprint of the study was released last year and has now been published in the peer-reviewed journal PAIN.

The 2023 surge in pain was observed in all age, gender, racial/ethnic groups, education levels, and in both rural and urban areas.

Pain increased in almost all body areas, including the back and neck; arms, shoulders and hands; hip, knees and feet; headache or migraine; and in the abdominal, pelvic, and genital areas. The lone area where pain declined was in the jaw or teeth.

Why did pain increase after the pandemic, but not during the pandemic — when people saw doctors less often and postponed or cancelled many health procedures?

One possible explanation is that Covid relief payments, expanded unemployment benefits, and eviction moratoriums eased financial stress.

Working from home and commuting less also lessened physical demands, while giving remote workers more opportunities for self-care.

PAIN journal

“The big question is why we saw this substantial increase in pain prevalence after the pandemic. We examined the role of long COVID and found that it explained about 13% of the increase,” said Grol-Prokopczyk. “None of the other measures we examined — including changes in income or physical health conditions — explained the increase.

“We speculate that abrupt termination of pandemic-era policies, such as remote work arrangements and expanded unemployment benefits, may have played a role.”

In addition to long Covid, researchers also noted an uptick in rates of health conditions that can cause pain, such as arthritis, cancer, cardiovascular disease, diabetes, depression, and anxiety.

The finding of an increase in pain rates conflicts with an FDA analysis that predicted the “medical need” for hydrocodone, oxycodone and other pain relieving Schedule II opioids would decline by 5.3% in 2023. The FDA also predicted a 7.4% decline in the medical use of opioids in 2024 and a 6.6% decline in 2025.

Those FDA projections are important because they are used by the DEA to establish annual production quotas for opioids, which have fallen for nine consecutive years. Since 2015, the DEA has reduced the supply of oxycodone by 68% and hydrocodone by 73%.

When short-term, acute pain is poorly treated, it can have long-term consequences for patients who may transition to chronic pain. Healthcare visits for non–Covid health issues declined dramatically in 2020 and 2021, particularly at hospitals and emergency departments, which are often the first site of care for acute pain management.

Researchers say the lack of adequate and timely pain management during the pandemic may have contributed to more people having chronic pain and high-impact pain in 2023.

“These findings highlight the importance of expanded epidemiological and clinical research on chronic pain to better understand population-level drivers of pain, and to improve national pain prevention and treatment efforts for the many Americans at risk of or affected by pain,” said Grol-Prokopczyk.

Brains Control Pain Differently, Depending Where It’s Felt

By Crystal Lindell

Different parts of the brain are more active when relieving pain — depending on where the pain originates — according to a new Australian study. The finding could lead to more targeted and effective treatments that utilize the body’s own pain relief system.  

Researchers  at the University of Sydney made the discovery while studying the placebo effect. They used MRI brain scans to monitor 93 healthy participants, while exposing them to painful heat on various parts of the face, forearm and leg. 

Before the test, participants were given a placebo analgesic cream and told it would help relieve their pain. In reality, the “lidocaine” cream was a placebo and researchers secretly lowered the temperature of the heat, tricking the participants to believe the cream was easing their pain. 

The heat stimulus was applied to the placebo-treated area, as well as a separate untreated area for comparison. Up to 61% of participants reported less pain in the area where the cream was applied, typical of a placebo response.

The MRI scans showed how the brain responded to the placebo effect. Researchers found that upper parts of the brainstem were more active when relieving facial pain, while lower regions of the brainstem were engaged for arm or leg pain. 

“This is the first time we’ve seen such a precise and detailed pain map in the human brainstem, showing us that it tailors pain relief to the specific part of the body that’s experiencing it,” lead author Lewis Crawford, PhD, a Research Fellow at the University of Sydney, said in a press release. 

Understanding which brainstem areas are linked to different parts of the body may open new avenues for developing non-invasive therapies that reduce pain.   

“The brain’s natural pain relief system is more nuanced than we thought,” said Crawford. “Essentially, it has a built-in system to control pain in specific areas. It’s not just turning pain off everywhere; but working in a highly coordinated, anatomically precise system.”     

“We now have a blueprint for how the brain controls pain in a spatially organised way,” said senior author Luke Henderson, PhD, a Professor in the School of Medical Sciences and the Brain and Mind Centre. “This could help us design more effective and personalised treatments, especially for people with chronic pain in a specific area of their body.”

It is important to note that none of the “healthy” participants had chronic pain, and thus these results may only apply to short-term, acute pain that is treated with a placebo.

Nevertheless, the study challenges long-held assumptions about how pain relief works. Instead of relying on medications that target opioid pain receptors in the brain, researchers say receptors in the brainstem could be targeted with cannabinoids. 

“Opioid-based pain relief typically activates central areas of the brain and can affect the whole body, whereas the cannabinoid circuit that we identified appears to operate in more targeted regions of the brainstem,” said Crawford. “This supports the idea that cannabinoids may play a role in localised, non-opioid pain control.”

Most oral pain medications today – including acetaminophen, ibuprofen and opioids – work by telling the brain to relieve pain throughout the entire body. This research opens the door to more targeted therapies that relieve pain in specific parts of the body.

When Headlines Lie: Misleading News About Opioids and Chronic Pain

By Neen Monty

The headline in Physician’s Weekly screams alarm:

“Rising Use of Potent Opioids in Chronic Pain Management”

And then the sub heading:

“Long-term opioid use for chronic pain doubled, with potent opioids rising, underscoring the need for stronger guideline adoption”

Terrifying, right? We must do something!

But now, read the article. It’s based on a study recently published in the European Journal of Pain on the prevalence of long-term opioid therapy (LTOT) when treating patients with chronic non-cancer pain.

The Dutch study looked at opioid use over a ten-year period, from 2013 to 2022, using a large dataset drawn from primary care records in the Rotterdam region. This database covered more than half a million patients and included data from over 240 general practitioners.

The researchers focused on adults aged 18 and over who had been prescribed opioids continuously for at least three months. They tracked how common LTOT was over time, and also explored which diagnoses, co-existing conditions, and other medications were associated with it. They reported their findings using basic descriptive stats and calculated LTOT prevalence per 100 patient-years to show trends over the decade.

And what did they find?

“The prevalence of LTOT increased twofold from 0.54% (95% CI: 0.51–0.58) per 100 patient years in 2013 to 1.04% (95% CI: 1.00–1.07) in 2022. The proportion of LTOT episodes solely involving potent opioids slightly increased between 2013 and 2022”

In plain English, the prevalence of long-term opioid use by patients at the end of the study was just over 1%.

Yes, that’s right: 1%.

And the prevalence increased by just half a percentage point over a decade.

Hardly a crisis. Hardly anything to scream about.

But we can’t have that! We need a clickbait headline to demonize opioids and stop their prescribing! So, instead of reporting accurately on the very small increase in opioid prescribing, they focus on the “twofold” increase. Trying to manufacture a crisis where there is none.

It’s true, the prevalence of LTOT did double, from half a percent to one percent. And that’s what the headline highlighted, to try and make it sound like there is an opioid crisis in Europe. There is not.

This tactic is often used in presenting medical research – using relative percentages rather than the actual numbers. That is because relative percentages -- “Opioid Use Doubled!” -- sounds worse than “Opioid Use Increased by Half a Percent.”

It’s a trick that researchers and the media use all the time.

Why do this? It’s dishonest. It’s deceptive. And it destroys our trust in science. They are trying to manufacture a crisis when there is none.

Why not research and report an actual crisis? Instead of making one up?

The Physician’s Weekly headline exemplifies the worst of scientific spin: inflating tiny fractional changes and omitting context. It potentially harms patients by reinforcing the myth that opioids don’t work long term and should be withheld. That myth persists because of misleading reporting like this.

Finally! An Honest Headline

It was nice to see some accurate reporting in Scimex, an Australian online news portal that tries to help journalists cover science. Instead of the usual deceptive, sensationalist headlines, this one tells the truth:

“Pain Reprocessing Therapy (PRT) could help those with mild chronic back pain”

This was so refreshing to see! Because it’s so very, very rare.

Most reporting on PRT glosses over a critical point: It has only been studied in people with mild, non-specific back pain. An average of 4 on the zero-to-10 pain scale.

That nuance is often lost in the hype about alternative treatments like PRT, cognitive behavioral therapy, mindfulness and TENS.

You do not treat 8/10 back pain the same way you treat 4/10 back pain.

What happens when people are misled about PRT? It gets recommended to people with severe, pathological pain — often with clearly identifiable causes — and everyone acts surprised when it doesn’t work.

Let’s be clear:

• PRT is not for severe back pain

• PRT is not for pain caused by pathology

• PRT is not a cure-all

But you wouldn’t know that from most headlines about PRT, such as “New therapy aims to cure back pain without drugs, surgery” and “A New Way to Treat Back Pain.”

Then you read the small print: All the participants in PRT studies had non-specific back pain from an unknown cause. And they had mild pain.

The researchers are often complicit, cherry-picking and hyping their own data. Why? Because they need funding. Because they’re writing a book. Because professors have to "publish or perish" to keep their jobs. Because it’s easier to mislead the public than to admit a therapy has limits. And you don’t get to be a guru if your therapy only works for a minority of patients with mild pain.

This kind of spin harms people with severe chronic secondary pain. It feeds the narrative that if you're still in pain, then it’s your fault. You didn’t try hard enough. You’re catastrophizing. You need to retrain your brain.

It feeds the stigma that all chronic pain is mild and easily curable. And that anyone who says their pain is severe has psychological problems.

No. Maybe their pain is caused by pathology, like tissue damage or herniated discs. Maybe their pain is nociceptive or neuropathic.

This is why chronic pain patients must be included on every research team. Someone with real-world, high-impact chronic pain would never let this kind of misrepresentation slide. And the rest of the team wouldn’t be able to claim ignorance.

We need more honesty and integrity in research and the media. We need headlines that reflect the actual findings. We need conclusions that match the data, not some predetermined narrative. Right now, most media coverage doesn’t even try.

Read the study, then read the headline. They rarely match. That’s how we ended up with a generation of healthcare providers who think opioids are bad, all chronic pain is primary pain, and that PRT is some miracle therapy.

It’s not. PRT may be helpful to people who are depressed or have anxiety, but should not be a first-line treatment for everyone. It’s only been tested in people with mild back pain for which there is no known physical cause. It has not been shown to work for people with severe pain or structural pathology.

But the researchers usually gloss over that. And the headlines and conclusions rarely reflect those facts or spell out who PRT is for and who it is not for.

Because here’s the truth: Pain Reprocessing Therapy is not a treatment for chronic pain. It’s a treatment for anxiety and depression.

That’s the real headline.

Neen Monty is a patient advocate in Australia who lives with rheumatoid arthritis and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), a progressive neurological disease that attacks the nerves.

Neen is dedicated to challenging misinformation and promoting access to safe, effective pain relief. She has created a website for Pain Patient Advocacy Australia to show that prescription opioids can be safe and effective, even when taken long term. You can subscribe to Neen’s free newsletter on Substack, “Arthritic Chick on Chronic Pain.”