Sounds Are More Intense When You Have Chronic Pain

By Crystal Lindell

Throughout the day, whenever I hear something particularly high-pitched or loud, I will often turn to my fiancé and say, “Turn it down. That sound is literally causing me pain.”

He always obliges, but I know he’s skeptical. And I understand that my complaint doesn’t really make sense. 

However, new research seems to support my experience.

A study at the University of Colorado Anschutz School of Medicine, published in the Annals of Neurology, found that people with chronic pain are significantly more sensitive to sound.

For the study, researchers recruited 142 adults with chronic back pain and 51 healthy people who were pain free. While receiving MRI brain imaging, both groups had mechanical pressure put on their bodies to stimulate pain, while being subjected to annoying sounds. Participants were then asked to rate how unpleasant the experience was.

The differences in responses between chronic pain patients and healthy controls was significant. On average, back pain sufferers reacted more strongly than 84% of people without pain.

The researchers also looked at brain activity during the experiments. The MRI scans showed stronger responses in brain regions that process sound (the auditory cortex) and emotional sensations (the insula). There was lower activity in regions that normally help calm or regulate emotions, like the medial prefrontal cortex.

Interestingly, the results overlap with other studies showing how patients with fibromyalgia react to painful stimuli.

"Our findings validate what many patients have been saying for years, that everyday sounds genuinely feel harsher and more intense. Their brains are responding differently, in regions that process both the loudness of sound and its emotional impact,” said senior author Yoni Ashar, PhD, Co-Director of the Pain Science Program at the Anschutz School of Medicine. 

“This tells us chronic back pain isn't just about the back. There's a broader sensory amplification happening in the brain, and that opens the door for treatments that can help turn that volume down." 

The researchers wanted to see which treatments could help reduce the brain’s response to noise. The pain patients were broken up into three groups that received either Pain Reprocessing Therapy (PRT), a placebo saline injection, or the usual care they were already getting for back pain. 

PRT is a type of mindfulness therapy, in which patients are encouraged to think differently about their pain in order to minimize it.

Out of all the treatments, PRT was the most effective. It reduced the heightened brain response to sound and increased activity in brain regions involved in regulating unpleasant experiences. But the effect was only minimal.

"These findings add to growing evidence that chronic back pain is not just a problem in the back. The brain plays a central role in driving chronic pain, by amplifying a range of sensations – such as sensory signals from the back, sounds and likely other sensations as well," said Ashar.

Overall, it’s great to see research like this validating what I know is a common experience for chronic pain patients.  

However, I do think there may be some “chicken and the egg” issues with this study. Which comes first: sensitivity to sound or back pain?

Maybe people who are more sensitive to sound are more likely to develop chronic pain. In other words, does the pain cause sound hypersensitivity, or does hypersensitivity cause the pain? 

Ashar and his research team plan further studies of senses other than hearing — such as light, smell or taste — to see if chronic pain causes sensitivity to those stimuli and how brain regions respond to them.

Many Rotator Cuff Surgeries May Be Unnecessary

By Pat Anson

Since I write about chronic pain and the many different treatments for it, it’s not uncommon for readers to ask if I’ve ever experienced it myself.

The answer, unfortunately, is yes. 

About 15 years ago, I started feeling a dull pain in my left shoulder that wouldn’t go away. It progressively grew worse, and my arm became so painful to move that I had trouble putting on a shirt or sleeping in the same position for more than a few hours. 

Only then did I finally see a doctor. An MRI confirmed there was a “wrinkle” in my rotator cuff,  and that the ligaments, muscles and tissue in my shoulder were inflamed. I had adhesive capsulitis, also known as a “frozen shoulder.” 

The doctor gave me a cortisone shot and prescription strength ibuprofen, and when neither of them helped, he recommended rotator cuff surgery or physical therapy. I opted for the latter. 

Everyone thinks their lived experience with pain is unique, and I’m no different. But it turns out my experience with shoulder pain is all too common and is likely a normal part of aging. 

According to a new study in JAMA Internal Medicine, almost everyone over the age of 40 will experience a rotator cuff injury.

Using MRI images, researchers in Finland studied the shoulders of over 600 people between the ages of 41 and 76. Although only 1 in 6 had complaints of shoulder pain, virtually everyone had a rotator cuff injury of some kind, ranging from a full tendon tear to age-related joint damage.

The findings challenge the value of advanced imaging like MRIs, which may be diagnosing shoulder problems that don’t need fixing — or at least don’t need to be treated with invasive injections and surgeries.

“In this population-based study, RC (rotator cuff) abnormalities were nearly universal after age 40 years and showed poor concordance with shoulder symptoms,” wrote lead author Thomas Ibounig, MD, an Orthopaedic Surgeon at Helsinki University Central Hospital.

“These findings suggest that RC abnormalities often represent normal age-related changes rather than disease and call into question the clinical value of routine imaging for atraumatic shoulder pain.”

Ibounig and his colleagues found that many people can have inflamed tendons (tendinopathy), full tendon tears (FTTs) and partial tendon tears (PTTs) in their shoulders without experiencing pain or any other symptoms. Only when they get medical imaging are the rotator cuff abnormalities found, which sets in motion a process that can lead to invasive treatments. 

About half a million rotator cuff repairs are performed annually in the United States, with the surgeries increasing at a rate of about 2% a year for patients 50-64 years of age. Their success rate is mixed, from about 90% for PTTs to as low as 50% for FTTs. Full recovery from rotator cuff surgery may take several months to a year. 

The Finnish study suggests that many of those surgeries are unnecessary and that shoulder pain should be accepted as a normal part of aging.  

“Given that tendinopathy, PTTs, and even FTTs may be incidental findings, clinicians should consider their high population prevalence when interpreting imaging results and deciding on interventions targeting these abnormalities. Reframing many of these findings as normal age-related changes rather than disease may help guide more appropriate care and reduce unnecessary interventions,” they concluded.

It took several months of physical therapy before my shoulder pain subsided. It still aches occasionally, but I no longer have the sharp stabbing pain that I used to get. And it’s no longer chronic.

I still use the stretches and exercises that I learned during physical therapy to keep my left shoulder from “freezing” again. It’s a good thing I learned how to do them, because now my right shoulder aches too. 

Why Are Women More Likely to Have Chronic Pain? Blame Hormones

By Crystal Lindell

Chronic pain typically lasts longer for women than men, and new research suggests hormones could be to blame. That’s according to a study at Michigan State University, published in Science Immunology. 

We’ve known for some time that women are more likely to have chronic pain, and that is likely because it takes longer for their pain to resolve. Acute pain becomes chronic when it lasts longer than three months. 

The researchers looked into the potential causes of this phenomenon, and found that differences in hormone-regulated immune cells, called monocytes, seem to be the culprit.

A subset of monocytes releases a molecule – called interleukin-10 or IL-10 – that can “switch off” pain. Those cells are more active in males because of higher levels of sex hormones such as testosterone. Females, however, experienced longer-lasting pain and delayed recovery because their monocytes were less active.

When the team tested their theory on laboratory mice, they discovered the same pattern they saw in human patients. They performed five different tests on the mice to make sure what they saw wasn’t an anomaly. Each time, the results were the same.

“The difference in pain between men and women has a biological basis,” lead author Geoffroy Laumet, an associate professor of physiology at MSU, explained in a press release. “It’s not in your head, and you’re not soft. It’s in your immune system.

“This study shows that pain resolution is not a passive process. It is an active, immune-driven one.”

These findings could mean those immune cells can be manipulated into producing more signals to calm pain.

Laumet hopes this research could one day help millions of people experience relief with non-opioid treatments — and ensure women’s pain is taken more seriously. Such treatments could help acute pain resolve faster, instead of relying on analgesics to block pain signals.

The next step is to investigate how treatments could target this pathway and boost IL-10 production, although Laument admits that could take years. 

“Future researchers can build on this work,” Laumet said. “This opens new avenues for non-opioid therapies aimed at preventing chronic pain before it’s established.”

In the meantime, hopefully this type of research will encourage medical professionals to believe women when they say their pain is not going away. 

The MSU study was funded by the National Institutes of Health and the Department of Defense.

Exercise Is Hard for Me. Now I Know Why

By Madora Pennington

Exercise is difficult for me. I’m lucky I can do it at all. I am extremely double-jointed because my tendons and ligaments are excessively stretchy as a result of hypermobile Epstein-Danlos Syndrome (hEDS), a connective tissue disorder I was born with.

When I play sports, go the gym or even swim, I see others moving with an ease that is out of my reach. I wonder what exercise feels like for them. I get so worn out — and no matter how fit I get — this does not change. What exactly is different about exercise for me, I never fully understood.

I am hardly alone. Here are some typical comments in online support groups from people with hEDS or Hypermobility Spectrum Disorders (HSD) looking for advice on exercise:

“I try now and then to walk on the treadmills for a slow 20 min, but it just makes me feel worse.”

“I’m 27. When I exercise, I get migraines and all over muscle tension. I always fail at physical therapy. My body does not respond like others.”

“Exercise intolerance hardly describes it. I can’t keep up with my peers. I have severe pain and fatigue. If I exercise, pain starts in my legs, builds and becomes intolerable.”

“I went to Disneyland. I couldn’t stay more than two hours before I was in so much pain, I could barely make it to the car.”

Recently, Canadian researchers published a study on the mechanics of walking in people whose joints are loose to better understand why it might be so painful and exhausting for them. They compared 11 hypermobile adults with 11 healthy (non-hypermobile) adults of the same age and gender, and found why walking can be such an arduous affair for those of us with loose joints.

Tendons and ligaments — the connective tissue that connect bones to bones and muscles to bones — should be like tight rubber bands. They should bend, but not stretch. Part of their job is to transfer force and energy like a coiled spring back to muscles.

When tendons and ligaments are stretchy or hypermobile, not only do they fail to hold joints in place, they cannot return unused energy back to the muscles to power more movement. Simply moving a body with loose joints is, in fact, a very big problem.

To understand the difference between the two groups, study participants had ultrasound images taken of their legs, the stiffness of their Achilles (ankle) tendon measured, and their ankles’ range of motion recorded. They walked on a treadmill and had their oxygen consumption and muscle electrical activity measured.

The results showed that if you are double-jointed:

• Your muscles have to shorten excessively to compensate for too much “give” in the tendons. This is extra work for a muscle that does not enhance performance.

• A stretchy tendon cannot send energy back to the muscle, so energy is drained, not recycled back into the system, even as muscles are working harder.

• Neighboring joints and muscles have to participate in walking in ways they normally would not to compensate for the lack of stability. That’s yet another energy drain.

In short, researchers found that each step takes more energy, and is less powerful and less efficient. That’s why walking with loose joints can be so exhausting and painful.  

“In this investigation, people with HSD/hEDS showed a significantly higher energy cost of walking and lower muscle strength. These differences were accompanied by significantly higher ratings of pain and higher muscle coactivation during stance following walking at, above and below their preferred walking speed,” researchers concluded.

Individualized physical therapy or gait training designed for people with hypermobility could help them become better walkers. After all, mobility —  being able to get around and do things for yourself — provides quality of life and better health. Good mobility also reduces the likelihood of falling injuries. 

While increasing strength and physical fitness won’t solve hypermobility issues, it can make exercise safer, less of an effort, and more enjoyable.

Can Fentanyl Be ‘Rewired’ to Make It Safer?

By Pat Anson

Scientists at Scripps Research have found a way to change fentanyl’s molecular structure to reduce the risk of overdosing, while at the same time preserving its pain-relieving properties. 

The findings, published in the ACS Medicinal Chemistry Letters, suggest that next-generation synthetic opioids could have less risk of addiction, respiratory depression, and death. 

Fentanyl has been used safely and effectively for over 50 years as a surgical analgesic, and by patients with severe pain from cancer and other intractable pain conditions. Only in the past decade has illicit fentanyl emerged as a potent and deadly street drug that fueled the U.S. overdose crisis.

That has given fentanyl a bad name – and led to efforts to “rewire” fentanyl and other opioids to make them safer, but still effective as pain relievers.

“For decades, the pharmaceutical industry has been constrained by the assumption that major structural changes to opioids would eliminate their analgesic properties,” says senior author Kim Janda, PhD, Professor of Chemistry at the Skaggs Institute For Chemical Biology. 

“Our research has identified a different possibility—that fundamental structural redesign can preserve pain relief while improving safety.”

Janda and his colleagues used a medicinal chemistry strategy known as “bioisosteric replacement,” a method used to redesign molecules to have different effects than the original molecules. 

To engineer the change in fentanyl, scientists replaced the central ring structure of fentanyl molecules with an entirely different one called “2-azaspiro[3.3]heptane.” The new compound doesn’t bind as much to nerve receptors in the brain that regulate breathing. 

When the redesigned fentanyl was tested on laboratory mice, the team arrived at a dose that remained effective as an analgesic, while the mice “appeared normal with no indication of distress or signs of acute toxicity.” 

Slowed breathing in the mice occurred only at very high doses and was temporary, with breathing returning to normal within 25-30 minutes. The new analog has a short half-life of about 27 minutes – the amount of time it takes for the liver to metabolize and break down the drug. Other medicines have a long half-life of several hours or even days — which makes them potentially more toxic.

“Finding ways to preserve the analgesic properties of the synthetic opioids without encumbering the perils of respiratory depression could help derisk the toxicity associated with synthetic opioid use while providing a new conduit for pain management,” says Janda.

The research appears promising and may someday benefit pain patients, but it overlooks the fact that illicit fentanyl is involved in most overdoses. The drug cartels and street dealers that sell it will have little interest in changing the chemical structure of illicit fentanyl to make it safer.

How Stress Makes Pain Worse

By Crystal Lindell

One of the easiest ways to spot a true chronic pain veteran is that they will be eerily silent during the worst pain of their lives.

That’s because people who endure pain day-in and day-out quickly learn that the worst thing you can do during a pain flare is panic and scream.

In practice, those things only serve to increase your stress levels, which will also increase your pain. The best response to pain is to keep yourself as calm and as quiet as possible.

I did not know this in the beginning. Back when I first started having chronic pain a little over a decade ago, the pain itself would stress me out. I’d end up in a devastating cycle where the pain increased, which made my stress increase, which made my pain increase. Usually, the only way to break the cycle would be to go to the emergency room.

A new study, published in the journal PAIN, offers some data proving this phenomenon. Belgian scientists found that stress heightens acute pain caused by electrical stimulation to the skin, and increases sensitivity to pinpricks.

While pinpricks and electrical stimulation are a far cry from the type of pain most chronic pain sufferers endure, it is still interesting to see data proving what many patients have already figured out: Stress makes pain worse.

The study was conducted on healthy women, using two different experiments. To measure their pain response, participants were asked to rank their pain on a scale of 0-100. 

To induce stress, researchers used the Mannheim Multicomponent Stress Test (MMST), a computer program that causes stress with difficult cognitive tests or disturbing noises and images.

In the first experiment, the researchers induced stress before they started administering electrical stimulation. They followed that up with pinpricks. 

They found that participants ranked their pain after the initial pinpricks as being 10 points higher. But pain decreased back to the normal range as they kept administering the pinpricks.

In the second experiment, stress was induced 20 minutes after they started administering electrical stimulation. They found that pinprick hypersensitivity significantly increased after the stress was induced.

In other words, if someone is stressed before electrical stimulation, it can make that stimulation hurt more. But it doesn't impact whether or not they become more sensitive to pinpricks. 

However, when someone becomes stressed after the electrical stimulation, the stress makes the sensitivity to pinpricks worse. 

While I still hate when people suggest yoga as a treatment for my chronic pain, I will admit that learning to keep myself calm during a flare can go a long way. And research like this helps prove why serenity is so important for pain patients. 

Scientists May Finally Know Why Statins Cause Muscle Pain

By Pat Anson

Many people stop taking cholesterol-lowering statins because they experience painful muscle cramps, weakness, and fatigue. I know, because I was one of them.

I started taking statins in my 40’s on the advice of our family physician, because of mildly elevated cholesterol and a family history of coronary artery disease. Soon I was having stinging cramps in my legs overnight, which were painful enough to wake me up. 

My doctor was skeptical that statins were the cause, but switched me from Lipitor to Vytorin and finally to Crestor. The muscle cramps continued. Only when I stopped taking statins did the symptoms disappear.

“I’ve had patients who’ve been prescribed statins, and they refused to take them because of the side effects. It’s the most common reason patients quit statins, and it’s a very real problem that needs a solution,” says Andrew Marks, MD, Professor and Chair of the Department of Physiology and Cellular Biophysics at Columbia University.

To find a solution, first you need to identify the cause, and Marks and his colleagues have finally discovered why about 10% of people on statins experience those muscular side effects.

Their research, recently published in The Journal of Clinical Investigation, found that a widely-used statin called simvastatin (Zocor) binds to a protein in muscle cells, which causes a leak of calcium ions inside the cells.

Using an electron microscope, researchers watched simvastatin molecules bind to two locations in a muscle protein called the ryanodine receptor, which opened a channel in the receptor that allowed calcium to flow through. 

Marks says the calcium leak could be weakening the muscle directly or by activating enzymes that degrade muscle tissue.

“It is unlikely that this explanation applies to everyone who experiences muscular side effects with statins, but even if it explains a small subset, that’s a lot of people we could help if we can resolve the issue,” Marks said in a press release.

The electron images suggest that statins could be redesigned so they don’t bind to the ryanodine receptor, but retain their cholesterol-lowering ability. 

Marks is now collaborating with chemists to create such a statin. He owns stock in RyCarma Therapeutics, a company developing compounds that target the ryanodine receptor.

Plugging the calcium leak could be another option: Statin-induced calcium leaks in laboratory mice can be closed with an experimental drug developed by Marks for other muscle conditions involving calcium leaks.

“These drugs are currently being tested in people with rare muscle diseases. If it shows efficacy in those patients, we can test it in statin-induced myopathies,” Marks says.

The first statin was approved by the FDA in 1987, but it took the agency nearly three decades to listen to patients like me and update warning labels on statins in 2014, cautioning that statins can cause myopathy. In rare instances, the FDA says statins can also cause liver injury, diabetes and memory loss.   

Chronic Pain and Complications Common After Outpatient Surgery

By Pat Anson

Outpatient surgeries are often touted for their convenience and cost savings. The surgeries are often minimally invasive, less painful, reduce trauma and recovery time, and save patients (and insurers) thousands of dollars because they don’t have to spend a night or two in the hospital in post-op care. 

But two new studies in the UK – where outpatient procedures are called “day-case” surgeries – show the benefits of outpatient surgery are not universal and often make pre-existing pain conditions worse.

The studies, published here and here in the journal Anaesthesia, involved nearly 17,500 patients, and were conducted by a team of researchers at the NHS Foundation Trust and University Hospitals Plymouth. 

In the first study, researchers found that 1 in 8 patients (11.8%) who had day-case surgery did not go home the same day and were admitted to hospital for various complications. For some patients who had prostate procedures (including those for cancer and benign prostate growth), the hospital admission rate was higher than 50%.

In the second study, one in 14 patients (7.2%) developed chronic pain or had their pain worsen at the surgery site. Some procedures had higher rates of chronic pain after 3 months, including orthopaedic (13.4%) and breast (10%) surgeries. Patients with chronic post-surgical pain also had lower quality of life scores than they did before the surgeries.

To be fair, many of the patients in the studies had chronic pain before their surgeries. Pain was already present at the surgery site in 39% of patients and was moderately severe. Chronic pain elsewhere in the body was also common. About one in four patients had opioid prescriptions prior to their surgeries, and a little over one in 10 used opioids daily. 

These were the first studies of their kind in the UK, and fill an important gap in information about the outcomes of outpatient surgery. Because the UK’s National Health Service seeks to have 85% of eligible elective operations be done as day-case surgeries, researchers expect the outpatient workload to increase and the numbers of patients with chronic post-surgical pain to also grow..

“In summary, this large multicentre UK observational study on day-case surgery provides valuable new insights into a key patient group. We have shown that chronic pain is prevalent within this cohort, with a significantly higher burden than the general population,” the authors found.

“While most patients undergoing day-case surgery were discharged on the same day, the rate of unplanned inpatient admissions was unacceptably high, at twice the national target. This finding underscores a critical area for improvement, as reducing unplanned admissions would enhance the efficiency of day-case surgery and improve outcomes for patients. We highlight the complexity of day-case surgery, where even procedures that are generally seen as straightforward can still carry potential risks, especially for certain patient groups.”

Previous studies have found that female patients had higher rates of chronic post-surgical pain. The new studies found no difference in outcomes between males and females overall, but did show that gynaecological and breast surgeries (almost all female patients) had higher rates of chronic post-surgical pain. This suggests that medical specialties –  rather than being female –- were behind the increased risk.

The studies also found that wealthier patients were less likely to have chronic post-surgical pain compared to the poorest ones. Patients of Asian, Black and mixed ethnicity were also more likely to report chronic post-surgical pain, which may be due to healthcare inequities and cultural difference in pain perception.

Rural Cancer Survivors More Likely to Have Chronic Pain

By Crystal Lindell

Rural cancer survivors are more likely to have chronic pain after cancer treatment than those who live in urban areas. And as a rural resident myself, I’m not surprised.

The findings are from a new study published in JAMA, led by Hyojin Choi, PhD.

Choi and her colleagues at the University of Vermont looked at over 5,500 U.S. adults with a cancer diagnosis in the last 5 years. The patients were then categorized as rural or urban residents, based on the population of counties where they lived. 

The study found a pretty striking difference between rural and urban cancer patients. Specifically, the prevalence of chronic pain was 43% among rural cancer survivors, compared to 33.5% among urban survivors.

The authors say the results suggest an association between chronic pain and the availability of pain specialists, survivorship resources, and insurance challenges accessing pain care in rural counties.

“Policymakers and health systems should work to close this gap by increasing the availability of pain management resources for rural cancer survivors. Approaches could include innovative payment models for integrative medicine in rural areas or supporting rural clinician access to pain specialists,” Choi wrote.

While the suggestions are well-intentioned, I’m not sure how practical or effective they would be. “Innovative payment models” sounds like they want rural patients to borrow money to pay for their healthcare. That’s not a true solution.

As someone who lives in rural Illinois and who has chronic pain, albeit not from cancer, I have some other thoughts on all this.

First, I want to note that I actually did live in an urban area when I first developed chronic pain in 2013. Within six months though, I made the decision to move in with family members who were living in a rural area, and I’ve been here ever since.

While, at the time, I was hoping to gain some much-needed emotional support by moving in with the family, the decision was largely driven by finances. I could no longer work the long hours and multiple jobs that it took for me to afford living in a more expensive urban area.

So, I suspect that a large part of why urban cancer survivors fare better than rural ones is that the rural cost of living is so much cheaper and thus it attacks people who have less money overall. The study, in fact, found that rural cancer survivors were nearly twice as likely to have household incomes below the federal poverty level than their urban counterparts (12% vs. 6.9%). 

We all know that more money gives access to better treatment. Of course, that doesn’t mean my rural area doesn’t have rich people. We definitely have rich people out here. But the next hurdle is the complete lack of providers near us. 

I personally drive about two hours each way to see my primary care doctor, because I want to get care at a university hospital and that is the closest option. A lot of other people who live near me also make that drive to the same university hospital system for the same reason.

However, even if you have money, and you can get care that far from home, having to drive such a long distance severely limits your healthcare treatments. It means that if you need a treatment that is required weekly, it either massively disrupts your life, or you just end up not doing it.

The easiest and cheapest way to treat pain is to send in a prescription for pain medication. That may not be the best way to address the pain long-term, but alternative treatments like physical therapy and massage are more of a hassle when you have to drive long distances to get them.

It’s also a lot more common to minimize both appointments and even emergency room visits when you know that doing either will require a lengthy drive. I assume that those tendencies also could contribute to post-cancer chronic pain.

My hope is that advances in treatment and technology solutions like virtual appointments will eventually help close the gap between rural and urban patients. Nobody should have to endure chronic pain simply because of where they live, but that is often the case.

Study Shows Anger Makes Chronic Pain Worse

By Crystal Lindell

A new study claims that the angrier someone is about their chronic pain, the worse their pain will be. But to be honest, the whole thing kind of pisses me off.

All kidding aside, the research published in The Journal of Pain, looked at four distinct “multidimensional anger profiles” in pain sufferers.

Researchers followed 735 adult patients with different types of chronic pain, assessing how they experience, express and control anger, and how strongly they feel about being wronged by their situation. About a third of the participants completed follow-up assessments 5 months later.

They found that people with medium to high levels of anger and feelings of “perceived injustice” had some of the most severe pain. They reported greater pain intensity, more widespread pain, and higher levels of disability and emotional distress. 

In contrast, people who seemed to manage their anger more effectively and viewed their condition with less resentment tended to have less pain..

However, the researchers did not clarify which treatments the patients had access to or how being denied treatment impacted their pain. Instead, they encouraged doctors to make an “early assessment” of patients that emphasizes “the need for tailored, anger-focused, patient-specific interventions.”

One of the biggest issues I have with this study is that it sets up doctors to blame the patient’s demeanor and mood for their physical pain – something they are often already prone to do. 

I can hear the in-office conversations now.

“Have you tried being less angry?” the doctor asks, as though he’s offering an actual treatment option to the patient sitting on a cold exam table.

The question would rightly be infuriating, which would then just lead the doctor to type in their notes that the patient’s pain is partly caused by their inherent anger and sense of injustice.

Leaving the insulted patient in a state of untreated limbo. 

Yes, people whose pain is left untreated or poorly treated are more likely to be justifiably angry overall. And they are especially more likely to feel like their pain is unjust.

In fact, anger is a very appropriate response to such suffering. It inspires you to push those around you to help you find relief. And unfortunately, it’s often required to get real help from medical doctors. 

In the study's conclusion, the authors admit as much.

"Anger is not inherently harmful - when adaptive, it can be a strong motivator, helping individuals set boundaries and navigate challenges," wrote lead author Gadi Gilam, PhD, a psychologist and neuroscientist at the Hebrew University of Jerusalem. "Rather than eliminating anger, interventions should harness this adaptive potential while mitigating its harmfulness."

Perhaps they could also focus on interventions that actually treat physical pain? Especially since the most effective treatment for many types of pain – opioids – has been severely restricted over the last decade.

Anyone who tells you they’d be calm and accepting while dealing with chronic pain, while at the same time knowing there was an effective treatment they weren’t allowed to have, is lying to you.

It’s actually very normal to be angry in that situation and to feel a strong sense of injustice. The situation itself is not just. 

I have long said that lack of sleep will make you crazy so much faster than you expect, and a version of that applies to pain as well. Unrelenting pain will make you angry so much faster than you expect.

Rather than trying to treat the anger, doctors should focus on the source, and treat the pain itself. 

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 nerve medications such as pregabalin (Lyrica), which are collectively known as gabapentinoids. 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 were 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 health consequences. Patients on gabapentinoids may be prescribed sleep aids, anti-depressants and other medications to counteract the drugs’ many side effects.

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 and sometimes appropriate, 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.