A Biopsy of a Decade of American Pain Policy

By Josh Bloom and Lynn Webster

Ten years after the publication of the 2016 CDC opioid guideline, enough time has passed to examine what followed. Consider this a biopsy of a decade of American pain policy — not an examination of what policymakers intended, but of what the tissue now shows. 

What happened to opioid prescribing? What happened to overdose deaths? What happened to physicians? And, most importantly, what happened to people living in pain?

Although the war on pain patients arguably began in the early 2010s, its nadir was reached with the publication of the CDC Guideline for Prescribing Opioids for Chronic Pain in 2016.

While the war on drugs has been an unmitigated disaster, the accompanying war against people in pain was an unqualified "success." And much of it was built on bad science and pharmacology.

Bad science is bad enough. But bad science turned into policy is worse, because real people have to live with it. That is, if day after day of under- or untreated pain really can be called living.

MME: The Illusion of Precision

The CDC's reliance on Morphine Milligram Equivalents (MME) had one very attractive feature: simplicity. Assign every opioid a number based on its potency relative to morphine, do some menial arithmetic, and you've solved a very complicated pharmacological problem.

Except you haven't.

The idea sounds reasonable. Morphine is assigned a value of 1.0. Other opioids are given conversion factors relative to morphine. In the 2016 CDC table, oxycodone was assigned a value of 1.5 and oxymorphone 3. So, according to the table, 60 mg of oxycodone or 30 mg of oxymorphone was equivalent to 90 mg of morphine.

Simple. Convenient. The arithmetic works perfectly. But the pharmacology doesn't.

The problem is that neither the drugs nor the people who take them fit neatly into an Excel sheet.

Consider oxycodone and oxymorphone, both strong opioids. They are chemically related, yet the body handles them very differently. Oral oxycodone has a bioavailability of roughly 60–87%; for oxymorphone, it is only about 10%. Their metabolism differs as well: oxycodone undergoes extensive metabolism involving CYP enzymes, while oxymorphone undergoes extensive glucuronidation mediated by an entirely different family of enzymes.

These are not trivial pharmacological differences, but MME reduces them to a pair of numbers that look far more meaningful than they are.

Genes Make the Numbers Even Worse

And then there are genetics. Two people can take the same drug at the same dose and process it very differently, sometimes very differently.

Yet MME ignores all this, squeezing pharmacological variation into a single, geneless number.

Even the CDC acknowledged the problem. Its 2016 guideline cautioned that equianalgesic conversions are only estimates and cannot account for individual variability in genetics and pharmacokinetics. It also warned physicians not to use calculated MME values to determine doses when switching patients from one opioid to another because doing so could cause an overdose.

Someone wasn't paying attention.

The numbers aren't reliable enough to tell a physician precisely how much of Drug B should replace Drug A for an individual patient. Yet those same "approximate" conversions were considered reliable enough to determine whether that patient had crossed an official dosage threshold.

And then things got bad.

Enter the Thresholds

The CDC advised physicians to "carefully reassess" benefits and risks when increasing a patient's dose to 50 MME per day and to avoid—or carefully justify—doses of 90 MME or more. The guideline itself acknowledged that a single dosage threshold for safe opioid use could not be identified. 

Nevertheless, 50 and especially 90 MME rapidly acquired significance far beyond what the underlying pharmacology could justify.

This is false precision.

MME can be useful as a rough measure of opioid exposure. It allows researchers to put different opioids into approximately comparable units. But an approximate population-level tool is a very different thing from a scientifically determined limit for an individual patient.

There is no pharmacological cliff at 50 MME. Nor does something suddenly happen to a patient when the dose reaches 90.

Yet numbers have a way of acquiring authority once they appear in an official government document. What began as a rough conversion method became embedded in prescribing policies, insurance rules, state laws, and medical practice.

And that's where a questionable pharmacological construct stopped being merely a scientific problem.

It became a human one; more accurately, an inhumane one.

Impact on Physicians and Patients

The 2016 guideline accelerated a fundamental change in how medicine viewed pain, people living with pain, and opioid therapy itself. Insurers, policymakers, and the medical community increasingly shifted their attention away from the undertreatment of pain and toward reducing opioid exposure. Although addiction and overdoses were stated public health concerns, reducing opioid prescribing became a principal policy response.

This shift was reinforced by a wave of opioid litigation that portrayed prescription opioids, and often the physicians who prescribed them, as central contributors to the overdose crisis. A relatively simple narrative became dominant: that prescription opioids were inherently highly addictive, broadly ineffective for chronic pain, and responsible for an extraordinary number of overdose deaths.

Important distinctions were often lost in the process: prescription opioids versus illicit opioids, therapeutic use versus misuse, physical dependence versus addiction, association versus causation, and population-level risk versus the needs of an individual patient.

The result was not simply a change in prescribing recommendations. It was a change in the culture of medicine.

For physicians, the incentives became increasingly clear. Prescribing fewer opioids was viewed as safer and more defensible. Continuing opioid therapy could bring scrutiny from medical boards or law enforcement. Physicians reduced doses, tapered established patients, became reluctant to accept patients already receiving long-term opioid therapy, and in some cases stopped treating pain altogether. 

The message was unmistakable: opioids were a risk not only to patients but to physicians as well.

Federal enforcement amplified that message. The DEA and Department of Justice made highly visible the consequences of being identified as an excessive opioid prescriber. Physicians watched colleagues be investigated and raided, lose DEA registrations, face prosecution, and sometimes receive lengthy prison sentences. 

At the same time, federal and state agencies increasingly used data analytics, peer-prescribing comparisons, and warning letters to identify prescribing outliers.

But patients living with pain paid a substantial price.

As clinicians became more reluctant to prescribe, patients encountered increasing difficulty finding physicians willing to assume their care or continue treatments that had been stable for years. Some experienced involuntary dose reductions or discontinuation. Others struggled to maintain continuity of treatment or felt increasingly viewed with suspicion simply because their medical care included an opioid.

Remarkably, the 2022 CDC guideline acknowledged much of what had gone wrong. It noted that policies derived from the 2016 guideline had sometimes gone "well beyond" its recommendations, including rigid dosage thresholds, rapid tapers, abrupt discontinuation, insurance and pharmacy limits, and even patient abandonment. The CDC concluded that these misapplications had contributed to patient harm, including untreated or undertreated pain, withdrawal, psychological distress, overdose, and suicidal ideation.

There is also a paradox that any ten-year assessment must confront. Opioid prescribing declined substantially during this period, yet the overdose crisis did not end. Instead, mortality became increasingly dominated by illicitly manufactured fentanyl and other hazards of an unpredictable illicit drug supply. 

This does not establish that reductions in prescribing caused subsequent overdose deaths. But it does raise a fundamental question about the strategy: did reducing prescription opioid exposure become confused with addressing the causes of the overdose crisis itself?

The most consequential legacy of the post-2016 era, therefore, is not simply the reduction in opioid prescribing. It is the transformation of pain treatment from an effort to relieve suffering and preserve function into one increasingly organized around physicians avoiding opioid-related risk.

The lesson of the last decade is not that opioids are harmless, that every prescription was appropriate, or that the country should return to the prescribing practices of the 1990s. It is that public-health policy can cause harm when uncertainty is converted into certainty, population averages are applied to individuals, and a complex epidemic is reduced to a single measurable target.

In trying to protect patients from opioids, medicine lost sight of an equally important obligation: protecting people in pain from unnecessary suffering.

Josh Bloom, PhD, is Director of Chemical and Pharmaceutical Sciences at the American Council on Science and Health (ACSH).

Lynn Webster, MD, is a pain and addiction medicine specialist, and Senior Fellow at the Center for U.S. Policy. He is the author of “Deconstructing Toxic Narratives: Data, Disparities, and a New Path Forward in the Opioid Crisis.”

This article originally appeared in the American Council on Science and Health and is republished with permission.

I May Not Look Like I’m in Pain – But I Am

By Crystal Lindell

When my mom had a sudden perforated ulcer in her stomach in 2022, she fell to the ground at work and was taken to the hospital via ambulance. While waiting in the ER, she alternated between the floor and the bed in eerie silence.

She didn’t scream, she didn’t cry. She just stayed quiet while waiting for help. 

My mom had been dealing with a very bad hip for years, so extreme pain wasn’t new to her, and she had long ago trained her mind and body to stay calm when she was in pain.  

However, because she wasn’t screaming at the top of her lungs, all the nurses assumed she was fine.

It took the staff 9 hours to finally order a cat scan, which showed the hole in her stomach. They immediately rushed her into emergency surgery, which barely saved her life.

Perhaps I inherited some of that ability to be quiet anytime my pain flares up. But I think it’s more likely that I learned what anyone who’s dealt with pain for long periods of time knows: The worst thing you can do is scream.

That does not align with the common media portrayal of pain though. In movies and TV shows, extreme pain involves obscene levels of screaming, buckets of tears, and facial expressions that actually match the number 10 emoji on the pain scale.

The patient we see in the media always has the vibe of a screeching red fire alarm.

In real life though, that’s not what extreme pain always looks like – at least not for chronic pain patients.

In real life, deep, unrelenting pain often arrives with a scary level of calmness, an odd silence, and maybe – on the especially bad days –  a few quiet tears streaming down the face.

Unfortunately, this disconnect between how pain is portrayed vs. what it actually looks like can lead to some very upsetting consequences. If you’re not screaming at the top of your lungs when you’re in pain, then everyone assumes you must be faking it.

By everyone, I don’t just mean friends and family – I also mean important people like bosses, clients, and even doctors.  

There are two main reasons why living with chronic pain usually changes how you react to level 11 pain flares.

One, you realize pretty quickly that staying calm is the best way to keep the pain from escalating even higher. 

And two, our vocal chords just aren’t designed to scream at full volume for very long.

Even though I have some days where the pain drops down to as low as a 2 or a 3, I spend most days trying to keep level 7-9 pain from ruining my life. 

I take multiple substances to try to accomplish that, but still spend lots of time coping with pain levels that healthy people would probably go to the ER for.

The reality is that it just isn’t physically possible for me to scream at the top of my lungs until the pain subsides. It would be like having the fire alarm go off every single day.  

Eventually, you realize that the only thing the alarm was doing was making things worse. 

All this means that most of the time, you aren’t able to tell if someone is in pain just by looking at them. In fact, it’s the people in the most pain who are often the best at hiding it.

As such, the best way to handle the situation as an outsider is this: If someone tells you they are in pain, believe them. 

It really is that simple. 

Thousands of Public Comments Support Keeping 7-OH Legal

By Pat Anson

Over 3,000 additional comments were posted in the Federal Register during the 15-day extension of the public comment period on the Trump administration’s plans to set a legal threshold for the kratom alkaloid 7-OH (7-hydroxymitragynine). 

Almost all of the additional comments oppose the DEA’s plan to set a limit of 1 mg per 7-OH tablet, gummy or shot, saying there is no evidence to support it.

Left unchanged, the DEA order would classify 7-OH products containing more than 1 mg (or more than 0.05% of a product by weight or volume) as illegal Schedule One controlled substances.

Pain sufferers who use 7-OH – often because they can’t get opioid pain medication – say 1 mg is too low of a dose and is far below what they are already taking.

“I currently take 15 mg twice a day every 4-6 hours as needed for my pain,” said April Sikes, a licensed practical nurse. “Please do not take another tool away from people who are simply trying to function, work, and live with dignity.” 

“I am a 31-year-old adult with severe chronic pain and a complex medical history who has used 7-OH for years. My typical amount is approximately 25 to 50 milligrams at a time, generally every 6 to 8 hours as needed,” wrote Veronika Livinska. 

“I currently use approximately 20 mg of 7-OH per day,” said Amy Cullen, who lives with chronic joint pain, anxiety and depression. “7-OH has personally been beneficial to me because it helps me manage my pain and makes it easier for me to function.” 

“I am a responsible member of the 7oh community and found 20mg 3 times a day is an appropriate dosage in maintaining my flare ups of lupus,” wrote Terry Matilda. “Please consider a reasonable threshold for 7oh rather than completely taking the one thing that keeps many pain patients functional.”

‘Little Information’ on 7-OH Safety

Exactly what a “reasonable threshold” is for 7-OH is difficult to determine. The alkaloid occurs naturally in whole leaf kratom – in trace amounts – and many people find those natural levels effective for pain relief, as well as other conditions such as anxiety, depression and withdrawal symptoms.

But manufacturers have developed ways to concentrate 7-OH – turning a mild pain reliever into a potent analgesic that has “opioid-like” side effects, such as withdrawal and addiction. 

Several states and dozens of cities and counties have already banned 7-OH, relying mainly on anecdotal stories about a surge in calls to poison control centers and reports of overdoses and hospitalizations involving 7-OH.

Despite the growing alarm about 7-OH and its characterization as “an imminent threat to public health,” there are no clinical trials or toxicological studies showing that 7-OH is toxic or unsafe in humans. Conversely, no studies have been conducted to establish what a “safe” 7-OH threshold is.

In a 2025 scientific assessment of 7-OH, the FDA acknowledged there is “little information” available on the safety profile of 7-OH. The few studies that exist were done on animals – rodents primarily – which found that 7-OH is a potent analgesic 4 to 6 times stronger than morphine when injected. 

But, when taken orally, researchers say 7-OH did not cause the same respiration depression in animals that causes overdoses in humans.

“If researchers couldn’t kill mice with oral 7OH, how would humans be dying from ingesting the same substance?” asked Joseph Garnella in his public comment. “Millions of 7OH doses have been consumed with zero overdose deaths. The only related deaths had multiple drugs and alcohol in their system.”

“No concentration or quantity of 7-OH has been identified as an imminent hazard,” said Chris O’Donoghue, who like other 7-OH users supports some degree of regulation. “I support age limits and lab testing. Licensed retail so you can get it out of gas stations.”

“It most certainly must be regulated in some way. It absolutely must not be allowed to be sold at gas stations and head-shops," said William Baldwin. “A license (akin to a tobacco or liquor license) should be required by any business involved selling it in the US, and quality control measures amongst the suppliers should be rather stringent.”

“I know people that would be alive today if they had a drug as safe as 7-OH to use, instead of things like heroin or fentanyl. If we ban this compound we are guaranteed to see a massive rise of fentanyl deaths or other dangerous black-market opioids,” said Collin Lomelino.

“I understand that we should probably regulate 7-OH, but the outright banning of this compound is going to leave hundreds of thousands of people no option but to turn to the street, which is filled with highly deadly drugs that will kill so many people.” 

In all, nearly 36-thousand public comments were made in the Federal Register since the Department of Health and Human Services (HHS) made its initial request for information on a 7-OH threshold in early July.

It’s unclear what, if any, impact all those comments will have on the DEA, which reports to U.S. Attorney General Todd Blanche – not HHS. 

DEA could amend its scheduling threshold to allow for more than 1 mg. Or it could implement the scheduling order at any time as it is currently written – making the manufacture, sale and possession of 7-OH illegal – and turning law-abiding 7-OH consumers into felons overnight.  

Damaged Nerve Cells May Cause Shingles 

By Andrew Bubak

Shingles can cause pain that is notoriously difficult to manage and can last for months to years for some people. The pain can be so severe that it causes a significant decline in quality of life and can be accompanied by suicidal thoughts and emotional distress.

If the pain lasts longer than three months, doctors call the condition post-herpetic neuralgia. Because the underlying mechanisms driving this persistent pain are unknown, treatment options are centered on relieving symptoms but largely fall short. Less than 50% of patients achieve meaningful pain relief.

However, new research from my team published in the journal Annals of Neurology uncovered that microparticles circulating in the blood called exosomes may provide an explanation for some of the most puzzling features of this neuropathic pain condition as well as new targets that could lead to new treatments.

Chickenpox Virus Reawakens

The varicella zoster virus that causes chickenpox (herpes zoster) has infected over 90% of the world’s population. Most people contract the virus during early childhood in temperate regions, but in tropical regions, initial infection typically occurs later in adolescence and early adulthood.

After this first infection, the virus enters a state of dormancy within pain-sensing neurons. Even children vaccinated for varicella, such as those in the United States since 1995, still have dormant virus in their neurons, since the vaccine uses a live but weakened strain.

In approximately a third of the world’s population, the virus will reactivate decades later to cause the infamously painful shingles rash; for reasons yet unknown, rates of shingles are increasing worldwide

For most people, the pain will resolve in a couple of weeks. However, about 10% to 18% of patients will progress to post-herpetic neuralgia months after the rash has cleared. In some cases, the pain can persist for years or the rest of their lives.

While anyone who has shingles is at risk of developing post-herpetic neuralgia, the risk rises significantly with age.

Exosomes and Irritated Neurons

Researchers and clinicians do not fully understand what causes post-herpetic neuralgia. In patients with post-herpetic neuralgia, while the shingles rash has cleared with seemingly normal-looking skin, skin biopsies show a puzzling reduction in sensory nerve fibers in the painful areas. 

Counterintuitively, this decrease in nerve fibers in the skin can lead to heightened pain in many patients. What prevents these nerve fibers from repairing after the infection has cleared is unknown.

Researchers have proposed that ongoing or intermittent viral replication within sensory neurons is likely continuing to damage or kill these cells months after the virus reactivates. However, antiviral treatment that shuts down viral replication does not reliably prevent or reduce post-herpetic neuralgia. Thus, neurovirologists like me have been looking for noninfectious contributors to this condition.

In our newly published research, my team and I investigated the role that noninfectious microscopic particles circulating in the blood called exosomes may play in the development of post-herpetic neuralgia. 

Exosomes are released from every type of cell in the body. They carry bioactive cargo – material such as proteins and nucleic acids that can change a recipient cell’s behavior or specific cellular process – and shuttle them from one cell to another. This process helps cells communicate with each other and is essential for normal bodily functions.

My laboratory previously discovered that exosomes in the blood of patients with an active shingles rash can increase stroke risk and inflammation. Thus, we hypothesized that circulating exosomes in the blood of post-herpetic neuralgia patients may also be contributing to their severe pain.

My team and I isolated exosomes from the blood of seven patients with post-herpetic neuralgia and compared them to those in the blood of seven patients without the condition. The contents of the exosomes of those with post-herpetic neuralgia had significantly higher concentrations of proteins known to suppress the growth of neurons. 

Did this finding mean that patients with post-herpetic neuralgia have particles in their blood that are preventing their pain sensory neurons from fully regenerating?

To test this assumption, we exposed human sensory neurons in a petri dish to exosomes isolated from the blood of people with or without post-herpetic neuralgia. Using live-cell imaging, we tracked and measured the ability of these neurons to extend and interact with each other in the petri dish. 

As suspected, neurons exposed to post-herpetic neuralgia exosomes were significantly stunted and unable to form a strong network with other neurons. In comparison, neurons exposed to the exosomes of people without the condition saw no measurable disruptions to their function.

When we measured the genetic activity of pain sensory neurons following exposure to post-herpetic neuralgia exosomes, we found that these neurons underwent changes that actively prevent the formation of growth cones – structures neurons need to grow and repair themselves.

Furthermore, we found evidence that post-herpetic neuralgia exosomes keep pain-sensing neurons in an overactive state, rendering them hypersensitive to pain signaling.

Future of Neuropathy Treatment

Our findings suggest that targeting the underlying cause behind nerve irritation and failed regeneration could help lead to more effective treatments for post-herpetic neuralgia by targeting the source of the pain.

Furthermore, my team and I believe this phenomenon is not unique to post-herpetic neuralgia. It could likely extend to other painful neuropathies, such as diabetic neuropathy, which is also associated with failed nerve regeneration.

Currently, my team is collecting sequential blood samples for up to a year from patients with shingles who later develop post-herpetic neuralgia, as well as from patients with shingles that resolves with no lingering pain. This comparison will be crucial to determine specifically what cargo exosomes are carrying that contribute to this debilitating chronic pain condition.

Andrew Bubak, PhD, is an Associate Professor of Neurology at University of Colorado Anschutz.

He studies viral-contributions to multi-system disease states, including Alzheimer’s disease, cardio- and cerebrovascular disorders, diabetes, cancer, and pain. 

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

Researchers To Use AI to Study Chronic Pain in Rural Older Adults

By Crystal Lindell

Virginia Tech researchers will receive nearly half a million dollars from the federal government to use artificial intelligence (AI) to study chronic pain in older adults living in rural areas.

The study is being led by Huaiyang Zhong, PhD, an Assistant Professor in the Grado Department of Industrial and Systems Engineering at Virginia Tech. He was awarded a $460,260 grant from the National Institute on Aging.

People in rural areas have significantly higher rates of chronic pain than those who live in big cities. They’re also at a big disadvantage when it comes to getting their pain treated, due to the distances many have to travel to see a doctor. 

Zhong and his team hope AI can help improve pain assessments and clinical decision making by doctors, with the goal of reducing pain and pain-related complications in older patients.

“I became interested in chronic pain because it's incredibly common, but also incredibly complicated,” Zhong said in a press release. “Pain is not just a single diagnosis, and it's not a number on a scale like a lot of medical diagnoses. Pain itself can affect mobility, mental health, sleep, cognitive functions, and overall quality of life. It's a multidimensional thing.”

Zhong hopes to learn how chronic pain evolves, which patients are more vulnerable to poor outcomes, and how healthcare systems can treat them more effectively. 

It all starts with the information that is sometimes buried in clinical notes. Researchers will use machine learning and natural language processing to analyze patient records and create “risk dashboards” to help doctors recognize when a patient is at risk of complications, such as depression or cognitive impairment.

“I ultimately want to help clinicians move toward more personalized pain management,” Zhong said. “This means understanding not just how much pain somebody has, but the broader health context surrounding that pain.”

Zhong is not a medical doctor, but has a PhD in Management Science and Engineering from Stanford University. He thinks his background in industrial and systems engineering (ISE) can help solve complex healthcare problems. 

“Machine learning can tell us which patients are at elevated risk, but as ISE researchers, we ask the next questions: What should we do with that information? How should limited healthcare resources be allocated? How does this information feed into clinical workflows? How does using this actually improve clinical outcomes?” Zhong said. 

Robert McNamara, PhD, a clinical psychologist and Associate Professor in Virginia Tech’s  School of Medicine, is a collaborator on the project. He looks forward to investigating the medical problems faced by rural older adults with chronic pain.

“We foresee this work leading to early, actionable insight for providers in rural areas, enabling appropriate intervention and referral, and ultimately improving quality of life for this vulnerable population,” said McNamara.

As a rural resident myself, who also suffers from chronic pain, I am always glad to see more resources going to research like this. It will be interesting to see if AI is actually able to offer new insights. 

Many of the older adults I know in northern Illinois who have chronic pain already know how to improve their healthcare and quality of life. First and foremost, they want access restored to opioid medication. 

There’s also a high need for making telehealth doctor appointments easier for older adults to access. In-home care is another high priority. It’s a chore to go to a doctor who might be a two-hour drive away. If there was a program where a traveling doctor could come to a rural community for a day, that would be a massive help.

Hopefully, AI offers real, practical insights into these types of problems, and all the other issues rural chronic pain patients suffer from.

More Than Distraction: How Music Relieves Pain 

By Pat Anson

Music won’t cure chronic pain, but there is some evidence that listening to your favorite tunes helps reduce pain levels temporarily. And it’s not just distraction.

The type of music doesn’t seem to matter – whether it’s Mozart or heavy metal – the key seems to be that listeners like what they hear and choose it themselves. Singing or humming along, moving in sync to music, or even playing the air guitar are also good ways to ease pain.

That’s what researchers at Drexel University found when they reviewed 57 clinical studies that evaluated the effects of music on pain.

Like a lot of pain research, many of the studies were small and induced pain in a laboratory by having healthy volunteers briefly dunk their hands in cold water – not the daily pain that comes from arthritis, migraine or an aching back.  

"Researching how music affects pain may sound simple, but it is actually very challenging because of the complexity of music and the complexity of pain," says lead author Joke Bradt, PhD, Professor and Program Director of the PhD in Creative Arts Therapies program at Drexel University.

"In my clinical work, I mostly use active music-making, such as singing, vocal improvisation and playing instruments because I have seen this to be much more effective for chronic pain than merely listening to music.” 

The study findings, recently published in PAIN Reports, suggest that there’s more to music than simple distraction. To be effective, it’s important for the music to be pleasant to the listener to help counteract the unpleasant sensations of pain. Someone who prefers country music or jazz may not get any pain relief listening to heavy metal.  

“Although distraction is often cited as a potential mechanism, current evidence suggests that attentional capture alone is insufficient for hypoalgesia. Unpleasant music or neutral sounds, while engaging attention, typically fail to reduce pain,” researchers found.

“Thus, music does not appear to reduce pain merely through the automatic capture of attention by an auditory stimulus. However, it remains possible that listeners sustain attention toward the music in a more deliberate and controlled manner.”

Active participation also plays a role. The simple act of choosing your own music and humming or singing along helps overcome the passive role that pain often induces. 

 "The findings from our study help explain why music can be an effective, low-risk approach for pain management and how we can maximize its potency," said Bradt.

Why is 7-OH Called ‘Gas Station Heroin’ but Caffeine and Alcohol Are Not?

By Crystal Lindell

I think it’s because I work as a manager at a truck stop that the phrase “gas station heroin” particularly pisses me off.

If you haven’t seen the coverage, “gas station heroin” is the favorite phrase used by the media and anti-7-OH groups to describe kratom and the alkaloid 7-OH (7-hydroxymitragynine).

But it’s not based on anything real, because kratom and 7-OH are not even close to being heroin.

So as the DEA nears a potential nationwide ban on 7-OH, and state and local governments ban kratom, it’s a good time to really look at the ways media and advocacy groups try to justify these bans. Notice how their labeling never extends to other substances like caffeine, nicotine, or alcohol. 

Indeed, calling 7-OH and kratom “gas station heroin” is about as accurate as calling coffee and energy drinks “gas station meth.” Or calling beer “gas station LSD.”

Lots of mind-altering and addictive things are sold at gas stations. But something being a little addictive and a little bit mind-altering does not mean it should be lumped in with more dangerous and more mind-altering substances like heroin.

Take this New York Post article trying to scare readers about 7-OH. Large portions of it focus on the idea that 7-OH is sold at gas stations, as though that’s a reason to ban it in and of itself. 

"People can buy 7-OH at vape shops and truck stops with little guidance on how much they’re actually supposed to take," the Post warned.

Okay, so does that apply to the nicotine products sold at vape shops? Or the alcohol sold at truck stops? I mean, there’s little to no guidance for those substances too. 

The Post also includes a quote from Dr. Oliver Grundmann, a kratom specialist at the University of Florida.

“Even if 7-OH can help people wean themselves off stronger opioids, it has no business being peddled at bodegas,” Grundmann said. “It should be appropriately labeled and also only available in the hands of someone who can provide professional guidance, like a licensed pharmacist. Not a clerk at a gas station.”

Here again, we can easily flip this around to apply to the beer and cigarettes that are readily available at gas stations and “bodegas” – a fancy way of describing a neighborhood convenience store. 

Imagine saying: ““Even if alcohol can help people relax, it has no business being peddled at bodegas.” 

Or this: "Nicotine should be appropriately labeled and also only available in the hands of someone who can provide professional guidance, like a licensed pharmacist. Not a clerk at a gas station.”

In fact, when it comes to things like alcohol and nicotine, we as a society have decided that even if something causes thousands of deaths a year, it can still be sold at gas stations.

The thing is, kratom and 7-OH do not cause thousands of deaths a year. If they did, the DEA would no doubt have thousands of deaths they could point to to justify a ban. Instead, they had to really stretch to find any deaths to share.   

In fact, the DEA could identify only one man in Norway who supposedly died from using 7-OH. The only problem was the death occurred in 2014, long before concentrated 7-OH actually became available in the U.S. in 2022.

By that logic, caffeine should also be turned into a Schedule One drug. After all, a U.S. teen died from cardiac arrhythmia after chugging three caffeinated drinks in 2017. And a young woman died in 2022 after going into cardiac arrest hours after drinking caffeinated lemonade.

Oh, and in regards to the Norway death, that man also had a sedative, antidepressant, and anti-seizure medication in his blood and urine. So it was clearly a case of polysubstance use.

Someone having 7-OH or kratom in their system at the time of death should not be enough reason to classify those substances in the most restrictive DEA drug category.

Imagine if we tracked how many people had caffeine in their blood when they died. Or nicotine. We don’t even bother because when it comes to those drugs, we all understand that simply having a substance in your blood when you die does not mean that it caused your death.

I’m not saying kratom and 7-OH should be sold without any regulations or age restrictions. Rather, just the opposite. I believe the industry should be heavily regulated and nobody under 21 should be able to buy any kratom products.

The good news is that we already have a model for how to implement that: We just need to look to the other drugs already sold at gas stations, like nicotine, alcohol and caffeine. 

‘Hyperactive’ Stem Cells May Cause Spinal Stenosis

By Pat Anson

Stem cells are often touted for their ability to reduce pain, restore damaged tissues and joints, and even treat cancer.

But researchers at Weill Cornell Medicine and Hospital for Special Surgery have found that when a certain type of stem cell becomes hyperactive in the lower spine, it can lead to lumbar spinal stenosis – a painful back condition that affects over 100 million people worldwide.

These specialized stem cells help generate and restore tendon and ligament cells – normally a good thing –  but in the lower spine they can grow too rapidly, pressing against nerves in the spinal canal, causing pain, numbness and difficulty walking.

“Given that this cell appears to be the ultimate origin of all tendon and ligament cells, defects in this cell are likely at the heart of a wide range of tendon and ligament disorders,” said Matthew Greenblatt, MD, Associate Professor of Pathology and Laboratory Medicine at Weill Cornell and co-author of a study published in the journal Cell.

Greenblatt and his colleagues first identified the stem cell in mice and then looked for it in humans, finding it in kneecaps, Achilles tendons and spines.

“Everywhere we looked, we found this cell,” said Greenblatt. “So, we think this is the universal stem cell for tendons and ligaments throughout the body.”

MRI image of spinal stenosis with two arrows that show narrowing of the spinal canal. (Credit: Dr. Sravisht Iyer)

The researchers found unusually high stem cell numbers in ligaments taken from people with spinal stenosis. When these stenosis-derived cells were transplanted into mice, they produced more tendon cells than healthy stem cells did. The cells showed higher levels of calcium signaling than their healthy counterparts, a sign they are growing too quickly. 

“Though spinal stenosis is a complex condition, this really showed us that these cells are contributing to the pathology,” said Greenblatt.

The good news here is that once you identify the problem, you can start looking for solutions.

Researchers think a class of drugs currently used to manage high blood pressure -- calcium channel blockers – could be repurposed to treat spinal stenosis by reducing calcium signals and slowing the growth of the specialized stem cells. Clinical studies will be needed to explore that theory.

“This is probably the first work that's shown a potential therapeutic target for one of the most common spine conditions in the world,” said co-author Stravisht Iyer, MD, an Associate Professor of Orthopedics at Weill Cornell and a spine surgeon at Hospital for Special Surgery. “The findings are exciting for their potential to change the way we deliver spinal care.

“Identifying these specialized stem cells unlocks a new area of research that allows us to address this disease much more mechanistically, rather than just waiting until a patient’s condition worsens and requires surgery to relieve the nerve compression.”

Spinal stenosis is currently treated with painkillers, physical therapy and steroid shots. If those methods don’t provide enough relief, surgery can be used to remove bone and tissue pressing on spinal nerves or “spacers” can be inserted to relieve pressure on the spine.

In addition to stenosis, researchers hope to explore the role that specialized stem cells play in other conditions, such as Marfan syndrome, a genetic disorder that affects the body’s connective tissues.

The findings could also lead to new treatments for tendons and ligaments that heal poorly after injuries, including rotator cuff tears, Achilles tendon injuries, ligament reconstruction and chronic tendon degeneration.

California Seizes More Kratom and 7-OH, but Online Orders Continue 

By Pat Anson

With 7-OH consumers still awaiting final word from the DEA on whether the concentrated kratom alkaloid will be classified as an illegal Schedule One controlled substance, individual states are pursuing regulatory action of their own.  

In California, Governor Gavin Newsom announced the state’s enforcement efforts have so far resulted in nearly 8,000 “deadly kratom/7-OH items” being removed from store shelves. 

Trace amounts of 7-OH (7-hydroxymitragynine) alkaloid occur naturally in whole leaf kratom, but manufacturers have developed ways to concentrate 7-OH in tablets, gummies and shots, which are potent pain relievers with opioid-like effects.  

Although the DEA is only considering a ban on 7-OH – leaving natural leaf kratom alone – California says kratom and 7-OH products both pose “serious health risks.” 

California’s crackdown began last October, when state health officials issued a consumer warning claiming that kratom and 7-OH caused several overdose deaths. Enforcement actions stepped up in January, with state agents seizing millions of dollars worth of kratom and 7-OH products. To date, they’ve issued 181 citations. 

The state also warned vendors they could lose their licenses to sell alcohol if they sold kratom and 7-OH. That threat – in effect saying it was safe to sell beer, wine and other intoxicating beverages, but not kratom and 7-OH – has resulted in a 98% compliance rate by Alcoholic Beverage Control licensees.

“If a product is sold in California, people should be able to trust that it follows the law. We’ve made the rules clear, giving businesses the opportunity to comply, and we’re holding accountable those who don’t. That’s how you protect kids and consumers while standing up for responsible businesses doing things the right way,” Gov. Gavin Newsom said in a news release.

But California’s enforcement efforts are uneven because they mainly target brick-and-mortar stores. Some online vendors are still shipping kratom and 7-OH products directly to California consumers, even though the California Department of Public Health (CDPH) said it has taken “significant enforcement action” against out-of-state kratom distributors.  

“CDPH has taken enforcement action on multiple orders of kratom shipped from out-of-state to California distribution facilities,” the agency said in a statement to PNN. "CDPH continues to monitor and enforce compliance with state law, including when products are sold or shipped directly to consumers in California. When CDPH becomes aware of unlawful kratom shipments, CDPH may take appropriate regulatory or enforcement action in coordination with local partners." 

The CDPH says it has the legal authority to ban kratom and 7-OH because they are “adulterated and misbranded” products that violate the California Health & Safety Code.

North Dakota Amends Kratom Ban

Dozens of other states, counties and cities have enacted laws banning or regulating kratom and 7-OH sales.

On Friday, North Dakota Governor Kelly Armstrong signed legislation that bans the sale, possession and use of 7-OH and other synthetic kratom products, and restricts the sale of natural kratom products to adults 21 and older.

Armstrong signed an executive order last month banning all kratom products, but under the new law passed by the North Dakota legislature during an emergency session, it will be legal again to sell natural leaf kratom as long as there are accurate labels and age restrictions.

“This is a victory for public health and safety, keeping dangerous synthetic kratom products off the shelves and protecting our young people from the adverse and unknown long-term effects of natural kratom, which is not regulated by the FDA but will now be subject to strict state regulations,” said Armstrong, who preferred a total ban on kratom.

Meanwhile, the DEA continues to slow walk enforcement action against 7-OH, even though it’s considered “an imminent threat to public health.” It’s been over a year since the FDA asked DEA to classify concentrated 7-OH as an illegal Schedule One substance, explicitly saying such a ban should not include natural kratom leaf.

DEA finally began the formal scheduling process for 7-OH in July, but federal health officials recently extended the public comment period until September 10. It’s not clear when DEA will act once that deadline passes or if it will make any changes in its scheduling order. 

As currently written, the order limits the amount of 7-OH to no more than 0.05% of a product by weight or volume, the equivalent of about 1 mg per tablet or gummie. That is well below the current dosage levels of 7-OH products. 

Pain Can Make You Mean. Don’t Let It

By Crystal Lindell

As a child, I grew up hearing stories about just how viciously mean my late great-grandmother was. Her son, my late grandpa, was also described as “mean.”

Nobody wanted to be around them. Everybody wanted to be different from them. 

The moral of the tale – as I was so often told as a little girl – was to make sure I didn’t grow up to be “mean.”

As I got a little older though, I started to also hear the stories about their various medical ailments.  

My great grandma suffered from rheumatoid arthritis. She moved to Arizona in her later years hoping the dry desert air would bring her relief. And she started drinking a single beer every day to treat the pain, because her only other option was aspirin.  

Meanwhile, my grandpa regularly spent months in the hospital because of his scoliosis. He wore a back brace, and when he was home, he was either in bed or sitting at the kitchen table chain smoking cigarettes.

As an adult, with my own medical ailments, the picture has become much clearer. My great-grandmother and grandpa probably were very mean – but it’s only because they were both in a lot of pain.

They suffered every day. And they did what millions of others before them have done in that situation – they let the pain make them mean.

The healthy adults who told me these family fables never seemed to make the connections between the pain and temperament. They saw the mean personalities as something inherent in both my great grandma and my grandpa, as though it were some wholly separate thing from the health conditions that ravaged their bodies.

To my relatives, they were mean because they were bad people.

As an adult with chronic pain myself, I have come to understand things that were impossible for me to grasp as a child: They weren’t bad people, they just had bad bodies.

When you’re dealing with chronic pain, even the nicest, kindest person will develop an insatiable urge to lose their temper on those around them. After all, you can’t waste time with fake pleasantries and patience when your body feels like it’s been through a war zone.

I don’t want to be mean though.

Even on my worst pain days, I make a specific effort to ensure that I’m not taking out my physical pain on those around me.

But I struggle. There are so many times that I want to snap at my fiancé, yell at my mom, lose my temper on my friend. Can’t they see? I’m in pain! Why are they talking to me and annoying me when I’m in pain?

I stop myself though. Or, worst case, when I don’t have enough strength to stop myself, I apologize afterwards.

Beyond that though, when I know someone is struggling with physical pain, I don’t take their meanness personally. Instead, I offer sympathy.

All of us are just a few bad pain days away from becoming mean. Knowing that can help us offer understanding to others. But more than that, it can help us fight off the urge within ourselves.

So yes, pain can make someone “mean” - and those of us with chronic pain often are. But if we’re diligent, it doesn’t have to become our whole personality.

Cannabis Detected in One in Five U.S. Overdose Deaths

By Pat Anson

A new study by the CDC seems likely to revive an old debate about cannabis: Can you overdose on cannabis?

The study, published in the CDC’s Morbidity and Mortality Weekly Report (MMWR), looked at U.S. overdoses from 2021 to 2025 and found that cannabis was “detected” in 43,880 deaths. That’s over one in five overdoses (21%).

It’s an alarming statistic, and also misleading because it doesn’t tell us the cause of those deaths – only that cannabis was detected in a toxicology test after someone died.

A deeper reading of the study shows that cannabis was listed as causing death (i.e., involved) in 0.8% of drug deaths and was the only drug involved in 0.004% of them. That represents just nine deaths over a five year period. 

Most of the cannabis-related deaths also involved more risky substances, such as illicit fentanyl (73.5%) and stimulants like cocaine or methamphetamine (60.4%).

“This evidence indicates that overdose deaths caused by cannabis are rare, and detection of cannabis among overdose deaths is primarily indicative of polysubstance use,” wrote lead author Lauren Tanz, ScD, Senior Scientist of Overdose Prevention in the National Center for Injury Prevention and Control.

“Because cannabinoids are rarely implicated in the cause of death, cannabinoid screening and confirmatory testing is not universally conducted. Thus, the identification of cannabis use among overdose deaths is likely underestimated.”

The CDC study is in line with previous ones, which found that the risk of death due to cannabis poisoning is “negligible.” Unlike opioids, cannabis doesn’t cause respiratory depression, which can stop people from breathing. 

But even the caveat of a cannabis overdose being “rare” is a bridge too far for cannabis advocates.

“Since it is well understood and acknowledged that cannabinoids are incapable of causing overdose death, and since the DEA continues to acknowledge even now that "no deaths from overdose of marijuana have been reported,” it seems irresponsible for the authors to put this statement out there at face value,” said Paul Armentano, Deputy Director of NORML, which advocates for marijuana legalization.

Armentano says the nine fatal overdoses in which cannabis was the only drug detected could be laboratory coding errors. Or some untested substance or health condition may have played a role.      

“Perhaps it’s also possible that a person suffered cardiac arrest following cannabis use and this death was miscoded as an overdose involving cannabis. Again, neither I nor anyone else have any idea because this report is presented without any details necessary to give it any sort of probative value whatsoever,” Armentano said in an email.

A cannabis overdose may be rare or unlikely, but you can become impaired by consuming too much cannabis, which increases the risk of an accident or a traumatic physical injury. Regular consumption can also contribute to cannabis use disorder (CUD), cognitive decline, mental health problems, or lung disorders if cannabis is smoked or vaped.

With the potency and availability of cannabis increasing, it’s not surprising that CUD rates are also rising. A recent study by the National Institute of Drug Abuse (NIDA) estimates that 19.4 million Americans have CUD, or about 7.3% of all adults. 

Increasingly, those adults tend to be older. The steepest increases in CUD occurred among adults aged 35 to 49 years and males 50 or older.

While CUD rates are going up, the number of Americans abusing alcohol has stabilized and is going down for some age groups, such as adults aged 21 to 34 years – the prime drinking age for earlier generations.

“This divergence may reflect behavioral and cultural shift – including increasing cannabis preference over alcohol – and declines in binge or heavy drinking,” wrote senior author Nora Volkow, MD, NIDA’s Director. “Findings repudiate conventional assumptions that cannabis carries a low addiction risk and that most young adults with CUD have mild symptoms.”    

In the end, the biggest risk from cannabis isn’t the “negligible” or “rare” risk of an overdose – it’s the risk of dying from something else. 

A recent JAMA study found that 3.5% of patients receiving hospital-based care for CUD in Canada died within five years — a rate 6 times higher than the general population. CUD patients had an elevated risk of dying from suicide, trauma, opioid poisoning, and lung cancer. 

Fans of Heavy Metal Music Have More Pain Tolerance

By Crystal Lindell

Angry and loud heavy metal music may not be good for your hearing, but it might actually be good for increasing pain tolerance. That’s according to a new study published in Nature by German researchers.  

The researchers asked attendees at the German Wacken Open Air festival in 2023 if they experienced “music-induced analgesia” while listening to heavy metal music. 

Sixty people were recruited before the festival began and put through a series of tests. Their results were then compared with those of 62 people who were recruited on the third and fourth day of the festival.

Before we go any further, take a look and listen to a sample of the Wacken Open Air festival, which bills itself as “the biggest metal festival on planet earth.” 

Researchers from the Max Planck Institute for Human Cognitive and Brain Sciences did several tests to see if being at the festival had any impact on pain tolerance, pain sensitivity, or unpleasantness. 

To test pain tolerance, they had participants place their hand and forearm in cold water for as long as they could tolerate it, up to four minutes maximum. An electrocardiogram was also used to measure their heart rate and “emotional processing.”

The researchers hypothesized that accepting unpleasant emotional experiences or difficult situations plays a central role in being resilient and tolerating pain – as opposed to masking those unpleasant emotions. Heavy metal music is known to help people express unpleasant emotions like anger.

“This aligns with common themes in metal music, which often expresses difficult emotions and life challenges, avoiding attempts to mask them with happiness,” the researchers wrote. “Combining such expression of negative emotionality with an energetic and activating soundscape may foster self-efficacy, an important component of resilience.”

Researchers found the music had no effect on pain sensitivity or unpleasantness, but they did find that pain tolerance was significantly increased for those who attended the festival.

"Participants perceived their pain during the festival not as less unpleasant or were less sensitive in perceiving it, but they could endure it for a longer time,” the authors said. “This seems to indicate that participants got more resilient, which means that they might have to a greater degree accepted feelings of unpleasantness towards the pain experience.”

Of course, it’s hard to say how much of a role heavy metal music played in the increased pain tolerance, since it could have also been caused by the social aspects of attending a music festival that is known to be “especially inclusive and friendly.” 

One might guess the 85,000 people who attended the festival also engaged in some drug and alcohol use, which may have impacted pain tolerance. The researchers say any individual displaying observable signs of intoxication was excluded from the study.  

In the end though, the only takeaway here is that sometimes you just need to scream along to some metal music to better tolerate pain – and honestly, that tracks.

Little Evidence Back Braces Work for Chronic Low Back Pain

By Pat Anson

Lumbar supports – also known as back braces – are widely used around the world for low back pain. They’re designed to stabilize the lower back and apply gentle compression to the abdomen, giving relief to sore muscles and aching backs.

There’s also little evidence that they work, according to a new Cochrane review by Italian researchers, who looked at the findings of eight randomised controlled trials involving over 500 adults with chronic low back pain. Five of the studies were conducted in low and middle-income countries and three were in high-income countries. 

Researchers found that lumbar supports showed little to no benefit, with the possible exception of a small short-term reduction in pain intensity when used with pain relievers like ibuprofen. The authors were cautious about drawing any further conclusions from the eight trials, and rated the quality of evidence as very low.

“Lumbar supports are widely used in clinical practice despite the fact we know virtually nothing about their effectiveness,” says lead author Chiara Arienti, PhD, an Assistant Professor in the Clinical Epidemiology Research Centre at Humanitas University in Milan. “Drawing from a very thin research base, we still don’t have enough evidence to make broad recommendations for or against their use.”

Arienti and her colleagues say lumbar supports may provide pain relief for three to four weeks when combined with nonsteroidal anti-inflammatory drugs (NSAIDs), but offer little to no benefit when used alone. They were also “very uncertain” about the benefits of lumbar support when combined with exercise and education.

None of the studies tested mobility devices like walking aids or wheelchairs, which could potentially be helpful for older adults and people with disabilities.

Lumbar Supports More Common in Poorer Countries

One interesting finding was the geographic distribution of the research. Most of the trials were conducted in low- and middle-income countries, where lumbar supports are used more routinely. 

In higher income countries, patients are more likely to get exercise therapy, education, and cognitive behavioral therapy for chronic low back pain. Those “active” therapies are less likely to be offered in poorer countries.

"It's striking that most of the research on lumbar supports is coming from areas where active treatments are harder to access," says senior author Stefano Negrini, PhD, a Professor in Physical and Rehabilitation Medicine at the University of Milan. “There’s enough data now showing that active treatments have a clinical effect on low back pain, but these treatments can be very expensive because they require rehabilitation professionals' involvement.”

As the population ages around the world, demand for low-cost treatments is likely to grow. The authors say more research is needed in low to middle-income countries to better understand the value of lumbar supports, particularly for older adults who may not have access to other treatments. 

“We have to ask ourselves whether we are looking at this problem only through the lens of the Global North, and whether that is the right perspective. These devices may play a different and important role in contexts where the alternative simply isn't available," Negrini said.

Chronic lower back pain is the leading cause of disability worldwide. Over 72 million U.S. adults suffer from it, according to a 2022 Harris Poll. About a third of those surveyed rated their pain as severe and nearly half said they experienced chronic back pain for at least five years. 

Although lower back pain is quite common, there is little consensus on how to treat it. Most of the clinical trial evidence is considered low or very low quality, a persistent problem.in many medical guidelines dealing with pain. 

Guideline for Migraine Prevention Finds Strongest Evidence for CGRP Inhibitors

By Pat Anson

New guidelines for medications that prevent migraines show that the strongest evidence supports the use of three CGRP inhibitors: Emgality, Ajovy and Aimovig. There is also strong evidence for using Botox injections to prevent chronic migraine.

The updated guideline was developed by the American Academy of Neurology and American Headache Society, and published in the journals Neurology and Headache. The update is the first since 2012 and incorporates several new treatments that have been developed since then, such as medications that inhibit calcitonin gene-related peptides (CGRPs), a protein that triggers migraine pain. 

Migraine affects about 39 million people in the United States and 1.1 billion worldwide. In addition to headache pain, migraine can cause nausea, blurriness, and sensitivity to light or sound. Women are three times more likely to suffer from migraines than men.  

Acute migraine medications help treat headache pain and other symptoms as they occur, while preventive medications stop migraines from starting. Oral migraine preventive medications need to be taken every day or every other day, while injectable medications are taken once a month or once every three months.Only one oral medication (Nurtec) both treats and prevents migraine attacks.

“There are a variety of effective preventive medications that work in different ways, including newer classes of medications that have been released in the past several years,” said guideline co-author Tamara Pringsheim, MD, a Professor at the University of Calgary. “For people experiencing frequent migraine attacks or attacks that affect the ability to function normally, this guideline can help clinicians determine which preventive medications may be able to help.”

The guideline update is based on a review of 217 studies that evaluated dozens of medications, and includes recommendations for preventing both chronic and episodic migraine. People with chronic migraine have 15 headache days or more each month, while episodic migraine occurs less often.

The guideline ranks each medication based on the evidence being either strong, moderate or weak. No evidence was found to support the use of over a dozen medications sometimes prescribed off-label for migraine, including Klonopin and Cymbalta. 

While the strongest evidence supports the newer CGRP inhibitors, moderate evidence exists for some old-line medications such as beta-blockers and anti-seizure medications. However, many of the older drugs are more likely to have side-effects, such as constipation and weight loss. 

Some medications, like antidepressants or medications that lower blood pressure, are primarily intended for other health conditions but have been effective in reducing migraine pain for some patients. 

“The research shows many different types of medications may be effective for preventing migraine attacks and reducing symptoms,” said co-author Rebecca Burch, MD, Associate Professor at the University of Vermont Larner College of Medicine. “The guideline includes recommendations for both previously established and newer medications. If one type of medication is not working well, a different type may still be effective. It is important for clinicians and patients to know that there are many options.”

The guideline says preventive treatments should be offered to adults who experience four or more migraine days per month or four or more moderate to severe headache days per month, or if migraine is affecting their ability to work or complete daily tasks.

When working with patients to choose medications, the guideline says clinicians should discuss the strength of the evidence, possible side effects, insurance coverage and out-of-pocket expenses. While CGRP inhibitors are some of the most effective medications, they often cost substantially more than older treatments.

A 2023 study found that some cheaper drugs are just as effective at preventing migraine as CGRP inhibitors. Researchers at the Norwegian Center for Headache Research found that two drugs commonly used to treat depression and high cholesterol – amitriptyline and simvastatin – help reduce the use of medications used to treat acute migraine pain. Both drugs are used off-label for migraine prevention. 

How I’m Able to Work Again with Chronic Pain

By Crystal Lindell

How do I do it?

On my days off, I sleep for 15 hours, waking up only to eat and pet my cats.

I can’t get out of bed without Norco, morphine, Advil, 7-OH, and Tums.

And I have a super supportive partner who does all the house work, all the grocery shopping, and changes all the litter boxes.  

That’s the short answer for how I manage to work a full-time job outside of the home while living with debilitating chronic pain. It takes a lot of drugs, a lot of sleep, a lot of support, and a lot of luck.

I also eat the same meals nearly every day to make food prep and decision-making easier. And I make zero plans for days off.

I started working again in April – my first full-time job in over four years. 

Despite my years of experience as a professional journalist working in the corporate world, I took a job as a gas station cashier close to home. I was fed up with corporate culture and just wanted to see if I could even handle working full-time again in any capacity with my health issues.

I also needed health insurance and the gas station offered me that after just one month.

Now that it's been a little over three months, it felt like a good time to reflect on how it’s going.

To be honest with you, I absolutely love it!

I love going to work every day. I love interacting with the public and making friends with my co-workers. I love getting out of the house. And I have already been promoted to the first level of management, with hopes of continuing up the ladder.

But it has taken a major toll on my body. 

I wake up in so much pain that walking to the bathroom feels like I’m using muscles for the first time in years. And after my shifts, I only have enough energy to change out of my work clothes and get into bed. 

I really don’t know if I’ll be able to keep it up if 7-OH is officially made into a Schedule One controlled substance.

I really, really want to keep it up though. 

I want to keep working, being good at my job, and forming surprisingly deep connections with my fellow employees. I want to keep feeling productive and living like I have a purpose in this world – even if that purpose is just helping truckers get back on the road.

That’s because, despite all the stereotypes about people with chronic illnesses, I desperately want to work. 

In reality, it’s the people constantly trying to take away my access to opioids and 7-OH who want me to be unemployed and bed bound. 

They may soon get their wish if 7-OH is banned – a policy being pushed in the name of “protecting me.”

Protection I do not want and didn’t ask for.

If it happens, the anti-7-OH advocates and federal health officials won’t take any responsibility. They won’t even offer me health insurance. Instead, I suspect they will tell me to go out and get a job.