How to Inhibit Reactivation of the Epstein-Barr Virus

By Dr. Forest Tennant

The Epstein-Barr virus (EBV) is a parasite that normally lives a dormant, harmless life in nasal and throat membranes and in our white blood cells. We are all carriers of EBV.

EBV usually enters the body and first activates during infancy, often resulting in a case of the "sniffles." In teenagers or young adults, it may trigger infectious mononucleosis. After the initial infection, the virus becomes dormant.

Unfortunately, EBV has the ability to reactivate, duplicate, and travel in the blood inside lymphocytes (white blood cells) to harm tissues and cause pain. How does this happen?

Biologic stress, meaning a physical or psychological situation that cause the hormones cortisol and adrenaline to elevate for more than a few hours, may lower one's immune system. That gives EBV the opportunity to reactivate, produce auto-antibodies, infiltrate tissue, and silently produce a painful condition.

The usual stressors that cause reactivation are physical trauma or injury, an infection, or emotional distress. People with medical conditions such as a genetic connective tissue disease (Ehlers-Danlos syndrome), diabetes, or stroke may have an immune deficiency that also makes them more prone to EBV reactivation.

EBV reactivation is similar to herpes or shingles reactivation. Like EBV, herpes and shingles are usually dormant and harmless viral infections, but they may reactivate and cause blisters or a skin rash.  

Unfortunately, EBV reactivation can be totally asymptomatic and unknown to the individual, until chronic reactivations cause a painful condition. This could result in fibromyalgia, small fiber neuropathy, burning mouth, herniated disc, arachnoiditis or even a cancer such as Hodgkin's disease or lymphoma. 

How to Diagnose and Treat EBV Reactivation

Persons with chronic pain severe enough to require daily pain relief medication may have EBV reactivation as a cause of their condition and should take steps to inhibit it. We recommend antibody testing for EBV reactivation in any person who has severe chronic pain for over 90 days and needs to take pain relievers daily.

Two antibodies are formed during EBV reactivation: the Viral Capsid Antibody (VCA) and Epstein-Barr Nuclear Antibody (EBNA).

Major laboratories offer three quantitative tests for VCA, EBNA and early EBNA antibodies. Qualitative tests (positive or negative) are not specific enough to make a diagnosis of EBV reactivation.

When VCA and EBNA antibodies are elevated above normal levels, a diagnosis of past reactivation is made, and the individual can properly be called a "chronic reactivator." We recommend that levels of VCA and EBNA be two or more times above normal, plus a patient having pain in two or more anatomic sites, to warrant a diagnosis of EBV reactivation.

If the early EBNA antibody is elevated above normal, therapeutic trials of antivirals and corticosteroids should be considered to reverse reactivation.

If both VCA and EBNA are elevated but the early EBNA is negative, we recommend the use of these vitamins and supplements to inhibit EBV reactivation:

• Vitamins C and D

• Astragalus

• Zinc

• Resveratrol

• Curcumin

• Selenium

• Luteolin

• Andrographis

• Lysine

Our research has found that about 90% of patients with adhesive arachnoiditis (AA) have EBV reactivation.  The good news is that once it is determined that a person has reactivation and autoimmunity, there are simple treatment measures that can be implemented.   

In our experience, the treatment measures tend to provide about 20% to 50% more pain relief when used with standard pain therapies. Failure to take therapeutic measures to control EBV may allow increased disease deterioration and pain. 

More information about the Epstein-Barr Virus and its relationship to chronic pain conditions can be found in our new book: "The Epstein-Barr Virus: A New Factor in the Care of Chronic Pain."  

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain and arachnoiditis. Readers interested in learning more about this research should visit the Tennant Foundation’s website, Arachnoiditis Hope. You can also subscribe to its bulletins here.   

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.   

The Link Between Collagen Deficiency and Arachnoiditis

By Dr. Forest Tennant

A major finding in our studies of adhesive arachnoiditis (AA) is that most AA patients also have hypermobile Ehlers-Danlos syndrome (hEDS) or a related disorder now called hypermobile spectrum disorder (HSD).

AA is a chronic inflammatory condition that causes nerves in the spinal canal to form adhesions that “glue” them together, while hEDS and HSD cause deficiencies in collagen and the immune system.

How are these conditions connected?

Normal collagen is in thick strands that hold connective tissues together and helps resist infections, tearing, and autoimmune degeneration. When collagen is deficient, the strands may be thin, broken, shortened or non-existent. This allows viruses and bacteria to invade, infiltrating tissues and causing more infections than in individuals with healthy immune systems.

Spinal tissue normally contains considerable amounts of collagen, but in patients with hEDS or HSD they are weak and susceptible to deterioration, inflammation, adhesions and scarring. These spinal tissues include intervertebral discs, vertebrae, spinal canal cover (dura and arachnoid layers), ligaments, and cauda equina nerves.

Weaknesses in spinal tissue make persons with hEDS and HSD more susceptible to AA. It’s also not uncommon for them to develop one or more of these conditions before AA:   

• Tavlov cyst

• Spinal fluid leaks

• Chiari

• Tethered spinal cord

• Herniated disc

• Back pain

• Neck pain

• Spinal arthritis

We have found that persons with hEDS and HSD are also susceptible to Lyme disease, cytomegalovirus, herpes 6 virus, and especially the Epstein-Barr virus (EBV). Almost everyone has EBV, which is typically dormant, but the virus may reactivate from its parasitic life in throat membranes or lymphocytes to infiltrate the brain and spinal tissues.

Persons with hEDS or HSD who have back or neck pain for over 90 days should be screened with the new EBV 4 panel test and take measures to hopefully prevent AA. We highly recommended that they take collagen supplements.

In our studies of patients with MRI-documented AA, essentially 100% have EBV autoimmunity and about 70% show EBV reactivation. About half of those that we review do not know they have hEDS or HSD.

For more details on the link between AA, hEDS and HSD, our new book "The Ehlers-Danlos / Arachnoiditis Connection" is recommended.

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain and arachnoiditis.

Readers interested in learning more about this research should visit the Tennant Foundation’s website, Arachnoiditis Hope. You can also subscribe to its bulletins here.  

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.   

Researchers Closer to Finding the Gene for Hypermobile EDS

By Crystal Lindell

We may be one step closer to discovering the specific gene mutations behind hypermobile Ehlers-Danlos syndrome (hEDS) — a connective tissue disorder that weakens collagen, muscles, ligaments and organs throughout the body, and makes joints highly flexible.

A research team at the Medical University of South Carolina has released the results of a genetic study of a family with high rates of hEDS. Five out of 11 family members met the clinical diagnostic criteria for hEDS and three were considered “probable.” 

Before we get too far into its conclusions though, it’s important to note that findings were released as a preprint in Research Square, which means they have not yet been peer-reviewed by a journal. As such, it’s in the early stages of release, and further scrutiny may result in changes to the conclusions.

That said, the researchers claim to have found what could be a variant linked to hEDS in the Kallikrein-15 gene, which is primarily expressed in the thyroid gland and other organs.

To check if this gene change actually causes hEDS, researchers used laboratory mice. After modifying the mice to have the same genetic variant, they found that the mice had similar connective tissue problems as seen in people with hEDS.

This supports the idea that the Kallikrein gene changes may play a role in causing hEDS.

But the research does not seem to show an all-encompassing hEDS gene. In a cohort of 197 hEDS patients, they found that less than a third (32.8%) had at least one KLK variant. Which means that over 60% of hEDS patients in the study did not have the variant.

As of now, hEDS is the only type of Ehlers-Danlos syndrome that does not have a known specific genetic marker, so finding one would be monumental. And even if this research doesn’t get us all the way there, it’s a huge step in the right direction.

Previous research has also associated hEDS to a genetic variant that causes a deficiency of folate, the natural form of Vitamin B9.

I should note here that I was diagnosed with hypermobile-EDS in 2018, so I have a lot of interest in the topic on a personal level. Since there is no genetic test currently available for hEDS, I was diagnosed via a physical assessment, along with my family’s medical history.

A lot of hEDS patients worry that if there ever is some sort of confirmed, definitive test like a genetic marker, they may not have the marker and would then “lose” their diagnosis.

Based on my personal experiences with medical professionals, I think that’s a legitimate fear. Doctors already seem unwilling to diagnose clear cases of hEDS for a variety of reasons, and this could just give them another excuse to continue doing that.

All I can really say is that if it happened to me, I would feel confident in knowing that my body is clearly not “normal” — so even if it’s not hEDS, there is something else impacting my health.

Some patients diagnosed with hEDS may actually be suffering from something else -- so a genetic test might help them to get the right diagnosis and treatment. I know that probably sounds naively optimistic to many patients. The more likely result is doctors telling patients nothing is wrong with them, and then sending them on their way to suffer.  

On the other hand, I think hEDS is so under-diagnosed, that having a definitive test for it would result in many, many more people finally getting an hEDS diagnosis.

Discovering the exact gene responsible for hEDS could also result in better treatments going forward. As of now, most doctors tell hEDS patients that there’s no cure, so all they can really do is treat the symptoms as they arise and avoid activities that could make their condition worse.  

This is purely wishful thinking, but perhaps in the future researchers will someday discover a way to actually strengthen our collagen and connective tissue, which could have countless benefits for patients suffering from the pain and other common hEDS symptoms.

Advancements like that still feel a long way off though, so until they happen, helping people get an hEDS diagnosis through a genetic test would be progress for millions of patients.

Can Complex Regional Pain Syndrome Be Cured?

By Pat Anson

A recent study by Australian researchers is challenging the notion that Complex Regional Pain Syndrome (CRPS) cannot be cured.

CRPS is a nerve disorder that often starts with an injury to an arm or leg, with the skin in the affected area becoming warm, red and painful to touch. Most cases are mild and people soon recover, but in rare cases it gets worse, resulting in chronic nerve pain that spreads throughout the body.  Because CRPS is difficult to predict, diagnose and treat, there’s been a long-held belief that it’s a lifelong illness.

“In this research we challenge the prevailing notion that CRPS is a lifelong burden,” says Michael Ferraro, a clinical researcher at the Centre for Pain IMPACT at Neuroscience Research Australia. “By reviewing and consolidating the latest developments in understanding CRPS, we’ve found that unlike previous theories, recovery is likely for most people with CRPS, and may be more likely with early diagnosis and a comprehensive treatment approach to match the multi-system nature of the disorder.”

Ferraro is lead author of a review in The Lancet Neurology, which maintains that 80% of CRPS patients can recover, if they are treated within the first 18 months of being diagnosed. The key is to “tackle CRPS from all angles” by combining pain medication, rehabilitation, and psychology with patient education about the condition.

Although the authors admit that “effective treatment of CRPS remains a challenge,” they think providers have learned a lot over the past five years about early identification of patients at high risk of CRPS, which is also known as Reflex Sympathetic Dystrophy (RSD).

“This is a major step towards better understanding CPRS. While more research is needed, our review highlights that biological and psychosocial factors are involved, and successful management of the disorder should target these factors,” says co-author Lorimer Moseley, PhD, a Professor of Clinical Neurosciences at University of South Australia. “The next steps will require national and international networks of researchers to test the most promising treatments in clinical trials.”

One study that’s already underway is the MEMOIR trial, funded by the Australian government, which is testing an analgesic drug and a newly developed rehabilitation program as potential treatments for CRPS.

Another recent study identified a genetic variant that may be involved in about a third of CRPS cases, which could potentially lead to earlier diagnoses.

Some CRPS patients are also finding relief through novel treatments, such as Scrambler therapy and ketamine infusions.

Volunteers Needed for Arachnoiditis Study

By Pat Anson

Kathleen Haynes knows all about the physical and emotional pain that comes from adhesive arachnoiditis (AA), a progressive spinal disorder that causes severe intractable pain.  

She’s had AA for 50 years, after an oily contrast dye used for a myelogram imaging test was injected into her spinal column. The invasive test turned a simple back injury into a living nightmare, with the nerves in her lower spine becoming inflamed and sticking together.

“That oil stayed in my spinal column, surrounded my spinal nerves, and that’s why my nerves clumped together,” Haynes said. “And it just got worse and worse and worse, to the point where I use a wheelchair to get around.”

At the young age of 70, Haines is now pursuing a doctorate degree in Psychology at Walden University. For her dissertation, she’s doing a study about suicide ideation in AA patients. In the past, Haynes had suicidal thoughts herself.

“The pain was just unbearable. And not being believed that I was in pain and not getting the right medication,” she told PNN.

“One of the things that was a deciding factor in doing this study was because I belong to a couple of AA groups on Facebook. And I was struck by the amount of people who go on there and say they're suicidal or say can you please lead me to somebody who does euthanasia?”  

KATHLEEN HAYNES

Haines’ goal is to interview 10 people with AA in the next few weeks who are not currently having suicidal thoughts, but are willing to talk about them. To protect their privacy, participants will be assigned numbers and their real names will not be used. A list of other conditions and sample questions can be found here, along with Haynes’ contact information.  

It’s not the just the pain that makes AA patients suicidal, according to Haynes. Other common factors are being disbelieved, ignored or marginalized by family, friends and doctors. Thoughts about “ending it all” occur so frequently that she thinks every AA patient should be evaluated for suicide ideation.   

“I want to see what people's common denominator is, in talking to them about their suicidality. The goal is to get this study together and get it out to the medical community because they barely recognize AA, yet alone the suicidality their patients face,” she said.

“They need to treat their patients with AA in a way that gives them a desire to live. And get them the treatment team, the providers that they need in order to live fairly comfortable life, despite their pain.” 

Like many other AA patients, Haynes had trouble being believed. She suffered her initial back injury while working for the U.S. Postal Service in the 1970’s, but only recently did the federal government approve her workers’ compensation claim, even though her AA diagnosis and disability happened a long time ago. The Massachusetts woman is now getting appropriate treatment and pain medication.        

To learn more about Haynes’ study and/or make a donation to her research, visit her GoFundMe page.

The Tragic Connection Between Ehlers-Danlos and Arachnoiditis

By Pat Anson, PNN Editor

Before his retirement from clinical practice, Dr. Forest Tennant treated hundreds of patients suffering from intractable pain at his clinic in West Covina, CA. Many of those patients had adhesive arachnoiditis (AA), a chronic inflammatory condition that causes nerves in the spinal canal to form adhesions that “glue” them together.  

Over time, Dr. Tennant began to realize that many of his AA patients also had Ehlers-Danlos syndrome (EDS), a genetic disorder that weakens muscles, joints, skin and organs by disrupting the production of collagen. How could so many pain patients have both diseases?

In his latest book, "The Ehlers-Danlos / Arachnoiditis Connection," Dr. Tennant explains how someone with EDS can develop arachnoiditis after an invasive spinal procedure.

This interview with Dr. Tennant has been edited for content and clarity.

PNN: You were treating patients with arachnoiditis and discovered that many also had Ehlers-Danlos?

Tennant: That’s exactly what happened. I was treating intractable pain, which was my specialty, and adhesive arachnoiditis had become the number one reason for a referral to my clinic. And I found that at least half or more of them had EDS. These discoveries were a total surprise.

EDS and arachnoiditis are considered rare diseases, but seem to be increasing in the last couple of decades, both by actual disease incidence as well as the ability to diagnose cases that previously went undetected.

PNN: Are most doctors unfamiliar with these two disease?

Tennant: Absolutely. We actually heard yesterday about a doctor at a spine and pain center who had never heard of arachnoiditis. I don't know how this is possible. Medical practice has become so caught up and so compartmentalized that a very good institution or excellent physician can be totally left in the dark about something.

PNN: What is the connection between EDS and arachnoiditis?

Tennant: The primary relationship is collagen deficiencies. The cauda equina nerves and the arachnoid membrane that surrounds them in the spinal cord are very collagen laden. The number one reason why EDS patients develop intractable pain is not arachnoiditis, but small fiber neuropathy. EDS has its own autoimmune disease component.

What's been happening is that EDS patients often develop back problems due to the lack of collagen, and then they're operated on or have epidural injections. That doesn't cause it, but it accelerates the problem.

If you look at the number of surgeries, it’s just immense. There’s an incredible number of surgeries that have been done on people with a collagen deficiency disease. No wonder they've developed critical complications.

PNN: Are surgeons unaware that the patient has EDS?

Tennant: Totally unaware. One of the reasons I wrote this book is that anyone who has severe back pain that hasn't responded to standard therapy, such as chiropractic care, physical therapy or anti-inflammatory drugs, should be evaluated for both arachnoiditis and EDS. After 90 days, if you haven't recovered, you need to be evaluated for these diseases.

PNN: Can someone with EDS develop arachnoiditis without some triggering event or invasive procedure?

Tennant: It doesn't look like it, no. There's got to be some something to generate inflammation in the spinal cord. We've had no one who developed arachnoiditis who had not had spinal procedures. All of them had invasive procedures, whether it was epidural injections and/or surgery. In the book you can see the amazing number of interventions that they've had.

Adhesive arachnoiditis is a disease in which a whole lot of things have to go wrong. You don’t just stand on the street corner and catch this disease. A whole sequence of events has to occur. And they’re all bad.

One of my messages in the book is that children who are double jointed and who have hypermobility, these things have to be taken seriously. They can't just be ignored or seen as some kind of oddity. They may have a serious condition. Children need to be identified with EDS. And they need to be on a prevention program to stop the disease from progressing.

PNN: Is there any way to treat EDS?

Tennant: First of all, try not to cause further damage. A child with hypermobility, I mean the idea that they're going to be a gymnast or they're going play football, I hate to say it, but that’s going to cause more damage to their joints and aggravate the disease.

They also probably need to be on some kind of diet with collagen, a very healthy diet with protein and collagen. A lot of parents are starting to have their EDS child at least take a multivitamin once a day. Some are using collagen supplements and some are using low dosage hormones like colostrum.

My book is about prevention. AA can be prevented. And when the EDS person starts developing things like carpal tunnel syndrome or dysautonomia disease, these patients need to be aggressively treated and monitored for spinal canal problems and treated without invasive procedures, if at all possible.

Once you have the two diseases together, it’s catastrophic. You're probably going to have the worst pain imaginable. These people need aggressive pain treatment. I'm hoping that doctors will get the message that when someone has these two diseases, you don’t worry about the CDC opioid guidelines or anybody else's guidelines. You need maximum medical treatment for pain.

We've got people right now with these two diseases and some doctor is giving them a Butrans patch (buprenorphine) or Motrin for pain relief. These people have to be very aggressively treated. Otherwise, they're going to be bed-bound and die a miserable death. Suicides are very common.

Part of my goal here is to get doctors to recognize both diseases. These are the worst of the worst. I've never seen any cancer patients that were any worse than this.

PNN: If you have EDS and arachnoiditis, is that a hopeless situation? Can you have any quality of life?

Tennant: People with both diseases need palliative care and “Brompton cocktail” type medications. In our studies, about two-thirds of them can get some relief. But they were also on pretty aggressive treatment programs. You know, multiple opioids and benzodiazepines. So, it's not hopeless.

PNN: Thank you, Dr. Tennant.

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain. Readers interested in learning more about his research should visit the Tennant Foundation’s website, Arachnoiditis Hope. You can subscribe to its research bulletins here.

To order "The Ehlers-Danlos / Arachnoiditis Connection" and other books of interest to the pain community, visit PNN’s Suggested Reading section.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

Millions Lose Medicaid Benefits, Including Disabled

By Daniel Chang, KFF Health News

Jacqueline Saa has a progressive genetic condition called Ehlers-Danlos syndrome that leaves her unable to stand, walk on her own, or hold a job.

Every weekday for four years, Saa, 43, has relied on a home health aide to help her cook, bathe and dress, go to the doctor, pick up medications, and accomplish other daily tasks. She received coverage through Florida’s Medicaid program, until it abruptly stopped at the end of March.

“Every day the anxiety builds,” said Saa, who lost her home health aide for 11 days, starting April 1, despite being eligible.

The state has since restored Saa’s home health aide service, but during the gap she leaned on her mother and her 23- and 15-year-old daughters, while struggling to regain her Medicaid benefits.

“It’s just so much to worry about,” she said. “This is a health care system that’s supposed to help.”

Medicaid’s home and community-based services are designed to help people like Saa, who have disabilities and need help with everyday activities, stay out of a nursing facility

JACQUELINE SAA

But people are losing benefits with little or no notice, getting bad advice when they call for information, and facing major disruptions in care while they wait for the issue to get sorted out, according to attorneys and advocates who are hearing from patients.

In Colorado, Texas, and Washington, D.C., the National Health Law Program, a nonprofit that advocates for low-income and underserved people, has filed civil rights complaints with two federal agencies alleging discrimination against people with disabilities. The group has not filed a lawsuit in Florida, though its attorneys say they’ve heard of many of the same problems there.

Attorneys nationwide say the special needs of disabled people were not prioritized as states began to review eligibility for Medicaid enrollees after a pandemic-era mandate for coverage expired in March 2023.

“Instead of monitoring and ensuring that people with disabilities could make their way through the process, they sort of treated them like everyone else with Medicaid,” said Elizabeth Edwards, a senior attorney for the National Health Law Program. Federal law puts an “obligation on states to make sure people with disabilities don’t get missed.”

At least 21 million people nationwide have been disenrolled from Medicaid since states began eligibility redeterminations in spring 2023, according to a KFF analysis.

The unwinding, as it’s known, is an immense undertaking, Edwards said, and some states did not take extra steps to set up a special telephone line for those with disabilities, for example, so people could renew their coverage or contact a case manager.

As states prepared for the unwinding, the Centers for Medicare & Medicaid Services, the federal agency that regulates Medicaid, advised states that they must give people with disabilities the help they need to benefit from the program, including specialized communications for people who are deaf or blind.

The Florida Department of Children and Families, which verifies eligibility for the state’s Medicaid program, has a specialized team that processes applications for home health services, said Mallory McManus, the department’s communications director.

People with disabilities disenrolled from Medicaid services were “properly noticed and either did not respond timely or no longer met financial eligibility requirements,” McManus said, noting that people “would have been contacted by us up to 13 times via phone, mail, email, and text before processing their disenrollment.”

Benefits Cut Without a Call

Allison Pellegrin of Ormond Beach, Florida, who lives with her sister Rhea Whitaker, who is blind and cognitively disabled, said that never happened for her family.

“They just cut off the benefits without a call, without a letter or anything stating that the benefits would be terminating,” Pellegrin said.

Her sister’s home health aide, whom she had used every day for nearly eight years, stopped service for 12 days.

“If I’m getting everything else in the mail,” she said, “it seems weird that after 13 times I wouldn’t have received one of them.”

Pellegrin, 58, a sales manager who gets health insurance through her employer, took time off from work to care for Whitaker, 56, who was disabled by a severe brain injury in 2006.

Medicaid reviews have been complicated, in part, by the fact that eligibility works differently for home health services than for general coverage, based on federal regulations that give states more flexibility to determine financial eligibility. Income limits for home health services are higher, for instance, and assets are counted differently.

RHEA WHITAKER

In Texas, a parent in a household of three would be limited to earning no more than $344 a month to qualify for Medicaid. And most adults with a disability can qualify without a dependent child and be eligible for Medicaid home health services with an income of up to $2,800 a month.

The state was not taking that into consideration, said Terry Anstee, a supervising attorney for community integration at Disability Rights Texas, a nonprofit advocacy group.

Even a brief lapse in Medicaid home health services can fracture relationships that took years to build.

“It may be very difficult for that person who lost that attendant to find another attendant,” Anstee said, because of workforce shortages for attendants and nurses and high demand.

Nearly all states have a waiting list for home health services. About 700,000 people were on waiting lists in 2023, most of them with intellectual and developmental disabilities, according to KFF data.

Daniel Tsai, a deputy administrator at CMS, said the agency is committed to ensuring that people with disabilities receiving home health services “can renew their Medicaid coverage with as little red tape as possible.”

CMS finalized a rule this year for states to monitor Medicaid home health services. For example, CMS will now track how long it takes for people who need home health care to receive the services and will require states to track how long people are on waitlists.

Staff turnover and vacancies at local Medicaid agencies have contributed to backlogs, according to complaints filed with two federal agencies focused on civil rights.

The District of Columbia’s Medicaid agency requires that case managers help people with disabilities complete renewals. However, a complaint says, case managers are the only ones who can help enrollees complete eligibility reviews and, sometimes, they don’t do their jobs.

Advocates for Medicaid enrollees have also complained to the Federal Trade Commission about faulty eligibility systems developed by Deloitte, a global consulting firm that contracts with about two dozen states to design, implement, or operate automated benefits systems.

KFF Health News found that multiple audits of Colorado’s eligibility system, managed by Deloitte, uncovered errors in notices sent to enrollees. A 2023 review by the Colorado Office of the State Auditor found that 90% of sampled notices contained problems, some of which violate the state’s Medicaid rules. The audit blamed “flaws in system design” for populating notices with incorrect dates.

Deloitte declined to comment on specific state issues.

In March, Colorado officials paused disenrollment for people on Medicaid who received home health services, which includes people with disabilities, after a “system update” led to wrongful terminations in February.

Another common problem is people being told to reapply, which immediately cuts off their benefits, instead of appealing the cancellation, which would ensure their coverage while the claim is investigated, said attorney Miriam Harmatz, founder of the Florida Health Justice Project.

“What they’re being advised to do is not appropriate. The best way to protect their legal rights,” Harmatz said, “is to file an appeal.”

‘So Many People Are Calling’

But some disabled people are worried about having to repay the cost of their care. Saa, who lives in Davie, Florida, received a letter shortly before her benefits were cut that said she “may be responsible to repay any benefits” if she lost her appeal.

The state should presume such people are still eligible and preserve their coverage, Harmatz said, because income and assets for most beneficiaries are not going to increase significantly and their conditions are not likely to improve.

The Florida Department of Children and Families would not say how many people with disabilities had lost Medicaid home health services.

But in Miami-Dade, Florida’s most populous county, the Alliance for Aging, a nonprofit that helps older and disabled people apply for Medicaid, saw requests for help jump from 58 in March to 146 in April, said Lisa Mele, the organization’s director of its Aging and Disability Resources Center.

“So many people are calling us,” she said.

States are not tracking the numbers, so “the impact is not clear,” Edwards said. “It’s a really complicated struggle.”

Saa filed an appeal March 29 after learning from her social worker that her benefits would expire at the end of the month. She went to the agency but couldn’t stand in a line that was 100 people deep. Calls to the state’s Medicaid eligibility review agency were fruitless, she said.

“When they finally connected me to a customer service representative, she was literally just reading the same explanation letter that I’ve read,” Saa said. “I did everything in my power.”

Saa canceled her home health aide. She lives on limited Social Security disability income and said she could not afford to pay for the care.

On April 10, she received a letter from the state saying her Medicaid had been reinstated, but she later learned that her plan did not cover home health care.

The following day, Saa said, advocates put her in touch with a point person at Florida’s Medicaid agency who restored her benefits. A home health aide showed up April 12. Saa said she’s thankful but feels anxious about the future.

“The toughest part of that period is knowing that that can happen at any time,” she said, “and not because of anything I did wrong.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues.

Epstein-Barr Virus Emerging As Possible Cause of Chronic Pain

By Dr. Forest Tennant, PNN Columnist 

When most people hear about the Epstein-Barr virus (EBV), they may recall its reputation as the rather harmless "kissing disease" known as mononucleosis.  To the surprise of many, this previously unheralded virus has recently emerged as a cause of some cancers and painful disorders.

It is now clear that EBV must be contained and suppressed in order to relieve the pain and suffering of many persons with chronic pain. This column is an introduction to the critical involvement of EBV with several chronic pain conditions.

The Epstein-Barr virus is named after Drs. Anthony Epstein and Yvonne Barr. In 1964, they discovered the virus after they found it in a cancer common in Africa called Burkitt’s Lymphoma.  Since that time, EBV has been found to cause other cancers including nasopharyngeal, gastric, Hodgkin’s lymphoma, and leukemia.  Some estimate that EBV causes about 200,000 cancers a year.

About three years after Epstein and Barr discovered EBV, it was found to be the cause of infectuous mononucleosis, which is known to trigger autoimmune complications.  Autoimmunity is simply defined as some element in the body that attacks, erodes, and destroys tissue. 

In 1968, this author reported that mononucleosis could cause glomerulonephritis, an autoimmune renal disease.  Over the ensuing decades, EBV has also been associated with other autoimmune disorders, including hepatitis, rheumatoid arthritis, fibromyalgia, systemic lupus, and Sjogren's syndrome.

EPSTEIN-BARR VIRUS

In 2018, a seminal study documented that EBV could cause a number of painful medical conditions by activating specific genes.  Dr. John Harley and colleagues at Cincinnati Children's Hospital Medical Center, with funding from the National Institutes of Health, found that a viral protein called Epstein-Barr nuclear analog 2 (EBNA 2) binds to the deoxyribonucleic acid (DNA) of genes that promote autoimmunity and some chronic pain conditions.

The pain conditions that Harley and his colleagues associated with EBV are multiple sclerosis, rheumatoid arthritis, celiac disease, type 1 diabetes, inflammatory bowel disease, thyroiditis, and juvenile arthritis.  Subsequent studies added Sjogren's syndrome, mixed connective tissue disease, and polymyositis to the list of EBV autoimmune conditions.

The Harley research is compelling.  We urgently need clinical studies of EBV in severe chronic pain patients to help develop new diagnostic, prevention, and treatment measures.  To this end, I've chosen to study the EBV relationship to painful spine and connective tissue diseases, especially adhesive arachnoiditis (AA) and Ehlers-Danlos syndrome (EDS). These conditions are considered intractable pain conditions in clinical pain practice. 

So far, we have collected EBV laboratory test results from over 80 persons with confirmed AA. Every case has demonstrated abnormally high levels of EBV IgG antibodies, which suggests the presence of autoimmunity and the possible invasion of brain and spinal tissue by the virus. 

Every patient with high IgG antibody levels also has herniated discs, and the majority have hypermobile EDS. Prior to developing AA, all had conditions associated with autoimmunity, such as fibromyalgia and small fiber neuropathy. All of them now have intractable pain.

How It Begins

Patients and clinicians concerned about chronic pain need to understand the basics of how EBV causes and aggravates chronic pain conditions. 

EBV is a member of the herpes virus family, which includes the other herpes viruses and cytomegalovirus.  It is a natural, lifelong parasite that usually infects children before the age of two. 

When EBV first enters the body, it is an “active” virus that may cause a cold, sinusitis, bronchitis, or possibly even go unnoticed. Infants and young children often have the “sniffles” and it could be mistaken as a simple cold. Some children who initially become infected with EBV later develop mononucleosis in their teenage or young adult life.  

After the initial infection, EBV settles into one’s lymphocytes and lining of the throat and nasal cavity to remain for life. Under normal physiologic circumstances, it is a latent or dormant parasite that does no harm.

Over 95% of adults will test positive for low levels of IgG antibodies, decades after their initial contact with EBV during childhood. When chronic pain patients are tested, autoimmunity is suspected if IgG antibodies are above normal levels found in the great majority of adults.

Once EBV has settled into lymphocytes or the throat lining and becomes dormant, it is living a harmless, symbiotic, parasitic life with its human host.  It will remain in this state, unless the body undergoes some kind of stress, usually trauma or an infection, that lowers or degrades the body's innate or natural immunologic protection systems. 

At this time, the virus may vacate its dormant or latent state to begin what is called a "lytic" or duplicative state.  The term used to indicate this state is "reactivation," meaning that the virus is again active, and attacking and invading new tissues. 

Once reactivated, EBV may create an autoimmune state by altering genes or by developing what is called an auto-antibody that will attack tissues.  In either case, an autoimmune state has been created that attacks normal tissues to produce inflammation, adhesions, scarring, and pain. 

Lymphocytes infected with reactivated EBV may enter any number of tissues. They may cross the blood brain barrier, enter the spinal cord and brain, and attack tissues such as the cauda equina, arachnoid membrane, intervertebral discs, and glial cells. This is the pathologic process in which EBV reactivation may cause chronic pain.

It is likely that entry and invasion of spinal canal and brain tissues may be responsible for the autoimmune manifestations seen after a stroke, head trauma, or complex regional pain syndrome (CRPS).  EBV may also be a cause of centralized pain that is associated with over-sensitization, hyperalgesia, and intractable pain.  There are reports that such common chronic pain conditions as fibromyalgia, small fiber neuropathy, and some arthropathies are caused by EBV autoimmunity.

This article's major intent is to inform all concerned parties that deal with chronic pain that EBV is not just some virus that causes the "kissing disease." It is a new revelation that compels an understanding and awareness that has the distinct potential to improve the plight of chronic pain patients. 

Laboratories and clinical researchers, including this author, are scurrying to identify more diagnostic, treatment, and preventive measures for EBV-caused autoimmunity. I'm pleased to report that our EBV project has been able to identify some initial testing and treatment measures which appear to be effective and a good start in dealing with EBV autoimmunity.  We will share our findings in future articles.

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain and arachnoiditis. Readers interested in learning more about this research should visit the Tennant Foundation’s website, Arachnoiditis Hope. You can subscribe to its bulletins here.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

How to Recognize and Treat Intractable Pain

By Dr. Forest Tennant, PNN Columnist

The realization that a subgroup of chronic pain patients has intractable pain is finally spreading. Over half a dozen states now have laws protecting intractable pain (IP) patients and Wikipedia refers to IP as a disease that causes “a severe, constant, relentless, and debilitating pain.”

A major impediment to treatment of IP is simply that it is not commonly recognized by either patient or practitioner. Basically, the concept that pain alone can cause serious medical complications is not yet appreciated. This fact is evidenced in product advertising and lay person media articles about “chronic pain.” A close analysis implies that everyone has simple chronic pain and needs a “one size fits all” treatment.

The fact is that the IP subgroup of patients isn’t recognized by even the most sophisticated and prestigious medical institutions. For example, I hear almost daily about a person with IP who has severe hypertension, tachycardia, or even angina without any recognition that IP is the culprit.

Other examples are persons with IP who have hormonal deficiencies. Medical practitioners are treating their patients for such hormonal complications as osteoporosis, impotence, and depression, with no recognition that IP is the cause. Regrettably, some persons have had their pituitary or adrenal removed for a “tumor” when in reality the gland was over functioning and enlarged due to IP.

About half of the persons who develop IP have a genetic or inherited disorder. The most common high risk genetic conditions are Ehlers-Danlos Syndrome (EDS), ankylosing spondylitis, and scoliosis.  Other genetic, but less common, risk disorders include Marfan Syndrome, porphyria, and autoimmune diseases such as rheumatoid arthritis and ulcerative colitis. 

How IP Starts 

Thanks to research and studies in recent years, there is now an understanding of the pathologic sequences that lead to IP.  Basically, IP is the end product of multiple events and conditions that may affect a person.   

IP always has a starting or painful initiating event which is either traumatic or inflammatory. Typically, the initiating event takes place several months or years before IP symptoms develop. 

The most common traumatic events are falls, altercations or surgery. Trauma may be to the head, spinal cord, or a nerve in the arm or leg.  The most common initiating inflammatory disorders are fibromyalgia, severe respiratory infection or arthritis. 

The initiating event doesn’t usually cease but “smolders on” with pain that comes and goes.  A diagnosis of chronic pain is likely assigned, and a wide variety of medications and other measures are attempted.   

Interestingly, an initiating inflammatory event such as arthritis or fibromyalgia may seemingly spread. The person may develop additional inflammatory disorders such as thyroiditis, carpal tunnel syndrome, migraine, and irritable bowel. 

Trauma may be severe or minor and the sequelae quite variable. Neuropathies or intervertebral disc degeneration and herniation are the most common traumatic complications that lead to IP.  Pain after the initiating event is usually not constant, but at some point becomes constant. 

This constancy is associated with inflammation that develops in the brain and/or spinal cord of the central nervous system (CNS). Cells called glia or microglia promote CNS inflammation, which can damage the neurotransmitter-receptor systems that control pain.   

Exactly how injuries and inflammatory disorder activate glial cells to produce CNS is unclear. The two most discussed mechanisms are excess electromagnetic energy generated in the injury and inflammatory sites, and autoimmunity or viral invasion of CNS tissue.  The Epstein Barr virus is the most likely virus.

The first chapters of my new book, “Handbook for Intractable Pain,” are dedicated to how to recognize IP symptoms. The second section is a step-by-step treatment program of self-help.

IP doesn’t have to thrust a person into misery and a short life if a three-component protocol is followed:

1. Suppression of inflammation and autoimmunity

2. Restoration of damaged tissues

3. Pain control

To carry out this protocol, one has to become knowledgeable about IP and build, over time, an effective therapeutic program.

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain. To Tennant Foundation has launched a new website, IntractablePain.org, where you can learn more about the conditions that cause intractable pain and their many complications.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

Understanding the Difference Between Chronic Pain and Intractable Pain

By Dr. Forest Tennant, PNN Columnist  

The difference between simple chronic pain and intractable pain (IP) is what is known as pathologic sympathetic overdrive. This major medical complication is characterized by excessive electrical activity in the body's sympathetic nervous system. Excess electricity causes hyperarousal and pathologic overactivity of the sympathetic nervous system, which controls the body’s stress response. A comprehensive grasp of this complication is crucial for effective treatment.

Pathologic complication is the root cause of the disability, profound suffering and shortened lifespan often caused by intractable pain. Even though I recognized and published the difference between chronic and intractable pain in the Western Journal of Medicine over 20 years ago, it is still poorly understood in the mainstream medical practices of today. This contributes greatly to the undertreatment and mistreatment of IP patients.

The severe, constant and disabling pain of IP causes anatomical defects in the brain, which leads the cells in the brain to generate excess electricity. This is how pathologic sympathetic overdrive (PSO) starts. The brain must get rid of the excess electricity to prevent damage from the “burning” of brain tissue.

The brain rids itself of excess electricity by sending it into the sympathetic nervous system. This system is comprised of nerves that connect the brain to the heart, blood vessels, skin, lung and gastrointestinal system. The best-known neural connection in the network that connects the brain to bodily organs is the vagus nerve, but there are less known nerve connections in and along the spinal cord.

The “overdrive” of excess electricity produces a typical set of easily recognized symptoms and physical signs. These include an elevated pulse rate (tachycardia), high blood pressure, cold extremities (sometimes exhibiting a bluish hue), goosebumps, dilated pupils, and hyperactive reflexes. Another common symptom is temperature spikes and flushing, often followed by chills.

Amazingly, while the nation persistently clamors about the importance of controlling blood pressure, making Americans very aware that hypertension leads to serious medical conditions and is one of the leading causes of death in the U.S., I cannot identify a single lay magazine or medical journal that even refers to the undeniable correlation between severe, unmanaged pain and high blood pressure.  Strangely, there is also a conspicuous absence of discussions even in medical publications about the necessity of adequate pain management to reduce blood pressure.

Complications Caused by Intractable Pain

PSO interferes with normal respiratory function. The lungs may not expand and bring in the normal level of oxygen, and carbon dioxide may elevate in the blood. Inadequate oxygenation may lead to lethargy, fatigue, poor motivation, muscle weakness and mental impairment.

An IP patient’s ability to sleep, and especially achieving adequate REM sleep, is greatly reduced by PSO.  The hazards of inadequate sleep are well-known: fatigue, depression, amotivation, poor mental activity, and hormone imbalances. A tragic misunderstanding is the belief that somehow a lack of sleep is better than taking a bedtime sedative. This notion lacks any scientific merit.

There are lesser known but other serious and debilitating sequalae of PSO. The gastrointestinal system becomes so impaired by PSO to the point that loss of appetite, malabsorption (nutrients do not assimilate) and malnutrition is present in essentially all IP patients. The disturbed nutritional metabolic deficits can lead to either significant weight gain or loss. Constipation and diarrhea will often alternate, while stomach pain and bloating are routine. Patients are often misdiagnosed as having irritable bowel syndrome (IBS), with treatment that gives no consideration that bowel symptoms will persist without control of the underlying IP.

PSO has a significant impact on the endocrine system, similar to the body's "fight or flight" response during moments of stress. With IP the stress is constant. This physiological response involves an increase in adrenaline and cortisone levels in the bloodstream. Normally, this response to stress is temporary, allowing the adrenal and pituitary glands to recover and remain intact. But with the constant pain and electrical overdrive of IP, the glands hypertrophy (enlarge abnormally) trying to keep up their hormonal output to protect the body.

Unfortunately, the glands will often deplete. IP patients have died due to adrenal failure as the glands could not produce enough cortisone and adrenaline to maintain life. PSO tends to especially cause the pituitary gland to enlarge. Some uninformed surgeons have “removed the pituitary tumor” without understanding the root cause of the enlargement, or the imperative need to manage pain.

If PSO goes on long enough, and the pituitary and adrenal glands exhaust or wear out, testosterone and estradiol will deplete. While most people are aware of the impact of such depletion on libido and menstrual functions, what many medical practitioners miss is the critical role these hormones play in tissue healing, pain reduction, and various mental functions.

Since PSO raises cortisone for as long as one has IP, calcium is extracted from bones and teeth. Osteoporosis may develop and teeth may deteriorate. Sudden loss of a tooth is common in IP as is chronic dental cavities.

PSO in an adult IP patient will often cause some level of adult attention deficit disorder (ADD/ADHD), which is the exact clinical syndrome that occurs in a child with hyperactivity or attention deficit disorder. Furthermore, when the IP patient develops the same “attention deficits,” they will need the same medications that a child does to normalize attention span, carry out the 3R’s (“reading, riting, rithmetic”), and activities of daily living.

The mental aberrations caused by IP, unless treated with today’s hyperactivity medications (Ritalin, Adderall), can be so debilitating that the IP patient can become a lonely, despondent invalid, who becomes expensive to care for and totally dependent on family and society. The medical profession’s rejection or dismissal of ADD/ADHD in IP patients can only be classified as blatant professional oversight.

Diagnosing Intractable Pain

It is essential to point out that a medical practitioner who understands PSO can distinguish an IP patient from a simple chronic pain patient with a 5-to-10-minute physical examination. For starters, the IP patient with PSO will show some abnormality of pulse-rate, blood pressure, temperature or breathing rate. Some reflexes will be hyperactive, and the pupil may be dilated.  Hands and feet will be cold to touch and may show a blue discoloration. Teeth will be missing and/or show a lot of decay. Mental activity and speech may be slow and deliberate. Movement also may be slow.

These physical signs correlated with the history and symptoms provided by the patient and family will easily and quickly nail down the presence of IP and PSO, without the need for blood tests or brain scans.

This essay is a call for all parties concerned to fully understand the difference between chronic pain and intractable pain with PSO. Every IP patient, family and medical practitioner must fully understand that PSO will cause dire complications. IP patients and their families need to recognize them and record their PSO manifestations and present them to their medical practitioners.

Sadly, this author cannot identify a single education effort by a recognized medical publication, organization or academic institution that has or is currently trying to educate on the obvious and blatant clinical manifestations of the sympathetic pathological complications of IP. Like most things in medical science and practice today, the demand and education must “start at the bottom and work up.”

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain. To help patients and clinicians better understand intractable pain, the Tennant Foundation has launched a new website, IntractablePain.Org, where you can learn more about the conditions that cause intractable pain and their many complications.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

The Way Forward: California’s New Opioid Guidelines

By Dr. Forest Tennant and Kristen Ogden

The Medical Board of California recently published new guidelines for prescribing opioids and other controlled substances for pain, which emphasize “individualized care” that is customized for each patient. 

The guidelines are a remarkable, positive and practical way forward in pain care. All persons concerned about chronic pain treatment with opioids, benzodiazepines and other controlled drugs need to know the basic concepts embedded in them.    

As the medical board was updating its guidelines, we had great concern that they would bury California’s Pain Patient's Bill of Rights and Intractable Pain Treatment Act. When these laws were passed in the 1990’s, they were a godsend to patients with chronic intractable pain, who were given the right to “request or reject the use of any or all modalities in order to relieve his or her pain.”

That means patients, with the support of their doctors, could get opiate medication without first having to submit to surgery, medical devices and other forms of pain treatment.  

To our great pleasure, the medical board’s new guidelines recognize, define and support these worthy laws.  Importantly, the guidelines also state that they are “not in any way intended to limit treatment” of patients in hospice or palliative care. And they allow for doctors to prescribe high dose opioids, provided they keep good medical records that document a need for them.

Defining Intractable Pain

The California guidelines provide a classic definition of intractable pain as “a state in which the cause cannot be removed or otherwise treated and no relief or cure has been found after reasonable efforts.” 

The problem with this definition is that intractable pain may be mild or intermittent and not curable, but may still be treated with non-opioid modalities. To require and receive treatment with opioids and other controlled drugs, one really needs a specific causative diagnosis of the unremitting “high impact” pain that produces physiologic complications such as hypertension, tachycardia, and endocrine deficiencies. 

Put another way, is intractable pain an incurable but treatable problem? Or is it constant and incurable with potentially life-threatening complications? 

Physicians, as a group, are often mystified, confused and unaware of how to determine which patients have an incurable, but readily treatable problem, and which patients have the constant and incurable pain that causes complications and require opioid therapy.

Physicians need help to make sound, defensible treatment decisions in the face of this quandary.  Some patients with complex intractable pain are greatly impacted and require non-standard treatment, which may include high-dose opioids, benzodiazepines and stimulant drugs. 

Here are the recommended criteria to identify such patients and support non-standard treatment plans.

1. A specific medical cause of intractable pain has been identified.

2. Constant pain has impacted some physiological and/or mental functions such as sleep, eating, hygiene, reading, concentration, and mobility.

3. Trials of standard medications and dosages with such agents as anti-depressants, muscle relaxants, anti-inflammatories, stimulants, anti-seizure medications, and low-dose opioids have not controlled pain or normalized functions.

4. There is objective physical evidence of the causative disease or complications of the pain, such as hypertension, tachycardia, neurologic deficits, or anatomic structural abnormalities.

5. There is an objective, diagnostic test result that documents an abnormality of the cause of pain or its complications, such as a magnetic resonance imaging (MRI), hormone deficiency, elevated autoimmune or inflammatory marker, or an abnormal electrodiagnostic test.

It is the lack of adequate treatment of complex intractable pain that is really the crux of the suffering and deaths that have emerged due to overzealous and misinformed opioid regulations and guidelines.  These legitimate, complex patients comprise about 3 to 5% of chronic pain patients.

The California medical board’s new guidelines provide clinicians the opportunity to implement individualized and effective treatments for these unfortunate and deserving intractable pain patients. 

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain. Dr. Tennant was the lead physician in crafting California’s Intractable Pain Law and Pain Patient Bill of Rights, and worked with the legislature to get them passed. 

Kristen Ogden is a patient advocate from Virginia. Kristen and her husband Louis travel regularly to California for his intractable pain treatment and prescriptions, which are not available in their home state. Kristen testified during public hearings on the California guidelines and closely followed their development. 

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

Colostrum: A Regenerative Hormone for Arachnoiditis

By Dr. Forest Tennant, PNN Columnist

Persons with adhesive arachnoiditis (AA) and other severe painful conditions such as Ehlers-Danlos syndrome (EDS) have multiple tissues that become damaged, painful and dysfunctional.

Healing those damaged tissues and reversing the pain and neurologic impairments will require regenerative hormones. This is in contrast to other types of hormones that control inflammation (cortisone), metabolism (thyroid) or sexual functions (estradiol).

The human body makes some natural regenerative hormones, and they are now available for clinical use. Our first realization of their value in treating AA was with human chorionic gonadotropin (HCG). Other regenerative hormones that can be used to treat AA include colostrum, pregnenolone, dehydroepiandrosterone (DHEA), nandrolone, and human growth hormone (HGH). We have used all of these and believe that persons with AA should use at least one of them. But our first choice is colostrum.

Colostrum is in mother’s milk produced during the first few days after birth. It contains high levels of tissue growth factors, anti-inflammatories, pain relievers, and anti-infectious agents. Its natural purpose is to allow the newborn baby to initiate growth, protect against infection, and provide pain relief from the trauma of birth.

Colostrum supplements are sold by a number of companies and are usually made from the milk of cows that have recently given birth. Colostrum is recommended for use at least 3 to 5 days a week by persons with AA or EDS, who may wish to double the labeled recommended dosage. Colostrum is non-prescription, relatively inexpensive, and has few side effects. It can be taken with opioids and other drugs.

Regenerative hormones work best when they are used simultaneously with a high protein diet, collagen or amino acid supplements, vitamin C, B12, and polypeptides.

If a person with AA is not doing well or deteriorating, we recommend adding a second regenerative hormone such as nandrolone. A significant reversal of AA symptoms may require one or more regenerative hormones.

Several times a week we get inquiries from people who have just been diagnosed with AA and are pleading for information on what to do. 

The Tennant Foundation recently published an inexpensive short handbook for persons with newly diagnosed AA that gives a step-by-step plan that can hopefully slow progression of this disease.

If you have had AA for a while and aren't doing well, you may still benefit from some of our most up-to-date knowledge and recommendations in the “Handbook for Newly Diagnosed Cases of Adhesive Arachnoiditis.”

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain and arachnoiditis. This column is adapted from bulletins recently issued by the Tennant Foundations’s Arachnoiditis Research and Education Project. Readers interested in subscribing to the bulletins should click here.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

What Kind of Pain Care Would JFK Get Today?

By Pat Anson, PNN Editor

This year marks the 60th anniversary of the assassination of President John F. Kennedy, an event that shocked the world. Kennedy was only 46 when he died in 1963.

At the time, Kennedy was widely seen as a healthy, handsome and vigorous man. The truth, which emerged years later, is that JFK was chronically ill almost from birth. Scarlet fever nearly killed him as an infant, and as a child he was thin, sickly, and suffered from chronic infections and digestive problems.

Not until decades after his death did we learn that Kennedy was born with an autoimmune condition called polyglandular syndrome, and that a series of failed back surgeries may have led to adhesive arachnoiditis, a chronic and painful inflammation in his spinal canal. Historians and physicians also confirmed rumors that JFK suffered from Addison’s Disease, a well-guarded family secret.

Kennedy was given the last rites at least twice before becoming president and reportedly told his father that he would “rather be dead” than spend the rest of his life on crutches, paralyzed by pain.

In short, it’s a bit of miracle that JFK even lived to see his 46th birthday. The American public never had a full understanding of his health problems until long after he was dead.

How did Kennedy pull it off? The answers can be found in Dr. Forest Tennant’s latest book, “The Strange Medical Saga of John F. Kennedy.”

“The reason I decided to write it was mainly that I had become aware that he was an intractable pain patient,” says Tennant, a retired physician and one the world’s foremost experts on arachnoiditis and intractable pain. “Fundamentally, my book is really taking a lot of other people's work and putting it together in a historical chronological fashion. I just felt it needs to be done to really understand what happened to him.”

Although Kennedy’s chronic health problems were largely hidden from the public, many of his medical records still exist – a reflection of his family’s wealth and access to the best medical care available. Good doctors keep good medical records, especially when their patients are rich and famous.

“Until I got into doing this, it was not appreciated by me. Unless a person is very famous and has a lot of medical records, physicians never get to see a case from start to finish. Meaning from birth to death. I've never really realized how rare that is,” says Tennant.

A Controversial Drug Cocktail

In the mid 1950’s, Kennedy found a team of innovative medical experts who helped relieve his pain, elect him as president, and achieve his best health ever while living in the White House.

Dr. Max Jacobson put Kennedy on a controversial “performance enhancing” cocktail. The ingredients were secret, but Tennant says the cocktail probably included methamphetamine, hormones, vitamins and steroids.

Exhausted from months of campaigning, Kennedy was injected with the cocktail just hours before his first debate with Richard Nixon, a nationally televised debate that likely won the election for Kennedy because he appeared more energetic than Nixon.

Kennedy continued taking the cocktail as president, over the objections of White House physicians.

High Dose Opioids

Dr. Janet Travell also played a key role in revitalizing Kennedy’s health, putting him on a comprehensive pain management program that included physical therapy, hormone replacement, anti-inflammatory drugs, and the opioids methadone, codeine and meperidine (Demerol).

One of the first things she noticed was the callouses under Kennedy’s armpits from using crutches so often.

“On the day she met him, she put him in a hospital and started methadone that day, as a long-acting opioid, and then she also had him on Demerol and some other miscellaneous opioids. But his two main opioids were methadone and then Demerol for breakthrough pain,” said Tennant.

The precise dosage given to JFK is unknown, but Tennant estimates it was initially 300 to 500 morphine milligram equivalents (MME) a day, a level that would be considered risky under the CDC’s 2016 opioid prescribing guideline. The guideline recommended that dosages not exceed 90 MME.

“It would have exceeded the CDC guidelines by far,” says Tennant. “The methadone dose would have exceeded the CDC guidelines itself. But she knew to put him on methadone and if it hadn't been for methadone, he’d never have been president. He had to have something to stabilize himself right at that time. And he had to have a second opioid for breakthrough pain.”

Dosages that high today would likely attract the attention of the Drug Enforcement Administration, which investigates and prosecutes doctors for writing high-dose prescriptions. Tennant himself came under scrutiny from the DEA for giving intractable pain patients high doses, and his office and home were raided by DEA agents in 2017. Tennant was never charged with a crime, but he retired from clinical practice a few months later.

Raids like that have had a chilling effect on doctors nationwide. Many now refuse to see pain patients on opioids, regardless of the dose.

“JFK would not have been welcome today in pain clinics,” says Tennant. “My patients were very similar to JFK, almost same disease, same kind of doses, and the same kind of therapies. And of course, today that is taboo. But that was the standard in the 1950’s.  

“It's only been in the last few years that the government has decided that the standard treatment that has been there for half a century is now almost a crime.”

Dr. Travell never came under that kind of scrutiny, but Dr. Jacobsen did. Dubbed “Dr. Feelgood” by critics for his unconventional treatments, Jacobson’s medical license was suspended in New York state a few years after Kennedy’s death. The 1972 Controlled Substances Act ensured that his cocktail would never be prescribed again.

Tennant says there is no evidence the cocktail harmed or impaired JFK, who was never hospitalized or bed-bound during the 8 years he was under Jacobson’s care.

Without Jacobson and Travell, Tennant believes it unlikely Kennedy would have run for president or been elected.

“That's one of the reasons why I wrote the book. I think people need to know that JFK’s treatment was opioids. And his treatment was the standard of the day, up until the recent fiat by the federal government and state medical boards. The country got along for half a century with those standards quite well,” Tennant said.

In addition to his book about JFK, Tennant has written books about Howard Hughes and Elvis Presley, who also lived with -- and overcame -- chronic health problems.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.  

How Realistic Is a Possible Treatment for Hypermobile EDS?

By Crystal Lindell, PNN Columnist

Ever since I was diagnosed with hypermobile Ehlers-Danlos Syndrome (hEDS) back in 2018, I’ve spent countless hours contemplating what my life would be like if there was an effective treatment.

Last week, Tulane University School of Medicine pushed that question to the forefront. They announced that they may have found a potential cause of hEDS and hypermobility in general. They also theorized a potential treatment.

Ehlers-Danlos Syndrome (EDS) creates fragile connective tissue, which can cause a range of other symptoms including joint pain, digestive trouble, migraines and more.  

Tulane researchers proposed that a variation of the MTHFR gene that causes a deficiency of folate – the natural form of vitamin B9 – could hold the key to hypermobility and a range of connective tissue disorders such as EDS. As for treatment, they hypothesized that methylated folate — which is folate that is already processed — could be a possible treatment for the myofascial pain that’s common for hypermobile patients. They published these preliminary findings in the journal Heliyon.

First, it should be noted that none of this was based on a clinical study of patients. Rather, it’s a proposal that they believe should be researched further. As such, there’s been some valid criticism of Tulane’s announcement from the EDS community. Was it premature? Will any of this hold up in a peer-reviewed study? Or are they just giving false hope to the thousands of EDS patients desperate for some good news?

As an EDS patient myself, I understand those concerns and I very much sympathize with them. Many of us have spent too much time being dismissed by doctors, and too much money on treatments that don’t end up working.

Unfortunately, I think we’re going to have to live in the uncertainty right now. We won’t know if this is a viable option until we get a peer-reviewed study. But I am glad that they are looking into this and sharing these types of updates as the research progresses. I’d rather be informed along the way than only be told at the end of the process.

What Would a Treatment Mean for Patients?

What if their theory is correct though? Is that a good thing? I have to confess, my feelings about it are complicated.

The thing about EDS is that it’s different for everyone. As it stands, most doctors treat the symptoms, which, as mentioned above, vary widely. For me, the most debilitating one is intercostal neuralgia — which is not a type of myofascial pain. As such, it seems unlikely that methylated folate would do much to treat it.

But hey, maybe methylated folate is more of a preventative treatment? That alone would be an incredible advancement for hEDS patients.

The question is, would this treatment impact anything else? Do they know if it would only address myofascial pain? Or could it also help with other symptoms? And would that even be a good thing if it did?

EDS touches every aspect of my body and even most aspects of my personality. There’s the velvety skin everyone comments on when they shake my hand. And the constant comments about how I look for my age, which also seems to be related to how EDS impacts my skin. Would methylated folate treatment change that at all? How so? And what would I end up looking like?

The most well-known EDS symptom is probably loose joints, which means they easily overextend. For me, that’s meant a lifetime of sprained ankles and joint pain. But again, what happens if methylated folate changes that? My joints may be loose, but they’re the only ones I’ve ever known. Would stiffening them up actually help me at this point? Or would I have to re-learn how to move my own body?

What about my mind? EDS patients have higher than average rates of neurodivergence like autism and ADHD. They also have higher rates of mental health issues like depression and anxiety. Could this treatment change our brains too? Or, if not, what if they eventually find a treatment that does? Would it alter aspects of people’s personalities?

There’s also the more logistical issue of EDS as a name at all. According to the National Library of Medicine, a syndrome refers to a group of symptoms and physical findings without a direct cause. Once a cause is found, the symptoms are typically renamed as a “disease.” So, if the researchers at Tulane did find a cause, what do we have? Ehlers-Danlos disease? EDD?

One thing we do know is that EDS and hypermobility cause immeasurable pain and suffering for a lot of people, so we do need more research into potential treatments. Time will tell if folate treatment proves effective or not, but either way, I hope that there are a lot more potential treatments coming.

Crystal Lindell is a freelance writer who lives in Illinois. After five years of unexplained rib pain, Crystal was finally diagnosed with hypermobile Ehlers-Danlos syndrome. She and her fiancé have 3 cats: Princess Dee, Basil, and Goose. She enjoys the Marvel Cinematic Universe, Taylor Swift Easter eggs, and playing the daily word game Semantle. 

Researchers Find Possible Cause of Hypermobile EDS

By Crystal Lindell, PNN Columnist

Do we finally have a genetic link for hypermobile Ehlers-Danlos syndrome?

Researchers at Tulane University School of Medicine think so – and it could even point to an effective treatment that’s already available.

A variation of the MTHFR gene that causes a deficiency of folate – the natural form of vitamin B9 – could hold the key to hypermobility and a range of associated connective tissue disorders such as Ehlers-Danlos (EDS), according to preliminary findings published in the journal Heliyon.

“You’ve got millions of people that likely have this, and until now, there’s been no known cause we’ve known to treat,” said Gregory Bix, MD, director of the Tulane University Clinical Neuroscience Research Center. “It’s a big deal.”

People with the genetic variant can’t metabolize folate, which causes unmetabolized folate to accumulate in the bloodstream. The resulting folate deficiency in other parts of the body prevents key proteins from binding collagen to the extracellular matrix, which plays an important role in cell growth. This leads to more elastic connective tissue, hypermobility, and a potential cascade of associated conditions, researchers said.

The discovery could help doctors more accurately diagnose hypermobility and hypermobile EDS by looking for elevated folate levels in blood tests and the MTHFR genetic variant.

“Hypermobility is widespread and unfortunately under-recognized,” said Jacques Courseault, MD, medical director of the Tulane Fascia Institute and Treatment Center. “I’m excited about being able to treat the masses where people aren’t going their whole lives being frustrated and not getting the treatment they need."

Doctors discovered the connection between folate deficiency and the MTHFR gene by working with patients at Tulane’s Hypermobility and Ehlers-Danlos Clinic, the only clinic in the U.S. that focuses on fascia disorders. Blood tests of hypermobile patients revealed elevated levels of unmetabolized folate. Subsequent tests showed that most of those with elevated folate serum levels had the MTHFR genetic variant.

The good news is a treatment already exists. Methylated folate – folate that is already processed – is FDA-approved and widely available.

“It’s an innocuous treatment,” Bix said. “It’s not dangerous, and it’s a vitamin that can improve people’s lives. That’s the biggest thing: We know what’s going on here, and we can treat it.”

“We’ve discovered something in medicine that can help, not a small group of people, but potentially many across the world.”

— Dr. Jacques Courseault

Though more studies and clinical testing needs to be done, researchers say patients who have been treated with folate have shown improvement: less pain, less brain fog, fewer allergies and improved gastrointestinal function.

“We’ve discovered something in medicine that can help, not a small group of people, but potentially many across the world,” Courseault said. “This is real, it’s been vetted out well and clinically we’re noticing a difference.”

What Is Hypermobile EDS?

For those with hypermobile Ehlers-Danlos syndrome (EDS), the same conditions that create fragile connective tissue can cause a range of other symptoms that, on the surface, can seem unrelated: joint pain, chronic fatigue, thin tooth enamel, dizziness, digestive trouble and migraines, as well as psychiatric disorders such as anxiety and depression. Women with hypermobile EDS may also be at increased risk for endometriosis or uterine fibroids.

For years, researchers have struggled to find the cause of hypermobility and hypermobile EDS. Of the 13 subtypes of EDS, hypermobile EDS comprises more than 90 percent of cases. But until this study, hypermobile EDS was the only subtype without a known genetic correlate. As a result, symptoms have often been treated individually, without EDS being recognized as the likely cause.

Until now, hypermobility could only be diagnosed by the Beighton score, a somewhat controversial physical exam that involves measuring the bend of the spine, fingers and limbs. There has also been a historic lack of acceptance of hypermobility as a disorder that requires specialized treatment.

Many patients with hypermobile EDS never get a proper diagnosis. As a result, the number of people with hypermobility is unclear, though it could comprise more than half the world’s population.

“Hypermobility is not rare,” Courseault said. “Hypermobility is like a Ferrari that requires a lot of maintenance and the best synthetic oil. After knowing a patient's name and date of birth, I think it's prudent for clinicians to know which of these body types they have.”

Crystal Lindell is a freelance writer who lives in Illinois. After five years of unexplained rib pain, Crystal was finally diagnosed with hypermobile Ehlers-Danlos syndrome. She and her fiancé have 3 cats: Princess Dee, Basil, and Goose. She enjoys the Marvel Cinematic Universe, Taylor Swift Easter eggs, and playing the daily word game Semantle.