Monday, 20 May 2019

Low Blood Volume, ME/CFS and Slow, Chronic Sepsis

https://www.syndromea.org/2019/05/17/low-blood-volume-a-sepsis-like-syndrome-mcas/

Summary

A very common cause of sepsis is the leakage of bacteria into the blood from the gut. ME/CFS patients have signs of leakage of bacteria from the gut into the blood and our illness looks a lot like sepsis. Low blood volume and mast cell activation may have everything to do with this process.

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In a 2018 paper, Dr. Maureen Hanson’s group conducted a study on microbiota and ME/CFS patients.  The microbiota is the collection of microorganisms that live in the gut.

Hanson’s team found that a substance called LPS was significantly elevated in the blood of patients. LPS is a substance from the cell walls of certain bacteria.  LPS becomes elevated in the blood when there is an increased permeability or leakiness of the intestines.

Other researchers have had similar findings with regard to LPS and ME/CFS patients.

Dr. David Bell, a longtime ME/CFS physician and member of the Open Medicine Foundation has compared ME/CFS to a slow, chronic version of sepsis.  The commonalities between these two conditions include low blood pressure, low blood volume, a loss of energy production at the cellular level, and widespread inflammation.

LPS, from either a bacterial infection or a damaged or leaky gut, is the most common cause of sepsis, a body-wide inflammatory disorder that kills 40% of its victims. LPS is a powerful trigger of inflammation and, because it spreads through the blood, it can cause inflammation all through body.

At the most recent Open Medicine Foundation Symposium, Dr. Bell’s book on this subject was held up in front of the audience and the speaker said essentially that Dr. Bell was really on to something.

Does a chronic trickle of LPS from the gut into the bloodstream of ME/CFS patients trigger a slow, chronic sepsis? It seems obvious that it could.

What causes this slow leak, this elevated amount of LPS in the bloodstream of patients?

ME/CFS patients have consistently been found to have chronically low blood volume. The loss of blood volume is enough to apparently cause our hearts to shrink in size. In ME/CFS patients with orthostatic intolerance, the amount of blood we are missing is equivalent to stage II hemorrhagic shock.

If ME/CFS is like a slow, chronic sepsis, we might also say that it is like a slow, chronic hemorrhagic shock.

Shock entails a loss of blood delivery to tissues.  This is called a loss of perfusion and the gut is extremely sensitive to losses of perfusion, much more so than many other organs in the body. Hemorrhagic shock, the type of shock that occurs when you lose blood, readily causes the gut to become leaky and release LPS into general circulation.

Mast cells are powerfully activated by LPS and a chronic slow leak of LPS into the bloodstream could be an obvious trigger of Mast Cell Activation Syndrome (MCAS), which so many of us suffer from.

In addition, the damage caused to the gut by problems with perfusion that may be largely caused by mast cells. 

Perhaps an existing propensity towards mast cell activation provides a powerful push towards an illness that looks like ME/CFS. Many more women than men get ME/CFS and female hormones powerfully stimulate mast cells.

Monday, 13 May 2019

He pioneered technology that fueled the Human Genome Project. Now his greatest challenge is curing his own son

https://edition.cnn.com/2019/05/12/health/stanford-geneticist-chronic-fatigue-syndrome-trnd/index.html

By Ryan Prior, CNN

May 12, 2019

(CNN) - Multiple times a day, every day, Ron Davis sits with his head bowed, waiting outside his son's bedroom for a subtle signal that it's all right to come in.

He opens the door to the space where Whitney has spent most of the last decade.

Whitney lies motionless on a simple bed, his head shaved and his frame emaciated. He's fed by a tube directly into his stomach. His lips haven't uttered a word in five years.

Davis, who is 77, leads a lab that invented much of the technology that powered the Human Genome Project. Now he and his wife spend much of their days caring for their 35-year-old son, who is immobilized by myalgic encephalomyelitis, or chronic fatigue syndrome (ME/CFS).

Sunday is ME/CFS International Awareness Day. There is no cure. But Davis is leading a global push to root out the molecular basis of what is laying waste to Whitney and millions of other sufferers around the world so that scientists can better treat the disease.

Davis signals to his wife, Janet Dafoe, that Whitney is ready. She goes in and wipes her son's face. She pulls the covers up toward his head while he lies motionless.

She fixes an IV bag to a pole, which will drip water into her son's veins.

Davis sinks to his knees and takes Whitney's socks off. He clips his son's toenails. He washes his son's feet.

For the couple, it's a holy moment.

Davis led a revolution in science

Davis and Dafoe will celebrate their 50th wedding anniversary in July. Decades ago, they would have never predicted their current situation.

Now their everyday lives are consumed with caring for their son. At least one of them must be at home every day to attend to Whitney.

"My wife and I can't go away together anymore," Davis says. They used to go to the beach every year, but it's been more than seven years since they last went. On basically a single income, they struggle with finances.

"It has turned my life upside down in many respects. I decided to terminate everything I was working on before Whitney got sick," Davis says. "Everything is ME/CFS now. It's an emergency kind of effort."

The couple have spent their careers in and around Stanford University. Davis worked for decades in the school's biochemistry and genetics department while Dafoe, who just turned 70, works as a child psychologist. She has scaled back her hours to about five hours a week to care for her son.

After his PhD at Caltech, Davis completed his postdoc at Harvard studying under Nobel Laureate Jim Watson of "Watson and Crick" fame, who was immortalized in science textbooks for co-discovering the double-helix structure of DNA in 1953.

Davis joined Stanford's biochemistry department in 1972 as an associate professor and quickly began making a name for himself.

He co-wrote one paper that created a map with a new way to link genes to the traits they caused, which became a cornerstone of the field of genomics. It led Davis and his colleague to write a "proposal for a map of the whole human genome." The National Institutes of Health turned them down in 1979, saying their plan was too ambitious.

But Davis kept innovating, eventually accumulating more than 30 patents for technology he developed.

Finally, the world caught up to his vision. The $3.8 billion Human Genome Project began in 1990, with Davis' gene-sequencing technologies at its core. Completed in 2003, it launched a revolution in science. Handing researchers that foundational blueprint for human life gave biologists and doctors what up to that point was an unimagined power to diagnose, treat and ultimately prevent the full gamut of human disease.

Davis was shortlisted by The Atlantic, along with SpaceX founder Elon Musk and Amazon founder Jeff Bezos, as someone tomorrow's historians will consider today's greatest inventors.

The same prescient mind that dreamed up the Human Genome Project now devotes days to what Davis calls "the last great disease to conquer."

He may need all his brilliance to save his son.

But then his son got sick, and his priorities changed

Davis and Dafoe raised their two children in a quiet Palo Alto neighborhood. Each year they backpacked as a family in California's Sierra mountains, disappearing for weeks at a time.

"I carried Whitney up there when he was young," Davis says. On one of these trips 5-year-old Whitney impressed his father by walking nine miles in a single day. On another Sierras trip their baby daughter Ashley took her first steps at 5,000 feet above sea level.

"I haven't gone in 10 years now," Davis says. "I would love to do that with Whitney again."

By 2008, Whitney, was 24 and living in a small town in Nevada, knocking on doors for then-Sen. Barack Obama's presidential campaign.

But he often complained about being exhausted. A skilled photographer, Whitney captured images at Obama's inauguration in 2009, but even then he could no longer work a full day.

After years of declining health, seeing numerous doctors and not getting answers, Whitney was finally diagnosed with ME/CFS.

As his health worsened, he moved in with his parents in May 2011. He tried to keep working as a wedding photographer but soon gave that up because he needed a week to recover from shooting a single wedding. He soon became mostly bedridden.

In his last post on his photography website, Whitney lamented that "chronic fatigue syndrome" couldn't do justice to his condition. He preferred "total body shutdown."

Whitney has lost the ability to speak -- something a very small fraction of ME/CFS patients experience. Dafoe says he used to communicate with the family via text messages, but that skill is now lost too, as even the glow of a smartphone screen is too much stimulation for him. The heart emojis he sent to his caregivers are just memories now.

Eventually he could no longer eat solid food.

In one of his last texts to his parents, he wrote, "I'm sorry I'm ruining your golden years."

To seek a cure, Davis recruited a dream team of researchers

Over a life spent at the frontiers of science, Davis has collaborated with many accomplished researchers. He's cashing in on those relationships now in building a world-class team he hopes can find the molecular basis for ME/CFS.

"I made phone calls, and everybody I called said yes," Davis says.

Among those who picked up the phone were two Nobel Laureates: Paul Berg, who won the chemistry prize in 1980, and Mario R. Capecchi, who won it in the "Physiology or Medicine" category in 2007.

Some of his colleagues had never heard of the disease. He told them it affected 1% of the population, or about one in 300 Americans. He told them the National Institutes of Health at the time was dedicating less than $6 million annually to researching the disorder.

That poses a challenge in tackling an illness that lacks an FDA-approved treatment, doesn't have a known cause or a singular lab test for clinicians to diagnose it. ME/CFS has lagged behind in the bio-medical imagination compared with cousins like multiple sclerosis, which also affects the immune system and the nervous system.

Following outbreaks in the 1980s, some dismissively called chronic fatigue syndrome the "yuppie flu."

But its symptoms, which include constant exhaustion, pain, brain fog and unrefreshing sleep, can be as disabling as late-stage cancer. Taking a shower may leave someone with ME/CFS bed-bound and unable to do anything for days.

In 2017, NIH doubled its research spending on the disease to $12 million. But Davis argues that compared to other diseases of similar severity and prevalence, that's not nearly enough. Multiple sclerosis, a disease that affects fewer patients than ME/CFS, attracts more than $100 million a year in NIH-funded research.

Davis now regularly convenes top scientists via an advisory board he set up through the Open Medicine Foundation, a California-based non-profit that's raised $18 million to research the disease. Its hub is Davis' Stanford Genome Technology Center, making Davis unique among living scientists in his ability to coordinate the discovery of a cure.

But to make the kind of progress he and his colleagues envision, they need a lot more money.

They are making slow but steady progress

ME/CFS patients, like those with multiple sclerosis and other diseases, fall on a spectrum. Some are still able to go to an office and work, while others are bedridden 23 or more hours a day.

At research conferences, Davis sometimes sits and talks with ME/CFS patients for hours.

"I'm very sympathetic to them," he says. "It makes me feel that I have to solve this, but not in an arrogant way. I just know I have to put every ounce of energy into this to help all the patients, which also include my son."

Davis and Dafoe know there's a vibrant mind and spirit alive in their son's weakened body. Whitney is a devout Buddhist, and their house is strewn with prayer flags. Dafoe thinks Whitney spends much of his day meditating.

When Whitney's younger sister Ashley got married, Dafoe pointed to the ring on her finger to pantomime the happy news to her son. The two siblings had been very close. Whitney didn't speak, but held his hands to his heart and wept with joy.

At Davis' lab, Whitney's blood samples are among many churning away in sequencing machines, contributing to what his organization believes is the deepest study of ME/CFS patients ever attempted.

This wouldn't be the first time Davis has set his sights on a problem the scientific establishment found unsolvable. "You have to look for those," he says.

He and his team have been hard at work the past few years. One of their inventions, a "nanoneedle" for testing blood, speaks to the need to find a single biomarker in patients' blood.

A blood test which identifies a specific molecular abnormality unique to ME/CFS patients has long been a sticking point in researchers' quest to get the disease more recognized. Having one could spur more drug development, because pharmaceutical companies would understand the root of what's wrong with patients.

Davis' team has tested their nanoneedle with initial success and recently published their findings in a scholarly journal. They discovered ME/CFS patients' blood responds to the introduction of "stress" -- in this case, salt -- differently than the blood of healthy people. Davis hopes the device will ultimately produce a cheap clinical test by which doctors can identify ME/CFS quickly and accurately.

He also wants to explore measures to prevent the disease. For example, he wants to understand why people with mononucleosis often develop ME/CFS.

Those are just a few of many things Davis' team are working on.

"We don't have enough money, so we have to prioritize," he says.

Davis flew to Washington in early April for a symposium about ME/CFS. He almost didn't make the trip because it would leave his wife at home alone, caring for Whitney while she had the flu.

But she told him he had to go.

Caring for Whitney is a daily ritual

Davis and Dafoe sometimes wait for hours outside Whitney's room, peering through a keyhole to see whether he has assumed a position in bed indicating it's all right to come in. With words no longer an option, they must interpret Whitney's postures and occasional hand signals.

Six times each day, every day, they perform this ritual, silently, dutifully, shut off from the gaze of the world.

They start around 2:30 p.m., first hooking up Whitney's IV. On the next entry into his room, they hook up the pump for the "j-tube" that will send nutrients directly into their son's stomach.

On the third visit, they wash and clean the small plastic vessels next to Whitney's bed that he uses as urinals. Next they come back in to put the urinals on Whitney's stomach for when he's ready to use them again. On their last visit, often around 2:30 a.m., they'll put ice on Whitney's stomach to help soothe his excruciating digestive pains.

"I feel like I'm living in a different world. It's hard to say anything when people ask 'how are you doing?'" Dafoe says. "Our world has just been consumed by a chronic illness."

There's a disciplined intentionality behind their movements. For Whitney, the tiniest deviation in their procedure can be devastating.

"His cognitive processes don't work right," Dafoe says. She and her husband wear plain shirts with no lettering when they're in Whitney's room because the sliver of energy it takes his brain to process a word can cause him to crash. They even use tape to cover labels on tubes of Neosporin.

Such crashes cause Whitney severe stomach pain, which make it impossible for them to put more food in his feeding tube.

Dafoe wants her husband to get enough sleep so that he can stay fresh and focused on researching the disease. That means on many nights she's up until 5 or 6 a.m. helping Whitney.

By 5 p.m. she's back to caring for her son.

They hope their son's suffering can have a greater purpose

"I got a PhD. That was hard," Dafoe says. "I've climbed mountains. That was hard."

But she says enduring Whitney's illness is the most difficult thing she's done in her life, "by a factor of thousands."

One simple truth guides her. "He's my son. I just love him."

Dafoe receives messages from ME/CFS patients all over the world who say they are inspired by her husband and alarmed by her son's severe condition. She says she feels like a mother to these people, many of whom are suicidal -- a rational response to a life spent hovering just above death.

Many tell her Whitney is their north star. They say if he can go on living through hell, year after year, then their suffering must be endurable too.

"He's saving lives," Dafoe says. "Just by lying there."

Nearly all her and her husband's communication with Whitney is through pantomimed gestures. If he wants more of something he'll hold his hands together, then bring them apart.

But every so often the fog lifts a little and Davis and Dafoe can speak more complex ideas aloud to Whitney. A few months ago, they told him how prominent his father has become in the field of scientists researching his disease.

"He was really excited about that," Dafoe says.

Whitney punched the air like a boxer, signaling that he intends to fight on.

Ryan Prior is a cross-platform associate producer at CNN. He was diagnosed with chronic fatigue syndrome in 2007 and wrote about that experience here.

Thursday, 9 May 2019

Who hath blessed us with all spiritual blessings


C H Spurgeon's Morning Devotional for 9th May

"Who hath blessed us with all spiritual blessings."

Ephesians 1:3

All the goodness of the past, the present, and the future, Christ bestows upon His people. In the mysterious ages of the past the Lord Jesus was His Father's first elect, and in His election He gave us an interest, for we were chosen in Him from before the foundation of the world. He had from all eternity the prerogatives of Sonship, as His Father's only-begotten and well-beloved Son, and He has, in the riches of His grace, by adoption and regeneration, elevated us to sonship also, so that to us He has given "power to become the sons of God." The eternal covenant, based upon suretiship and confirmed by oath, is ours, for our strong consolation and security. In the everlasting settlements of predestinating wisdom and omnipotent decree, the eye of the Lord Jesus was ever fixed on us; and we may rest assured that in the whole roll of destiny there is not a line which militates against the interests of His redeemed. The great betrothal of the Prince of Glory is ours, for it is to us that He is affianced, as the sacred nuptials shall ere long declare to an assembled universe. The marvellous incarnation of the God of heaven, with all the amazing condescension and humiliation which attended it, is ours. The bloody sweat, the scourge, the cross, are ours for ever. Whatever blissful consequences flow from perfect obedience, finished atonement, resurrection, ascension, or intercession, all are ours by His own gift. Upon His breastplate he is now bearing our names; and in His authoritative pleadings at the throne He remembers our persons and pleads our cause. His dominion over principalities and powers, and His absolute majesty in heaven, He employs for the benefit of them who trust in Him. His high estate is as much at our service as was His condition of abasement. He who gave Himself for us in the depths of woe and death, doth not withdraw the grant now that He is enthroned in the highest heavens.

Monday, 6 May 2019

CBT for ME/CFS is not effective


Cognitive behavioural therapy for myalgic encephalomyelitis/chronic fatigue syndrome is not effective. Re-analysis of a Cochrane review

Mark Vink, Alexandra Vink-Niese

First Published May 2, 2019

Abstract

Analysis of the 2008 Cochrane review of cognitive behavioural therapy for chronic fatigue syndrome shows that seven patients with mild chronic fatigue syndrome need to be treated for one to report a small, short-lived subjective improvement of fatigue. This is not matched by an objective improvement of physical fitness or employment and illness benefit status. Most studies in the Cochrane review failed to report on safety or adverse reactions. Patient evidence suggests adverse outcomes in 20 per cent of cases. If a trial of a drug or surgical procedure uncovered a similar high rate, it would be unlikely to be accepted as safe. It is time to downgrade cognitive behavioural therapy to an adjunct support-level therapy, rather than a treatment for chronic fatigue syndrome.

Introduction

For years, the recommended treatments for chronic fatigue syndrome (CFS) have been cognitive behavioural therapy (CBT) and graded exercise therapy (GET). These recommendations have been based on Cochrane reviews (Larun et al., 2017; Price et al., 2008) and a large randomised controlled trial by White et al. (2011), informally referred to as the PACE trial (‘Pacing, graded Activity, and Cognitive behaviour therapy; a randomised Evaluation’). This trial concluded that CBT and GET were moderately effective treatments, leading to recovery in 22 per cent of patients. Due to its size (n = 640) and promotion, it has been very influential in the promotion of CBT and GET as effective treatments for CFS (Wilshire et al., 2018b). Recently, a number of re-analyses of the PACE trial, including a special issue of the Journal of Health Psychology (Marks, 2017), have raised significant concerns with the published outcomes of the trial. If the PACE trial had not made a significant number of outcome changes, which led to an overlap in entry and recovery criteria, then there would not have been a difference in recovery rate between CBT and GET and the two control groups (no treatment (specialist medical care) and adaptive pacing therapy) (Geraghty, 2017a; Vink, 2016; Wilshire et al., 2018b). Essentially, the recovery rate would have been the same as the natural occurring one (Cairns and Hotopf, 2005). The absence of objective improvement in the PACE trial (fitness and 6-minute walk test (6MWT)) and the increase in illness and unemployment benefits, matched the findings from the evaluation of the use of CBT and GET in the Belgium CFS knowledge centres (Stordeur et al., 2008). As noted by O’Leary (2018), ‘although PACE [has] dictated management of ME/CFS across the globe for many years, the study fails to meet basic standards of scientific methodology’. ‘Indeed, it is difficult to imagine how such a large-scale investigation could have developed, proceeded and passed through the review process unless its scientific failings were actually characteristic of its field’. Analysis of the Dutch FITNET trial of Internet CBT for adolescents (Ghatineh and Vink, 2017), of the Dutch FatiGo trial of multidisciplinary rehabilitation treatment (Vink and Vink-Niese, 2018a) and of five Dutch hallmark CBT studies (Twisk and Corsius, 2017) supported this observation. A recent re-analysis of the Cochrane exercise review for CFS (Vink and Vink-Niese, 2018b) revealed a number of methodological concerns with many of the studies reviewed as part of the Cochrane review of GET for CFS and a lack of objective evidence for improvement in physical function. It also showed that the problems noted by O’Leary are not confined to Dutch studies. O’Leary also concluded that ‘the PACE controversy suggests a need to evaluate the scientific credibility of psychosomatic medicine generally’. As such, we carried out an analysis of the Cochrane review of CBT treatment for CFS by Price et al. (2008), to ascertain if this review contained any of the problems identified in Vink and Vink-Niese (2018b), by O’Leary (2018) or Geraghty (2017a) and also to assess whether or not the conclusions of this Cochrane review – that CBT is somewhat effective with moderate size effects – is justified by the data contained within the primary studies included in the review. In our analysis, we concentrated on the objective outcome measures to establish if improvements in self-report (fatigue) translate to observable improvement in objective tests (physical ability, fitness, etc.) as there is an inverse relationship between fatigue and physical activity (Rongen-van Dartel et al., 2014).

To read the references and rest of this article, please go to –


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Wednesday, 1 May 2019

Something in the blood

https://mecfsresearchreview.me/2019/04/25/something-in-the-blood/


Remarkably, four independent groups have now found evidence that a factor in the blood can affect cell metabolism/mitochondria in ME/CFS and transfer the effect to healthy cells. Here is a summary of the provisional findings.


The first to find the effect were Dr Oystein Fluge and Professor Olav Mella in 2016.

They were studying energy production in the cell, a logical thing to do when trying to understand an illness where energy is in such short supply.

Cells have two ways to convert food molecules into usable energy. Glycolysis is a process in the cell cytoplasm that extracts a small amount of energy from carbohydrate molecules, producing lactate. But the real houses of energy production are mitochondria, which burn up food molecules with oxygen, producing large amounts of usable fuel.

Fluge and Mella used an expensive bit of kit called the Seahorse analyser, which measures glycolysis through the lactate production and mitochondrial activity through changes in oxygen levels.

They tested normal healthy muscle cells that had been grown in the lab. But they added to those cells serum taken from either ME/CFS patients or healthy controls. Serum is the fluid left over after blood has clotted and it contains small molecules and other soluble substances.

They have data for 12 people with ME/CFS and 12 healthy controls, a relatively small sample.

What they found was, surprisingly, that the muscle cells produced more lactate and burned more oxygen when they were incubated with ME/CFS serum than when incubated in serum from healthy controls. And the effect was particularly strong when the cells were made to work hard.

So something in the serum (which comes from blood) of ME/CFS patients is affecting healthy cells, and somehow making them work harder.

This is the only published study to date, but three other groups have revealed related findings at conferences.

Ron Davis

Dr Ron Davis provided the most dramatic demonstration of the effect in a plasma swap experiment using his nanoneedle test. Plasma is the liquid left over when solid matter has been removed from blood: the the red and white blood cells, and platelets.

The nanoneedle chip measures electrical impedance of cells. In the presence of salt (which stresses the cells because they have to use energy to pump the salt out) the impedance of cells in ME/CFS blood increases much more than cells in blood taken from healthy controls.

Davis’s group then ran an elegant experiment using this set up. They put blood cells from healthy donors in plasma from ME/CFS patients and found that the healthy cells behaved like ME/CFS ones did, with a big increase in electrical impedance. And when they put ME/CFS cells in plasma from healthy controls, they found that these ME/CFS cells behave like healthy cells.

So plasma from ME/CFS patients makes healthy cells behave like ME/CFS ones. And plasma from healthy controls makes ME/CFS cells behave like healthy ones. These are stunning findings.

We don’t know the sample size for this study but hopefully more details will be available soon as a paper has been accepted for publication in the Journal PNAS.

Karl Morten, Oxford university

Like Fluge and Mella, Dr Karl Morten looked at mitochondria/energy metabolism in lab grown muscle cells and also saw an effect.

His group used a molecular probe to measure oxygen concentration within cells to track the activity of mitochondria.

They found that adding plasma from healthy controls made no difference to oxygen levels of the muscle cells. But adding plasma from ME/CFS patients caused oxygen levels to fall, indicating that the mitochondria were working harder (a similar result to Fluge and Mella).

Morton said he didn’t know why the mitochondria were working harder: he said it might be that they were working less efficiently, but the goal was to find out.

The study used over 30 patients and Morton noted that on average the levels were lower for patients than for controls. He suggested this might be due to a subgroup effect, where only some patients had the effect, with around a third of patients scoring below the lowest oxygen level for healthy controls.

Bhupesh Prusty, Wuerzburg university

Dr Bhupesh Prusty has also looked at the effect of a blood factor on mitochondria, but his work focuses on a less well-known role of mitochondria, in immunity against viruses.

Although mitochondria are normally shown as single bacteria- or bean-like units, the reality is more complex. In living cells, mitochondria constantly fuse together and separate, and the fact that they are often fused together, like a string of beans, is important for their ability to fight viruses.

Some viruses, including HHV-6, fight back by causing mitochondria to fragment back into their single forms, reducing their ability to fight viruses.

Serum from ME/CFS patients causes mitochondria that were fused together to fragment, whereas plasma from healthy controls does not.

So far, the group have only looked at five patients and three controls, so these are very provisional results.

In a separate experiment, his group showed that the effect was reversible (they washed away patient serum after three days and mitochondria gradually resumed normal fusing behaviour).

So…

Fluge’s and Morten’s studies are directly linked to energy metabolism. Davis’s is indirectly: the salt added to the nanoneedle test forces the cell to use energy pumping sodium out of the cell. The Prusty research looks at mitochondria, but the changes in morphology are apparently linked to cell defence rather than to energy production.

At the recent NIH conference, Ron Davis said that their work indicates that the factor in the blood responsible for all this are exosomes, tiny membrane-bound packets of biomolecules released by cells. Exosomes are a type of extracellular vesicle, and these are taken up by cells and are believed to be involved in cell to cell communication, though their role is as yet unclear. Extracellular vesicles are being studied by Dr Maureen Hanson as part of her collaborative’s work.

So we have four groups finding that a factor in ME/CFS blood that has an effect on cells. These are still early days: only one study has been published so far, the sample sizes are relatively small and the findings need to be confirmed. But if things pan out, this development could prove to be an important step in understanding the biology of at least some types of ME/CFS.